Commentary

Rumination syndrome is a well-recognized functional disorder characterized by the regurgitation of food or liquid in the absence of retching or nausea.

Evidence suggests that the prevalence of rumination syndrome is increasing. In a 2022 health survey study conducted across 26 countries — the largest epidemiologic study to date on rumination syndrome — investigators reported that it had a global prevalence of 3.1% in adults. This was higher than reported in most prior country-specific studies. More recently, a systematic review and meta-analysis from 2024 reported the pooled prevalence of rumination syndrome as 3.7% in adults and 0.4% in children. Both reports noted that female gender, anxiety, and depression were independent risk factors associated with rumination syndrome.

Recognition of this disorder is crucial in order for clinicians to better diagnose and manage it in their patients.
 

Making the Diagnosis

The diagnosis of rumination syndrome is currently based on the Rome IV consensus criteria, which were last updated in 2016. These include three diagnostic criteria essential to remember as discriminant for rumination syndrome:

• Regurgitation is the effortless return of gastric contents (recognizable food) retrograde back into the esophagus and/or mouth.
• This is not preceded by retching and not associated with nausea.
• These symptoms must have started at least 6 months before evaluation, been evident over the past 3 months, and occurred at least two to three times per month.

Although this diagnosis will be highly suspected after taking an astute clinical history, you will still need to rule out the presence of underlying organic disease.

Nearly one quarter of patients with eating disorders — which commonly accompany gastrointestinal disorders — will not have been diagnosed by the time they visit with a gastroenterologist. Therefore, gastroenterologists should be vigilant in screening for eating disorders. Notably, severe weight loss, malnutrition, electrolyte abnormalities, and dental erosions (due to acid etching) are uncommon in rumination syndrome. If such symptoms are present, it increases the possibility of an underlying eating disorder rather than primary regurgitation.

Previously, there were no published, validated questionnaires to assess the diagnosis or symptomatic response to therapies for rumination syndrome. This has recently changed with the development of a novel eight-point questionnaire that assesses frequency, severity, type of regurgitant, timing of regurgitation in relation to the meal, weight loss, and use of and response to proton pump inhibitors.

This questionnaire was recently implemented in five patients diagnosed with rumination syndrome. Albeit an extremely small trial, it nonetheless showed clinical improvement in scores associated with therapeutic intervention. Further evaluation of this tool is needed.

The diagnosis of rumination syndrome can be confirmed using impedance manometry in persons with evidence of reflux extending to the proximal esophagus, which is associated with an intragastric pressure > 30 mmHg in adults or > 25 mmHg in children. 

Gastric emptying studies are typically not required to make a diagnosis unless the clinical symptoms are atypical and an alternative motility disorder is suspected. Endoscopy is performed to rule out a mechanical disorder.
 

Histopathologic Evidence

New data indicate that there may be specific histologic changes associated with rumination syndrome. A 2023 meta-analysis reported that patients with rumination syndrome had duodenal histologic evidence of increased lymphocytes and eosinophils, which have been associated with epithelial barrier dysfunction, microbial changes, and systemic immune activation in eosinophilic duodenitis.

If these histologic changes are validated, they may suggest future novel diagnostic and treatment approaches, at least for a subset of people with rumination syndrome.
 

Best Available Treatments

The first-line therapeutic treatment for rumination syndrome is diaphragmatic breathing.

I recommended using diaphragmatic breathing for this indication in a previous commentary, in which I noted that it can essentially serve as yoga for the diaphragm and abdominal muscles and advised patients to focus on breathing “through” their belly button.

Patients are instructed to breath in through their nose for 4-6 seconds, hold their breath for 2-3 seconds, and then breath out slowly against pursed lips. They can be supine or upright but should sense their abdominal muscles expand with inhaling, not move their chest wall, and completely relax their abdominal muscles upon exhaling.

Although there is no standard frequency or duration for diaphragmatic breathing, I routinely recommend patients try it after each meal for 10-15 minutes and, if possible, more during the day and in times of stress or anxiety.

Cognitive-behavioral therapies have been shown to be effective alternatives to diaphragmatic breathing.

There is some evidence that hypnosis and biofeedback-guided control of abdominothoracic muscle activity can also be effective options in treating rumination syndrome.

Robust data on pharmacologic treatments for rumination syndrome are lacking, with the exception of a randomized crossover study of baclofen. In this study, baclofen (10 mg three times daily) was significantly more effective than placebo (P = .04) in reducing regurgitation events. Investigators theorized that baclofen counteracts transient lower esophageal sphincter (LES) relaxations by increasing basal LES pressure, thereby potentially reducing regurgitation episodes. The most notable treatment side effects were somnolence, confusion, and dizziness, which may limit its extended use.
 

A Potentially Reversible Habit

Rumination syndrome is considered an acquired habit and, therefore, should be reversible.

Although there is no recent evidence in the literature that rumination syndrome contributes to a reduced survival rate, older data suggested adult mortality rates of 12%-20% (mostly in patients who were institutionalized). Additionally, rumination syndrome has been shown to diminish quality of life.

The best approach to improving the clinical outcomes of patients with rumination syndrome is to enlist a collaborative interprofessional team that includes physicians, behavioral therapists, and nurses to coordinate and optimize existing treatment strategies.

David A. Johnson, MD, is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He has disclosed the following relevant financial relationships: advisor to ISOTHRIVE and Johnson & Johnson.

A version of this article first appeared on Medscape.com.

Rumination syndrome is a well-recognized functional disorder characterized by the regurgitation of food or liquid in the absence of retching or nausea.

Evidence suggests that the prevalence of rumination syndrome is increasing. In a 2022 health survey study conducted across 26 countries — the largest epidemiologic study to date on rumination syndrome — investigators reported that it had a global prevalence of 3.1% in adults. This was higher than reported in most prior country-specific studies. More recently, a systematic review and meta-analysis from 2024 reported the pooled prevalence of rumination syndrome as 3.7% in adults and 0.4% in children. Both reports noted that female gender, anxiety, and depression were independent risk factors associated with rumination syndrome.

Recognition of this disorder is crucial in order for clinicians to better diagnose and manage it in their patients.
 

Making the Diagnosis

The diagnosis of rumination syndrome is currently based on the Rome IV consensus criteria, which were last updated in 2016. These include three diagnostic criteria essential to remember as discriminant for rumination syndrome:

• Regurgitation is the effortless return of gastric contents (recognizable food) retrograde back into the esophagus and/or mouth.
• This is not preceded by retching and not associated with nausea.
• These symptoms must have started at least 6 months before evaluation, been evident over the past 3 months, and occurred at least two to three times per month.

Although this diagnosis will be highly suspected after taking an astute clinical history, you will still need to rule out the presence of underlying organic disease.

Nearly one quarter of patients with eating disorders — which commonly accompany gastrointestinal disorders — will not have been diagnosed by the time they visit with a gastroenterologist. Therefore, gastroenterologists should be vigilant in screening for eating disorders. Notably, severe weight loss, malnutrition, electrolyte abnormalities, and dental erosions (due to acid etching) are uncommon in rumination syndrome. If such symptoms are present, it increases the possibility of an underlying eating disorder rather than primary regurgitation.

Previously, there were no published, validated questionnaires to assess the diagnosis or symptomatic response to therapies for rumination syndrome. This has recently changed with the development of a novel eight-point questionnaire that assesses frequency, severity, type of regurgitant, timing of regurgitation in relation to the meal, weight loss, and use of and response to proton pump inhibitors.

This questionnaire was recently implemented in five patients diagnosed with rumination syndrome. Albeit an extremely small trial, it nonetheless showed clinical improvement in scores associated with therapeutic intervention. Further evaluation of this tool is needed.

The diagnosis of rumination syndrome can be confirmed using impedance manometry in persons with evidence of reflux extending to the proximal esophagus, which is associated with an intragastric pressure > 30 mmHg in adults or > 25 mmHg in children. 

Gastric emptying studies are typically not required to make a diagnosis unless the clinical symptoms are atypical and an alternative motility disorder is suspected. Endoscopy is performed to rule out a mechanical disorder.
 

Histopathologic Evidence

New data indicate that there may be specific histologic changes associated with rumination syndrome. A 2023 meta-analysis reported that patients with rumination syndrome had duodenal histologic evidence of increased lymphocytes and eosinophils, which have been associated with epithelial barrier dysfunction, microbial changes, and systemic immune activation in eosinophilic duodenitis.

If these histologic changes are validated, they may suggest future novel diagnostic and treatment approaches, at least for a subset of people with rumination syndrome.
 

Best Available Treatments

The first-line therapeutic treatment for rumination syndrome is diaphragmatic breathing.

I recommended using diaphragmatic breathing for this indication in a previous commentary, in which I noted that it can essentially serve as yoga for the diaphragm and abdominal muscles and advised patients to focus on breathing “through” their belly button.

Patients are instructed to breath in through their nose for 4-6 seconds, hold their breath for 2-3 seconds, and then breath out slowly against pursed lips. They can be supine or upright but should sense their abdominal muscles expand with inhaling, not move their chest wall, and completely relax their abdominal muscles upon exhaling.

Although there is no standard frequency or duration for diaphragmatic breathing, I routinely recommend patients try it after each meal for 10-15 minutes and, if possible, more during the day and in times of stress or anxiety.

Cognitive-behavioral therapies have been shown to be effective alternatives to diaphragmatic breathing.

There is some evidence that hypnosis and biofeedback-guided control of abdominothoracic muscle activity can also be effective options in treating rumination syndrome.

Robust data on pharmacologic treatments for rumination syndrome are lacking, with the exception of a randomized crossover study of baclofen. In this study, baclofen (10 mg three times daily) was significantly more effective than placebo (P = .04) in reducing regurgitation events. Investigators theorized that baclofen counteracts transient lower esophageal sphincter (LES) relaxations by increasing basal LES pressure, thereby potentially reducing regurgitation episodes. The most notable treatment side effects were somnolence, confusion, and dizziness, which may limit its extended use.
 

A Potentially Reversible Habit

Rumination syndrome is considered an acquired habit and, therefore, should be reversible.

Although there is no recent evidence in the literature that rumination syndrome contributes to a reduced survival rate, older data suggested adult mortality rates of 12%-20% (mostly in patients who were institutionalized). Additionally, rumination syndrome has been shown to diminish quality of life.

The best approach to improving the clinical outcomes of patients with rumination syndrome is to enlist a collaborative interprofessional team that includes physicians, behavioral therapists, and nurses to coordinate and optimize existing treatment strategies.

David A. Johnson, MD, is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He has disclosed the following relevant financial relationships: advisor to ISOTHRIVE and Johnson & Johnson.

A version of this article first appeared on Medscape.com.

Rumination syndrome is a well-recognized functional disorder characterized by the regurgitation of food or liquid in the absence of retching or nausea.

Evidence suggests that the prevalence of rumination syndrome is increasing. In a 2022 health survey study conducted across 26 countries — the largest epidemiologic study to date on rumination syndrome — investigators reported that it had a global prevalence of 3.1% in adults. This was higher than reported in most prior country-specific studies. More recently, a systematic review and meta-analysis from 2024 reported the pooled prevalence of rumination syndrome as 3.7% in adults and 0.4% in children. Both reports noted that female gender, anxiety, and depression were independent risk factors associated with rumination syndrome.

Recognition of this disorder is crucial in order for clinicians to better diagnose and manage it in their patients.
 

Making the Diagnosis

The diagnosis of rumination syndrome is currently based on the Rome IV consensus criteria, which were last updated in 2016. These include three diagnostic criteria essential to remember as discriminant for rumination syndrome:

• Regurgitation is the effortless return of gastric contents (recognizable food) retrograde back into the esophagus and/or mouth.
• This is not preceded by retching and not associated with nausea.
• These symptoms must have started at least 6 months before evaluation, been evident over the past 3 months, and occurred at least two to three times per month.

Although this diagnosis will be highly suspected after taking an astute clinical history, you will still need to rule out the presence of underlying organic disease.

Nearly one quarter of patients with eating disorders — which commonly accompany gastrointestinal disorders — will not have been diagnosed by the time they visit with a gastroenterologist. Therefore, gastroenterologists should be vigilant in screening for eating disorders. Notably, severe weight loss, malnutrition, electrolyte abnormalities, and dental erosions (due to acid etching) are uncommon in rumination syndrome. If such symptoms are present, it increases the possibility of an underlying eating disorder rather than primary regurgitation.

Previously, there were no published, validated questionnaires to assess the diagnosis or symptomatic response to therapies for rumination syndrome. This has recently changed with the development of a novel eight-point questionnaire that assesses frequency, severity, type of regurgitant, timing of regurgitation in relation to the meal, weight loss, and use of and response to proton pump inhibitors.

This questionnaire was recently implemented in five patients diagnosed with rumination syndrome. Albeit an extremely small trial, it nonetheless showed clinical improvement in scores associated with therapeutic intervention. Further evaluation of this tool is needed.

The diagnosis of rumination syndrome can be confirmed using impedance manometry in persons with evidence of reflux extending to the proximal esophagus, which is associated with an intragastric pressure > 30 mmHg in adults or > 25 mmHg in children. 

Gastric emptying studies are typically not required to make a diagnosis unless the clinical symptoms are atypical and an alternative motility disorder is suspected. Endoscopy is performed to rule out a mechanical disorder.
 

Histopathologic Evidence

New data indicate that there may be specific histologic changes associated with rumination syndrome. A 2023 meta-analysis reported that patients with rumination syndrome had duodenal histologic evidence of increased lymphocytes and eosinophils, which have been associated with epithelial barrier dysfunction, microbial changes, and systemic immune activation in eosinophilic duodenitis.

If these histologic changes are validated, they may suggest future novel diagnostic and treatment approaches, at least for a subset of people with rumination syndrome.
 

Best Available Treatments

The first-line therapeutic treatment for rumination syndrome is diaphragmatic breathing.

I recommended using diaphragmatic breathing for this indication in a previous commentary, in which I noted that it can essentially serve as yoga for the diaphragm and abdominal muscles and advised patients to focus on breathing “through” their belly button.

Patients are instructed to breath in through their nose for 4-6 seconds, hold their breath for 2-3 seconds, and then breath out slowly against pursed lips. They can be supine or upright but should sense their abdominal muscles expand with inhaling, not move their chest wall, and completely relax their abdominal muscles upon exhaling.

Although there is no standard frequency or duration for diaphragmatic breathing, I routinely recommend patients try it after each meal for 10-15 minutes and, if possible, more during the day and in times of stress or anxiety.

Cognitive-behavioral therapies have been shown to be effective alternatives to diaphragmatic breathing.

There is some evidence that hypnosis and biofeedback-guided control of abdominothoracic muscle activity can also be effective options in treating rumination syndrome.

Robust data on pharmacologic treatments for rumination syndrome are lacking, with the exception of a randomized crossover study of baclofen. In this study, baclofen (10 mg three times daily) was significantly more effective than placebo (P = .04) in reducing regurgitation events. Investigators theorized that baclofen counteracts transient lower esophageal sphincter (LES) relaxations by increasing basal LES pressure, thereby potentially reducing regurgitation episodes. The most notable treatment side effects were somnolence, confusion, and dizziness, which may limit its extended use.
 

A Potentially Reversible Habit

Rumination syndrome is considered an acquired habit and, therefore, should be reversible.

Although there is no recent evidence in the literature that rumination syndrome contributes to a reduced survival rate, older data suggested adult mortality rates of 12%-20% (mostly in patients who were institutionalized). Additionally, rumination syndrome has been shown to diminish quality of life.

The best approach to improving the clinical outcomes of patients with rumination syndrome is to enlist a collaborative interprofessional team that includes physicians, behavioral therapists, and nurses to coordinate and optimize existing treatment strategies.

David A. Johnson, MD, is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He has disclosed the following relevant financial relationships: advisor to ISOTHRIVE and Johnson & Johnson.

A version of this article first appeared on Medscape.com.

Should we now recommend continuous glucose monitoring to all our patients, even those without diabetes? Most of us would instinctively say “no” to this question, but we are seeing opinions from doctors recommending it, and in recent years, scientific literature has focused on the subject. 

Today, anyone can get an arm patch that continuously measures interstitial glucose, which is closely related to blood sugar. The information can be read on a dedicated reader or on a mobile phone by scanning the patch or, with some models, without even doing anything.

There is a consensus for prescribing continuous glucose monitoring for patients with type 1 or type 2 diabetes who are treated with at least three insulin injections. Not only is the use of continuous glucose monitoring much more comfortable than self-monitoring with finger sticks, but continuous monitoring also helps reduce glycosylated hemoglobin while decreasing the risk for hypoglycemia. Recently, another indication has begun to be reimbursed in France: Type 2 diabetes under mono-insulin injection when the diabetes is not well controlled.

But alongside these situations, there are two questions that are worth considering.
 

Untreated Type 2 Diabetes 

First, is continuous glucose monitoring desirable for all patients with diabetes, even those not treated with insulin and even when blood sugar levels are well managed? Intuitively, one might think that it can’t hurt and that continuous monitoring of blood sugar can only improve things. We have some evidence supporting this idea, but the level of proof is quite weak. It is not clear that continuous monitoring can improve patients’ awareness of the impact of dietary choices or physical activity on blood sugar. Obviously, one can imagine that continuously monitoring glucose will encourage a shift toward more beneficial behaviors. But honestly, today, we do not have proof that wearing a continuous glucose monitor can improve behaviors in patients with type 2 diabetes who are treated with noninsulin antidiabetic medications.

Furthermore, a significant study has shown that while the effectiveness is more evident in patients treated with insulin, strong evidence suggests that continuous glucose monitoring could also reduce glycosylated hemoglobin in patients with type 2 diabetes who are not treated with insulin. A close examination of the results suggests that the benefits generally are less than those observed in insulin-treated patients with diabetes.

When we look at the scientific literature, two factors seem particularly important to consider if choosing to prescribe a continuous glucose monitoring sensor. The first is the method used, because the results can vary depending on the method. It appears that only self-monitoring that allows the patient to follow glucose in real time is effective, unlike blind monitoring that allows only a retrospective analysis of blood sugar levels. In the latter case, the patient wears the sensor, and after a week, 10 days, or 15 days, the results are analyzed, possibly with a health care provider. It seems that this is not very effective in improving glycosylated hemoglobin and dietary and physical activity behavior.

The second essential factor to consider is the need for an education program for the use of these sensors to be helpful. If sensors are used but nothing else is done, it does not seem logical. Seeing blood sugar levels without being able to understand them and act accordingly seems of little use. Scientific literature seems to confirm this idea. 
 

Patients Without Diabetes

Now there is another question. We have discussed patients with type 2 diabetes without insulin. It’s trendy to talk about the potential benefits of continuous glucose monitors in patients without diabetes. The idea is emerging that these monitors could be used to refine the diagnosis of diabetes or to better predict the onset of diabetes in the subsequent years.

Others claim that continuous glucose monitors are an effective way to induce a change in dietary and physical activity behaviors in patients with prediabetes. One can, for example, tell a patient, “You are at risk of developing diabetes, so by monitoring your glucose, you will change your behavior.” Honestly, the scientific data we have today do not support these ideas, and I sincerely believe that it is not advisable today to recommend, as some would like, the mass use of monitors, whether in patients with overweight or obesity, or in patients with prediabetes. This goes for suggestions for using the monitor for 7-10 days per year, in the form of a session to try to reduce the risk for diabetes by motivating patients to change their behavior. We have no evidence at all that this can work. And in my opinion, with this kind of discourse, we ultimately risk, as usual, encouraging patients who are already “fans” of self-checks and self-monitoring to get health data, even if they do not know how to interpret it. Maybe even the doctor they ask for interpretation will not be trained to interpret the results of these monitors.

Spreading the idea that monitors are useful for preventing diabetes has a side effect: It hinders progress on the essential issue. Today, one of the problems in diabetes and prediabetes is that screening is not done often enough, and 20% of patients with diabetes are still unaware of their diagnosis. The management of early diabetes or prediabetes, in my opinion, is not optimal in routine care today. So, I think that adding the idea that using monitors could be beneficial dilutes the main information.

Having said that, I sometimes offer continuous glucose monitoring to some of my patients on a case-by-case basis. I believe that with proper support and an educational program, it can be beneficial for certain patients.
 

In Practice

In summary, I am totally opposed to the normalization of the use of monitors. I think it is our role as health care professionals to warn the public that even if it is accessible — anyone can buy a reader, a sensor — it is not necessarily beneficial, and it may even distract us from what is essential. But as a specialist, I think that using a monitor within a genuine care plan seems reasonable. Ultimately, it’s just personalized medicine.

Dr. Hansel is an endocrinologist-diabetologist and nutritionist, Department of Diabetology-Endocrinology-Nutrition, Hôpital Bichat, and a university lecturer and hospital practitioner, Université Paris-Diderot, France. He discloses ties with Iriade, Sanofi-Aventis, and Amgen.

This story was translated from the Medscape French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Should we now recommend continuous glucose monitoring to all our patients, even those without diabetes? Most of us would instinctively say “no” to this question, but we are seeing opinions from doctors recommending it, and in recent years, scientific literature has focused on the subject. 

Today, anyone can get an arm patch that continuously measures interstitial glucose, which is closely related to blood sugar. The information can be read on a dedicated reader or on a mobile phone by scanning the patch or, with some models, without even doing anything.

There is a consensus for prescribing continuous glucose monitoring for patients with type 1 or type 2 diabetes who are treated with at least three insulin injections. Not only is the use of continuous glucose monitoring much more comfortable than self-monitoring with finger sticks, but continuous monitoring also helps reduce glycosylated hemoglobin while decreasing the risk for hypoglycemia. Recently, another indication has begun to be reimbursed in France: Type 2 diabetes under mono-insulin injection when the diabetes is not well controlled.

But alongside these situations, there are two questions that are worth considering.
 

Untreated Type 2 Diabetes 

First, is continuous glucose monitoring desirable for all patients with diabetes, even those not treated with insulin and even when blood sugar levels are well managed? Intuitively, one might think that it can’t hurt and that continuous monitoring of blood sugar can only improve things. We have some evidence supporting this idea, but the level of proof is quite weak. It is not clear that continuous monitoring can improve patients’ awareness of the impact of dietary choices or physical activity on blood sugar. Obviously, one can imagine that continuously monitoring glucose will encourage a shift toward more beneficial behaviors. But honestly, today, we do not have proof that wearing a continuous glucose monitor can improve behaviors in patients with type 2 diabetes who are treated with noninsulin antidiabetic medications.

Furthermore, a significant study has shown that while the effectiveness is more evident in patients treated with insulin, strong evidence suggests that continuous glucose monitoring could also reduce glycosylated hemoglobin in patients with type 2 diabetes who are not treated with insulin. A close examination of the results suggests that the benefits generally are less than those observed in insulin-treated patients with diabetes.

When we look at the scientific literature, two factors seem particularly important to consider if choosing to prescribe a continuous glucose monitoring sensor. The first is the method used, because the results can vary depending on the method. It appears that only self-monitoring that allows the patient to follow glucose in real time is effective, unlike blind monitoring that allows only a retrospective analysis of blood sugar levels. In the latter case, the patient wears the sensor, and after a week, 10 days, or 15 days, the results are analyzed, possibly with a health care provider. It seems that this is not very effective in improving glycosylated hemoglobin and dietary and physical activity behavior.

The second essential factor to consider is the need for an education program for the use of these sensors to be helpful. If sensors are used but nothing else is done, it does not seem logical. Seeing blood sugar levels without being able to understand them and act accordingly seems of little use. Scientific literature seems to confirm this idea. 
 

Patients Without Diabetes

Now there is another question. We have discussed patients with type 2 diabetes without insulin. It’s trendy to talk about the potential benefits of continuous glucose monitors in patients without diabetes. The idea is emerging that these monitors could be used to refine the diagnosis of diabetes or to better predict the onset of diabetes in the subsequent years.

Others claim that continuous glucose monitors are an effective way to induce a change in dietary and physical activity behaviors in patients with prediabetes. One can, for example, tell a patient, “You are at risk of developing diabetes, so by monitoring your glucose, you will change your behavior.” Honestly, the scientific data we have today do not support these ideas, and I sincerely believe that it is not advisable today to recommend, as some would like, the mass use of monitors, whether in patients with overweight or obesity, or in patients with prediabetes. This goes for suggestions for using the monitor for 7-10 days per year, in the form of a session to try to reduce the risk for diabetes by motivating patients to change their behavior. We have no evidence at all that this can work. And in my opinion, with this kind of discourse, we ultimately risk, as usual, encouraging patients who are already “fans” of self-checks and self-monitoring to get health data, even if they do not know how to interpret it. Maybe even the doctor they ask for interpretation will not be trained to interpret the results of these monitors.

Spreading the idea that monitors are useful for preventing diabetes has a side effect: It hinders progress on the essential issue. Today, one of the problems in diabetes and prediabetes is that screening is not done often enough, and 20% of patients with diabetes are still unaware of their diagnosis. The management of early diabetes or prediabetes, in my opinion, is not optimal in routine care today. So, I think that adding the idea that using monitors could be beneficial dilutes the main information.

Having said that, I sometimes offer continuous glucose monitoring to some of my patients on a case-by-case basis. I believe that with proper support and an educational program, it can be beneficial for certain patients.
 

In Practice

In summary, I am totally opposed to the normalization of the use of monitors. I think it is our role as health care professionals to warn the public that even if it is accessible — anyone can buy a reader, a sensor — it is not necessarily beneficial, and it may even distract us from what is essential. But as a specialist, I think that using a monitor within a genuine care plan seems reasonable. Ultimately, it’s just personalized medicine.

Dr. Hansel is an endocrinologist-diabetologist and nutritionist, Department of Diabetology-Endocrinology-Nutrition, Hôpital Bichat, and a university lecturer and hospital practitioner, Université Paris-Diderot, France. He discloses ties with Iriade, Sanofi-Aventis, and Amgen.

This story was translated from the Medscape French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Should we now recommend continuous glucose monitoring to all our patients, even those without diabetes? Most of us would instinctively say “no” to this question, but we are seeing opinions from doctors recommending it, and in recent years, scientific literature has focused on the subject. 

Today, anyone can get an arm patch that continuously measures interstitial glucose, which is closely related to blood sugar. The information can be read on a dedicated reader or on a mobile phone by scanning the patch or, with some models, without even doing anything.

There is a consensus for prescribing continuous glucose monitoring for patients with type 1 or type 2 diabetes who are treated with at least three insulin injections. Not only is the use of continuous glucose monitoring much more comfortable than self-monitoring with finger sticks, but continuous monitoring also helps reduce glycosylated hemoglobin while decreasing the risk for hypoglycemia. Recently, another indication has begun to be reimbursed in France: Type 2 diabetes under mono-insulin injection when the diabetes is not well controlled.

But alongside these situations, there are two questions that are worth considering.
 

Untreated Type 2 Diabetes 

First, is continuous glucose monitoring desirable for all patients with diabetes, even those not treated with insulin and even when blood sugar levels are well managed? Intuitively, one might think that it can’t hurt and that continuous monitoring of blood sugar can only improve things. We have some evidence supporting this idea, but the level of proof is quite weak. It is not clear that continuous monitoring can improve patients’ awareness of the impact of dietary choices or physical activity on blood sugar. Obviously, one can imagine that continuously monitoring glucose will encourage a shift toward more beneficial behaviors. But honestly, today, we do not have proof that wearing a continuous glucose monitor can improve behaviors in patients with type 2 diabetes who are treated with noninsulin antidiabetic medications.

Furthermore, a significant study has shown that while the effectiveness is more evident in patients treated with insulin, strong evidence suggests that continuous glucose monitoring could also reduce glycosylated hemoglobin in patients with type 2 diabetes who are not treated with insulin. A close examination of the results suggests that the benefits generally are less than those observed in insulin-treated patients with diabetes.

When we look at the scientific literature, two factors seem particularly important to consider if choosing to prescribe a continuous glucose monitoring sensor. The first is the method used, because the results can vary depending on the method. It appears that only self-monitoring that allows the patient to follow glucose in real time is effective, unlike blind monitoring that allows only a retrospective analysis of blood sugar levels. In the latter case, the patient wears the sensor, and after a week, 10 days, or 15 days, the results are analyzed, possibly with a health care provider. It seems that this is not very effective in improving glycosylated hemoglobin and dietary and physical activity behavior.

The second essential factor to consider is the need for an education program for the use of these sensors to be helpful. If sensors are used but nothing else is done, it does not seem logical. Seeing blood sugar levels without being able to understand them and act accordingly seems of little use. Scientific literature seems to confirm this idea. 
 

Patients Without Diabetes

Now there is another question. We have discussed patients with type 2 diabetes without insulin. It’s trendy to talk about the potential benefits of continuous glucose monitors in patients without diabetes. The idea is emerging that these monitors could be used to refine the diagnosis of diabetes or to better predict the onset of diabetes in the subsequent years.

Others claim that continuous glucose monitors are an effective way to induce a change in dietary and physical activity behaviors in patients with prediabetes. One can, for example, tell a patient, “You are at risk of developing diabetes, so by monitoring your glucose, you will change your behavior.” Honestly, the scientific data we have today do not support these ideas, and I sincerely believe that it is not advisable today to recommend, as some would like, the mass use of monitors, whether in patients with overweight or obesity, or in patients with prediabetes. This goes for suggestions for using the monitor for 7-10 days per year, in the form of a session to try to reduce the risk for diabetes by motivating patients to change their behavior. We have no evidence at all that this can work. And in my opinion, with this kind of discourse, we ultimately risk, as usual, encouraging patients who are already “fans” of self-checks and self-monitoring to get health data, even if they do not know how to interpret it. Maybe even the doctor they ask for interpretation will not be trained to interpret the results of these monitors.

Spreading the idea that monitors are useful for preventing diabetes has a side effect: It hinders progress on the essential issue. Today, one of the problems in diabetes and prediabetes is that screening is not done often enough, and 20% of patients with diabetes are still unaware of their diagnosis. The management of early diabetes or prediabetes, in my opinion, is not optimal in routine care today. So, I think that adding the idea that using monitors could be beneficial dilutes the main information.

Having said that, I sometimes offer continuous glucose monitoring to some of my patients on a case-by-case basis. I believe that with proper support and an educational program, it can be beneficial for certain patients.
 

In Practice

In summary, I am totally opposed to the normalization of the use of monitors. I think it is our role as health care professionals to warn the public that even if it is accessible — anyone can buy a reader, a sensor — it is not necessarily beneficial, and it may even distract us from what is essential. But as a specialist, I think that using a monitor within a genuine care plan seems reasonable. Ultimately, it’s just personalized medicine.

Dr. Hansel is an endocrinologist-diabetologist and nutritionist, Department of Diabetology-Endocrinology-Nutrition, Hôpital Bichat, and a university lecturer and hospital practitioner, Université Paris-Diderot, France. He discloses ties with Iriade, Sanofi-Aventis, and Amgen.

This story was translated from the Medscape French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

It’s time to renew two of my three narcotic prescribing licenses. For the first time in my career, I’ve waffled on whether the financial outlay to the US Drug Enforcement Agency (DEA) is worth it. 

At $888 each, I’ve considered letting two licenses lapse because I only work part-time in Montana. But several friends advised me to keep a “spare” in case I transfer to a new location. 

I thought about just paying the fees until I could do a little more research, but there is no mechanism for a refund unless I die within the first year of the 3-year cycle, provide incorrect credit card digits, or accidentally duplicate payments.

The renewal fee is just part of the issue.
 

Mandatory 8-Hour Training

I also received an alert about the requirement for more “narcotics prescribing education” thanks to the Medication Access and Training Expansion Act (MATE). 

The requirement seems counterintuitive because opioid prescribing has decreased for the 10th consecutive year, according to the AMA Overdose Epidemic Report. The continuing rise in overdose deaths is largely due to illegitimate manufacturing of synthetic opioids. 

I’ve written zero outpatient narcotics prescriptions in the past 6 years, and I’ve written very few in my 33 years of practice. My use is limited to intravenous morphine for flash pulmonary edema or refractory angina, but unless you graduated from a training program within 5 years of the June 2023 mandate or are boarded in addiction medicine, there is no way to escape the 8-hour education requirement.

The problem is that these courses are never just 8 hours in duration. After signing up for one such CME course that cost $150, I was still dying of boredom and at risk for DVT 4 days later. That’s how long it took to sit through.

Instead of the 30 seconds it should have taken to review the simple instructions to deliver Narcan, there were scores of screens followed by juvenile quizlets and cartoons. All but about 2 hours out of the 4 days is now relegated to that category of “hours of my life that I can never get back.” Additionally, none of that mandatory “education” will change my prescribing habits one whit. 

And beware the penalty. 

keshophucitotrumuhidruwrorobrubauestetowrirostakoswijocraviphuswuclumineketretichodanacromuclalislolo

vepribuspekucrukulemacrefrisoclutagaswegopregiprowrastauuchiclethasluslochouifricrecosteslobrijetumudraraprajotrufrauuchuuimevewrufradojashuthouejoshudrefracredriclofridrevechuchisivuphastaphusitinacredepavitrereswivupaprecrabrohosustivijukacludi

Changes Needed

The only good thing that came of those 4 long days of opioid education was a motivation to drive change in our current licensing and educational experience. Why not use this opportunity to reform the DEA-physician/prescriber relationship? 

The educational requirements should be curtailed for those of us who do not provide outpatient narcotic prescriptions even if we use inpatient opioids. Meds with low abuse potential should be rescheduled to minimize who gets caught in the broad net of the education requirement. 

We should reduce overregulation of the legitimate prescribers by lowering, instead of increasing, licensing fees. We should change to a single license number that covers every state. In this digital age, there is no legitimate excuse to prevent this from happening. 

After all, the settlements from opioid manufacturers and distributors will in time total $50 billion. It seems that at least some of the responsibilities of the DEA could shift to states, cities, and towns. 

My friend Siamak Karimian, MD, who provides locum services in multiple states, pays for seven active DEA licenses every 3 years. He pointed out the hypocrisy in the current regulatory system: “It’s funny that you can have only one DEA or state license and work for the government in all other states or territories with no limits, including the VA, Indian healthcare systems, or prison systems.”

All other prescribers require a separate DEA number for every state. Ultimately, you’d think tracking prescriptions for a single DEA number should be far simpler than tracking someone with seven. 

Competent physicians not guilty of criminal overprescribing seem to be the last to be considered in nearly every healthcare endeavor these days. It would be refreshing if they would reduce our fees and prevent this waste of our time. 

And while we are at it, perhaps a more fitting punishment is due for Richard Sackler and all the Purdue Pharma–affiliated family members. The Sacklers will pay out $6 billion in exchange for immunity against civil litigation. That doesn’t seem like much when they are worth $11 billion. 

Perhaps they should be made to take an 8-hour course on opioid prescribing, annually and in perpetuity. Let’s see them complete a few quizlets and sit through screens of instruction on how to administer Naloxone. Of course, that would be a mild punishment for those who manufactured a drug that killed hundreds of thousands. But it would be a start. 
 

Dr. Walton-Shirley, a clinical cardiologist in Nashville, Tennessee, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

It’s time to renew two of my three narcotic prescribing licenses. For the first time in my career, I’ve waffled on whether the financial outlay to the US Drug Enforcement Agency (DEA) is worth it. 

At $888 each, I’ve considered letting two licenses lapse because I only work part-time in Montana. But several friends advised me to keep a “spare” in case I transfer to a new location. 

I thought about just paying the fees until I could do a little more research, but there is no mechanism for a refund unless I die within the first year of the 3-year cycle, provide incorrect credit card digits, or accidentally duplicate payments.

The renewal fee is just part of the issue.
 

Mandatory 8-Hour Training

I also received an alert about the requirement for more “narcotics prescribing education” thanks to the Medication Access and Training Expansion Act (MATE). 

The requirement seems counterintuitive because opioid prescribing has decreased for the 10th consecutive year, according to the AMA Overdose Epidemic Report. The continuing rise in overdose deaths is largely due to illegitimate manufacturing of synthetic opioids. 

I’ve written zero outpatient narcotics prescriptions in the past 6 years, and I’ve written very few in my 33 years of practice. My use is limited to intravenous morphine for flash pulmonary edema or refractory angina, but unless you graduated from a training program within 5 years of the June 2023 mandate or are boarded in addiction medicine, there is no way to escape the 8-hour education requirement.

The problem is that these courses are never just 8 hours in duration. After signing up for one such CME course that cost $150, I was still dying of boredom and at risk for DVT 4 days later. That’s how long it took to sit through.

Instead of the 30 seconds it should have taken to review the simple instructions to deliver Narcan, there were scores of screens followed by juvenile quizlets and cartoons. All but about 2 hours out of the 4 days is now relegated to that category of “hours of my life that I can never get back.” Additionally, none of that mandatory “education” will change my prescribing habits one whit. 

And beware the penalty. 

keshophucitotrumuhidruwrorobrubauestetowrirostakoswijocraviphuswuclumineketretichodanacromuclalislolo

vepribuspekucrukulemacrefrisoclutagaswegopregiprowrastauuchiclethasluslochouifricrecosteslobrijetumudraraprajotrufrauuchuuimevewrufradojashuthouejoshudrefracredriclofridrevechuchisivuphastaphusitinacredepavitrereswivupaprecrabrohosustivijukacludi

Changes Needed

The only good thing that came of those 4 long days of opioid education was a motivation to drive change in our current licensing and educational experience. Why not use this opportunity to reform the DEA-physician/prescriber relationship? 

The educational requirements should be curtailed for those of us who do not provide outpatient narcotic prescriptions even if we use inpatient opioids. Meds with low abuse potential should be rescheduled to minimize who gets caught in the broad net of the education requirement. 

We should reduce overregulation of the legitimate prescribers by lowering, instead of increasing, licensing fees. We should change to a single license number that covers every state. In this digital age, there is no legitimate excuse to prevent this from happening. 

After all, the settlements from opioid manufacturers and distributors will in time total $50 billion. It seems that at least some of the responsibilities of the DEA could shift to states, cities, and towns. 

My friend Siamak Karimian, MD, who provides locum services in multiple states, pays for seven active DEA licenses every 3 years. He pointed out the hypocrisy in the current regulatory system: “It’s funny that you can have only one DEA or state license and work for the government in all other states or territories with no limits, including the VA, Indian healthcare systems, or prison systems.”

All other prescribers require a separate DEA number for every state. Ultimately, you’d think tracking prescriptions for a single DEA number should be far simpler than tracking someone with seven. 

Competent physicians not guilty of criminal overprescribing seem to be the last to be considered in nearly every healthcare endeavor these days. It would be refreshing if they would reduce our fees and prevent this waste of our time. 

And while we are at it, perhaps a more fitting punishment is due for Richard Sackler and all the Purdue Pharma–affiliated family members. The Sacklers will pay out $6 billion in exchange for immunity against civil litigation. That doesn’t seem like much when they are worth $11 billion. 

Perhaps they should be made to take an 8-hour course on opioid prescribing, annually and in perpetuity. Let’s see them complete a few quizlets and sit through screens of instruction on how to administer Naloxone. Of course, that would be a mild punishment for those who manufactured a drug that killed hundreds of thousands. But it would be a start. 
 

Dr. Walton-Shirley, a clinical cardiologist in Nashville, Tennessee, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

It’s time to renew two of my three narcotic prescribing licenses. For the first time in my career, I’ve waffled on whether the financial outlay to the US Drug Enforcement Agency (DEA) is worth it. 

At $888 each, I’ve considered letting two licenses lapse because I only work part-time in Montana. But several friends advised me to keep a “spare” in case I transfer to a new location. 

I thought about just paying the fees until I could do a little more research, but there is no mechanism for a refund unless I die within the first year of the 3-year cycle, provide incorrect credit card digits, or accidentally duplicate payments.

The renewal fee is just part of the issue.
 

Mandatory 8-Hour Training

I also received an alert about the requirement for more “narcotics prescribing education” thanks to the Medication Access and Training Expansion Act (MATE). 

The requirement seems counterintuitive because opioid prescribing has decreased for the 10th consecutive year, according to the AMA Overdose Epidemic Report. The continuing rise in overdose deaths is largely due to illegitimate manufacturing of synthetic opioids. 

I’ve written zero outpatient narcotics prescriptions in the past 6 years, and I’ve written very few in my 33 years of practice. My use is limited to intravenous morphine for flash pulmonary edema or refractory angina, but unless you graduated from a training program within 5 years of the June 2023 mandate or are boarded in addiction medicine, there is no way to escape the 8-hour education requirement.

The problem is that these courses are never just 8 hours in duration. After signing up for one such CME course that cost $150, I was still dying of boredom and at risk for DVT 4 days later. That’s how long it took to sit through.

Instead of the 30 seconds it should have taken to review the simple instructions to deliver Narcan, there were scores of screens followed by juvenile quizlets and cartoons. All but about 2 hours out of the 4 days is now relegated to that category of “hours of my life that I can never get back.” Additionally, none of that mandatory “education” will change my prescribing habits one whit. 

And beware the penalty. 

keshophucitotrumuhidruwrorobrubauestetowrirostakoswijocraviphuswuclumineketretichodanacromuclalislolo

vepribuspekucrukulemacrefrisoclutagaswegopregiprowrastauuchiclethasluslochouifricrecosteslobrijetumudraraprajotrufrauuchuuimevewrufradojashuthouejoshudrefracredriclofridrevechuchisivuphastaphusitinacredepavitrereswivupaprecrabrohosustivijukacludi

Changes Needed

The only good thing that came of those 4 long days of opioid education was a motivation to drive change in our current licensing and educational experience. Why not use this opportunity to reform the DEA-physician/prescriber relationship? 

The educational requirements should be curtailed for those of us who do not provide outpatient narcotic prescriptions even if we use inpatient opioids. Meds with low abuse potential should be rescheduled to minimize who gets caught in the broad net of the education requirement. 

We should reduce overregulation of the legitimate prescribers by lowering, instead of increasing, licensing fees. We should change to a single license number that covers every state. In this digital age, there is no legitimate excuse to prevent this from happening. 

After all, the settlements from opioid manufacturers and distributors will in time total $50 billion. It seems that at least some of the responsibilities of the DEA could shift to states, cities, and towns. 

My friend Siamak Karimian, MD, who provides locum services in multiple states, pays for seven active DEA licenses every 3 years. He pointed out the hypocrisy in the current regulatory system: “It’s funny that you can have only one DEA or state license and work for the government in all other states or territories with no limits, including the VA, Indian healthcare systems, or prison systems.”

All other prescribers require a separate DEA number for every state. Ultimately, you’d think tracking prescriptions for a single DEA number should be far simpler than tracking someone with seven. 

Competent physicians not guilty of criminal overprescribing seem to be the last to be considered in nearly every healthcare endeavor these days. It would be refreshing if they would reduce our fees and prevent this waste of our time. 

And while we are at it, perhaps a more fitting punishment is due for Richard Sackler and all the Purdue Pharma–affiliated family members. The Sacklers will pay out $6 billion in exchange for immunity against civil litigation. That doesn’t seem like much when they are worth $11 billion. 

Perhaps they should be made to take an 8-hour course on opioid prescribing, annually and in perpetuity. Let’s see them complete a few quizlets and sit through screens of instruction on how to administer Naloxone. Of course, that would be a mild punishment for those who manufactured a drug that killed hundreds of thousands. But it would be a start. 
 

Dr. Walton-Shirley, a clinical cardiologist in Nashville, Tennessee, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Minoxidil, a potent vasodilator, was approved by the US Food and Drug Administration (FDA) in 1963 to treat high blood pressure. Its application as a hair loss treatment was discovered by accident—patients taking oral minoxidil for blood pressure noticed hair growth on their bodies as a side effect of the medication. In 1988, topical minoxidil (Rogaine [Johnson & Johnson Consumer Inc]) was approved by the FDA for the treatment of androgenetic alopecia in men, and then it was approved for the same indication in women in 1991. The mechanism of action by which minoxidil increases hair growth still has not been fully elucidated. When applied topically, it is thought to extend the anagen phase (or growth phase) of the hair cycle and increase hair follicle size. It also increases oxygen to the hair follicle through vasodilation and stimulates the production of vascular endothelial growth factor, which is thought to promote hair growth.¹ Since its approval, topical minoxidil has become a first-line treatment of androgenetic alopecia in men and women.

In August 2022, The New York Times (NYT) published an article on dermatologists’ use of oral minoxidil at a fraction of the dose prescribed for blood pressure with profound results in hair regrowth.² Several dermatologists quoted in the article endorsed that the decreased dose minimizes unwanted side effects such as hypertrichosis, hypotension, and other cardiac issues while still being effective for hair loss. Also, compared to topical minoxidil, low-dose oral minoxidil (LDOM) is relatively cheaper and easier to use; topicals are more cumbersome to apply and often leave the hair and scalp sticky, leading to noncompliance among patients.² Currently, oral minoxidil is not approved by the FDA for use in hair loss, making it an off-label use.

Since the NYT article was published, we have observed an increase in patient questions and requests for LDOM as well as heightened use by fellow dermatologists in our community. As of November 2022, the NYT had approximately 9,330,000 total subscribers, solidifying its place as a newspaper of record in the United States and across the world.³ In April 2023, we conducted a survey of US-based board-certified dermatologists to investigate the impact of the NYT article on prescribing practices of LDOM for alopecia. The survey was conducted as a poll in a Facebook group for board-certified dermatologists and asked, “How did the NYT article on oral minoxidil for alopecia change your utilization of LDOM (low-dose oral minoxidil) for alopecia?” Three answer choices were given: (1) I started Rx’ing LDOM or increased the number of patients I manage with LDOM; (2) No change. I never Rx’d LDOM and/or no increase in utilization; and (3) I was already prescribing LDOM.

Of the 65 total respondents, 27 (42%) reported that the NYT article influenced their decision to start prescribing LDOM for alopecia. Nine respondents (14%) reported that the article did not influence their prescribing habits, and 27 (42%) responded that they were already prescribing the medication prior to the article’s publication.

Data from Epiphany Dermatology, a practice with more than 70 locations throughout the United States, showed that oral minoxidil was prescribed for alopecia 107 times in 2020 and 672 times in 2021 (Amy Hadley, Epiphany Dermatology, written communication, March 24, 2023). In 2022, prescriptions increased exponentially to 1626, and in the period of January 2023 to March 2023 alone, oral minoxidil was prescribed 510 times. Following publication of the NYT article in August 2022, LDOM was prescribed a total of 1377 times in the next 8 months.

Moreover, data from Summit Pharmacy, a retail pharmacy in Centennial, Colorado, showed an 1800% increase in LDOM prescriptions in the 7 months following the NYT article’s publication (August 2022 to March 2023) compared with the 7 months prior (January 2022 to August 2022)(Brandon Johnson, Summit Pharmacy, written communication, March 30, 2023). These data provide evidence for the influence of the NYT article on prescribing habits of dermatology providers in the United States.

The safety of oral minoxidil for use in hair loss has been established through several studies in the literature.^4,5 These results show that LDOM may be a safe, readily accessible, and revolutionary treatment for hair loss. A retrospective multicenter study of 1404 patients treated with LDOM for any type of alopecia found that side effects were infrequent, and only 1.7% of patients discontinued treatment due to adverse effects. The most frequent adverse effect was hypertrichosis, occurring in 15.1% of patients but leading to treatment withdrawal in only 0.5% of patients.⁴ Similarly, Randolph and Tosti⁵ found that hypertrichosis of the face and body was the most common adverse effect observed, though it rarely resulted in discontinuation and likely was dose dependent: less than 10% of patients receiving 0.25 mg/d experienced hypertrichosis compared with more than 50% of those receiving 5 mg/d (N=634). They also described patients in whom topical minoxidil, though effective, posed major barriers to compliance due to the twice-daily application, changes to hair texture from the medication, and scalp irritation. A literature review of 17 studies with 634 patients on LDOM as a primary treatment for hair loss found that it was an effective, well-tolerated treatment and should be considered for healthy patients who have difficulty with topical formulations.⁵

In the age of media with data constantly at users’ fingertips, the art of practicing medicine also has changed. Although physicians pride themselves on evidence-based medicine, it appears that an NYT article had an impact on how physicians, particularly dermatologists, prescribe oral minoxidil. However, it is difficult to know if the article exposed dermatologists to another treatment in their armamentarium for hair loss or if it influenced patients to ask their health care provider about LDOM for hair loss. One thing is clear—since the article’s publication, the off-label use of LDOM for alopecia has produced what many may call “miracles” for patients with hair loss.⁵

Minoxidil, a potent vasodilator, was approved by the US Food and Drug Administration (FDA) in 1963 to treat high blood pressure. Its application as a hair loss treatment was discovered by accident—patients taking oral minoxidil for blood pressure noticed hair growth on their bodies as a side effect of the medication. In 1988, topical minoxidil (Rogaine [Johnson & Johnson Consumer Inc]) was approved by the FDA for the treatment of androgenetic alopecia in men, and then it was approved for the same indication in women in 1991. The mechanism of action by which minoxidil increases hair growth still has not been fully elucidated. When applied topically, it is thought to extend the anagen phase (or growth phase) of the hair cycle and increase hair follicle size. It also increases oxygen to the hair follicle through vasodilation and stimulates the production of vascular endothelial growth factor, which is thought to promote hair growth.¹ Since its approval, topical minoxidil has become a first-line treatment of androgenetic alopecia in men and women.

In August 2022, The New York Times (NYT) published an article on dermatologists’ use of oral minoxidil at a fraction of the dose prescribed for blood pressure with profound results in hair regrowth.² Several dermatologists quoted in the article endorsed that the decreased dose minimizes unwanted side effects such as hypertrichosis, hypotension, and other cardiac issues while still being effective for hair loss. Also, compared to topical minoxidil, low-dose oral minoxidil (LDOM) is relatively cheaper and easier to use; topicals are more cumbersome to apply and often leave the hair and scalp sticky, leading to noncompliance among patients.² Currently, oral minoxidil is not approved by the FDA for use in hair loss, making it an off-label use.

Since the NYT article was published, we have observed an increase in patient questions and requests for LDOM as well as heightened use by fellow dermatologists in our community. As of November 2022, the NYT had approximately 9,330,000 total subscribers, solidifying its place as a newspaper of record in the United States and across the world.³ In April 2023, we conducted a survey of US-based board-certified dermatologists to investigate the impact of the NYT article on prescribing practices of LDOM for alopecia. The survey was conducted as a poll in a Facebook group for board-certified dermatologists and asked, “How did the NYT article on oral minoxidil for alopecia change your utilization of LDOM (low-dose oral minoxidil) for alopecia?” Three answer choices were given: (1) I started Rx’ing LDOM or increased the number of patients I manage with LDOM; (2) No change. I never Rx’d LDOM and/or no increase in utilization; and (3) I was already prescribing LDOM.

Of the 65 total respondents, 27 (42%) reported that the NYT article influenced their decision to start prescribing LDOM for alopecia. Nine respondents (14%) reported that the article did not influence their prescribing habits, and 27 (42%) responded that they were already prescribing the medication prior to the article’s publication.

Data from Epiphany Dermatology, a practice with more than 70 locations throughout the United States, showed that oral minoxidil was prescribed for alopecia 107 times in 2020 and 672 times in 2021 (Amy Hadley, Epiphany Dermatology, written communication, March 24, 2023). In 2022, prescriptions increased exponentially to 1626, and in the period of January 2023 to March 2023 alone, oral minoxidil was prescribed 510 times. Following publication of the NYT article in August 2022, LDOM was prescribed a total of 1377 times in the next 8 months.

Moreover, data from Summit Pharmacy, a retail pharmacy in Centennial, Colorado, showed an 1800% increase in LDOM prescriptions in the 7 months following the NYT article’s publication (August 2022 to March 2023) compared with the 7 months prior (January 2022 to August 2022)(Brandon Johnson, Summit Pharmacy, written communication, March 30, 2023). These data provide evidence for the influence of the NYT article on prescribing habits of dermatology providers in the United States.

The safety of oral minoxidil for use in hair loss has been established through several studies in the literature.^4,5 These results show that LDOM may be a safe, readily accessible, and revolutionary treatment for hair loss. A retrospective multicenter study of 1404 patients treated with LDOM for any type of alopecia found that side effects were infrequent, and only 1.7% of patients discontinued treatment due to adverse effects. The most frequent adverse effect was hypertrichosis, occurring in 15.1% of patients but leading to treatment withdrawal in only 0.5% of patients.⁴ Similarly, Randolph and Tosti⁵ found that hypertrichosis of the face and body was the most common adverse effect observed, though it rarely resulted in discontinuation and likely was dose dependent: less than 10% of patients receiving 0.25 mg/d experienced hypertrichosis compared with more than 50% of those receiving 5 mg/d (N=634). They also described patients in whom topical minoxidil, though effective, posed major barriers to compliance due to the twice-daily application, changes to hair texture from the medication, and scalp irritation. A literature review of 17 studies with 634 patients on LDOM as a primary treatment for hair loss found that it was an effective, well-tolerated treatment and should be considered for healthy patients who have difficulty with topical formulations.⁵

In the age of media with data constantly at users’ fingertips, the art of practicing medicine also has changed. Although physicians pride themselves on evidence-based medicine, it appears that an NYT article had an impact on how physicians, particularly dermatologists, prescribe oral minoxidil. However, it is difficult to know if the article exposed dermatologists to another treatment in their armamentarium for hair loss or if it influenced patients to ask their health care provider about LDOM for hair loss. One thing is clear—since the article’s publication, the off-label use of LDOM for alopecia has produced what many may call “miracles” for patients with hair loss.⁵

Minoxidil, a potent vasodilator, was approved by the US Food and Drug Administration (FDA) in 1963 to treat high blood pressure. Its application as a hair loss treatment was discovered by accident—patients taking oral minoxidil for blood pressure noticed hair growth on their bodies as a side effect of the medication. In 1988, topical minoxidil (Rogaine [Johnson & Johnson Consumer Inc]) was approved by the FDA for the treatment of androgenetic alopecia in men, and then it was approved for the same indication in women in 1991. The mechanism of action by which minoxidil increases hair growth still has not been fully elucidated. When applied topically, it is thought to extend the anagen phase (or growth phase) of the hair cycle and increase hair follicle size. It also increases oxygen to the hair follicle through vasodilation and stimulates the production of vascular endothelial growth factor, which is thought to promote hair growth.¹ Since its approval, topical minoxidil has become a first-line treatment of androgenetic alopecia in men and women.

In August 2022, The New York Times (NYT) published an article on dermatologists’ use of oral minoxidil at a fraction of the dose prescribed for blood pressure with profound results in hair regrowth.² Several dermatologists quoted in the article endorsed that the decreased dose minimizes unwanted side effects such as hypertrichosis, hypotension, and other cardiac issues while still being effective for hair loss. Also, compared to topical minoxidil, low-dose oral minoxidil (LDOM) is relatively cheaper and easier to use; topicals are more cumbersome to apply and often leave the hair and scalp sticky, leading to noncompliance among patients.² Currently, oral minoxidil is not approved by the FDA for use in hair loss, making it an off-label use.

Since the NYT article was published, we have observed an increase in patient questions and requests for LDOM as well as heightened use by fellow dermatologists in our community. As of November 2022, the NYT had approximately 9,330,000 total subscribers, solidifying its place as a newspaper of record in the United States and across the world.³ In April 2023, we conducted a survey of US-based board-certified dermatologists to investigate the impact of the NYT article on prescribing practices of LDOM for alopecia. The survey was conducted as a poll in a Facebook group for board-certified dermatologists and asked, “How did the NYT article on oral minoxidil for alopecia change your utilization of LDOM (low-dose oral minoxidil) for alopecia?” Three answer choices were given: (1) I started Rx’ing LDOM or increased the number of patients I manage with LDOM; (2) No change. I never Rx’d LDOM and/or no increase in utilization; and (3) I was already prescribing LDOM.

Of the 65 total respondents, 27 (42%) reported that the NYT article influenced their decision to start prescribing LDOM for alopecia. Nine respondents (14%) reported that the article did not influence their prescribing habits, and 27 (42%) responded that they were already prescribing the medication prior to the article’s publication.

Data from Epiphany Dermatology, a practice with more than 70 locations throughout the United States, showed that oral minoxidil was prescribed for alopecia 107 times in 2020 and 672 times in 2021 (Amy Hadley, Epiphany Dermatology, written communication, March 24, 2023). In 2022, prescriptions increased exponentially to 1626, and in the period of January 2023 to March 2023 alone, oral minoxidil was prescribed 510 times. Following publication of the NYT article in August 2022, LDOM was prescribed a total of 1377 times in the next 8 months.

Moreover, data from Summit Pharmacy, a retail pharmacy in Centennial, Colorado, showed an 1800% increase in LDOM prescriptions in the 7 months following the NYT article’s publication (August 2022 to March 2023) compared with the 7 months prior (January 2022 to August 2022)(Brandon Johnson, Summit Pharmacy, written communication, March 30, 2023). These data provide evidence for the influence of the NYT article on prescribing habits of dermatology providers in the United States.

The safety of oral minoxidil for use in hair loss has been established through several studies in the literature.^4,5 These results show that LDOM may be a safe, readily accessible, and revolutionary treatment for hair loss. A retrospective multicenter study of 1404 patients treated with LDOM for any type of alopecia found that side effects were infrequent, and only 1.7% of patients discontinued treatment due to adverse effects. The most frequent adverse effect was hypertrichosis, occurring in 15.1% of patients but leading to treatment withdrawal in only 0.5% of patients.⁴ Similarly, Randolph and Tosti⁵ found that hypertrichosis of the face and body was the most common adverse effect observed, though it rarely resulted in discontinuation and likely was dose dependent: less than 10% of patients receiving 0.25 mg/d experienced hypertrichosis compared with more than 50% of those receiving 5 mg/d (N=634). They also described patients in whom topical minoxidil, though effective, posed major barriers to compliance due to the twice-daily application, changes to hair texture from the medication, and scalp irritation. A literature review of 17 studies with 634 patients on LDOM as a primary treatment for hair loss found that it was an effective, well-tolerated treatment and should be considered for healthy patients who have difficulty with topical formulations.⁵

In the age of media with data constantly at users’ fingertips, the art of practicing medicine also has changed. Although physicians pride themselves on evidence-based medicine, it appears that an NYT article had an impact on how physicians, particularly dermatologists, prescribe oral minoxidil. However, it is difficult to know if the article exposed dermatologists to another treatment in their armamentarium for hair loss or if it influenced patients to ask their health care provider about LDOM for hair loss. One thing is clear—since the article’s publication, the off-label use of LDOM for alopecia has produced what many may call “miracles” for patients with hair loss.⁵

Recently, I had an interesting conversation while getting my hair cut. It gave me a great deal of insight into some of the problems we have right now with how medical information is shared and some of the disconnect our patients may feel.

The young woman who was cutting my hair asked me what I did for an occupation. I said that I was a physician. She said, “Can I please ask you an important question?” She asked me what my thoughts were about the COVID vaccine. She prefaced it with “I am so confused on whether I should get the vaccine. I have seen a number of TikTok videos that talk about nano particles in the COVID vaccine that can be very dangerous.”

I discussed with her how the COVID vaccine actually works and shared with her the remarkable success of the vaccine. I asked her what side effects she was worried about from the vaccine and what her fears were. She said that she had heard that a lot of people had died from the vaccine. I told her that severe reactions from the vaccine were very uncommon.

Paauw_Doug_SEATTLE_2019_web.jpg

She then made a very telling comment: “I wish I could talk to a doctor about my concerns. I have been going to the same health center for the last 5 years and every time I go I see a different person.” She added, “I rarely have more than 5-10 minutes with the person that I am seeing and I rarely get the opportunity to ask questions.”

She thanked me for the information and said that she would be getting the COVID vaccine in the future. She said it is so hard to know where to get information now and the very different things that she heard confused her. She told me that she thought her generation got most of its information from short sound bites or TikTok and Instagram videos.

Why did she trust me? I still think that the medical profession is respected. We are all pressured to do more with less time. Conversations where we can listen and then respond go a long way. We can always listen and learn what information people need and will appreciate. I was also struck by how alone this person felt in our health care system. She did not have a relationship with any one person whom she could trust and reach out to with questions. Relationships with our patients go a long way to establishing trust.
 

Pearl

It takes time to listen to and answer our patients’ questions. We need to do that to fight the waves of misinformation our patients face.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

Recently, I had an interesting conversation while getting my hair cut. It gave me a great deal of insight into some of the problems we have right now with how medical information is shared and some of the disconnect our patients may feel.

The young woman who was cutting my hair asked me what I did for an occupation. I said that I was a physician. She said, “Can I please ask you an important question?” She asked me what my thoughts were about the COVID vaccine. She prefaced it with “I am so confused on whether I should get the vaccine. I have seen a number of TikTok videos that talk about nano particles in the COVID vaccine that can be very dangerous.”

I discussed with her how the COVID vaccine actually works and shared with her the remarkable success of the vaccine. I asked her what side effects she was worried about from the vaccine and what her fears were. She said that she had heard that a lot of people had died from the vaccine. I told her that severe reactions from the vaccine were very uncommon.

Paauw_Doug_SEATTLE_2019_web.jpg

She then made a very telling comment: “I wish I could talk to a doctor about my concerns. I have been going to the same health center for the last 5 years and every time I go I see a different person.” She added, “I rarely have more than 5-10 minutes with the person that I am seeing and I rarely get the opportunity to ask questions.”

She thanked me for the information and said that she would be getting the COVID vaccine in the future. She said it is so hard to know where to get information now and the very different things that she heard confused her. She told me that she thought her generation got most of its information from short sound bites or TikTok and Instagram videos.

Why did she trust me? I still think that the medical profession is respected. We are all pressured to do more with less time. Conversations where we can listen and then respond go a long way. We can always listen and learn what information people need and will appreciate. I was also struck by how alone this person felt in our health care system. She did not have a relationship with any one person whom she could trust and reach out to with questions. Relationships with our patients go a long way to establishing trust.
 

Pearl

It takes time to listen to and answer our patients’ questions. We need to do that to fight the waves of misinformation our patients face.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

Recently, I had an interesting conversation while getting my hair cut. It gave me a great deal of insight into some of the problems we have right now with how medical information is shared and some of the disconnect our patients may feel.

The young woman who was cutting my hair asked me what I did for an occupation. I said that I was a physician. She said, “Can I please ask you an important question?” She asked me what my thoughts were about the COVID vaccine. She prefaced it with “I am so confused on whether I should get the vaccine. I have seen a number of TikTok videos that talk about nano particles in the COVID vaccine that can be very dangerous.”

I discussed with her how the COVID vaccine actually works and shared with her the remarkable success of the vaccine. I asked her what side effects she was worried about from the vaccine and what her fears were. She said that she had heard that a lot of people had died from the vaccine. I told her that severe reactions from the vaccine were very uncommon.

Paauw_Doug_SEATTLE_2019_web.jpg

She then made a very telling comment: “I wish I could talk to a doctor about my concerns. I have been going to the same health center for the last 5 years and every time I go I see a different person.” She added, “I rarely have more than 5-10 minutes with the person that I am seeing and I rarely get the opportunity to ask questions.”

She thanked me for the information and said that she would be getting the COVID vaccine in the future. She said it is so hard to know where to get information now and the very different things that she heard confused her. She told me that she thought her generation got most of its information from short sound bites or TikTok and Instagram videos.

Why did she trust me? I still think that the medical profession is respected. We are all pressured to do more with less time. Conversations where we can listen and then respond go a long way. We can always listen and learn what information people need and will appreciate. I was also struck by how alone this person felt in our health care system. She did not have a relationship with any one person whom she could trust and reach out to with questions. Relationships with our patients go a long way to establishing trust.
 

Pearl

It takes time to listen to and answer our patients’ questions. We need to do that to fight the waves of misinformation our patients face.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

Beta-blockers are excellent drugs. They’re cheap and effective; feature prominently in hypertension guidelines; and remain a sine qua non for coronary artery disease, myocardial infarction, and heart failure treatment. They’ve been around forever, and we know they work. Good luck finding an adult medicine patient who isn’t on one.

Beta-blockers act by slowing resting heart rate (and blunting the heart rate response to exercise. The latter is a pernicious cause of activity intolerance that often goes unchecked. Even when the adverse effects of beta-blockers are appreciated, providers are loath to alter dosing, much less stop the drug. After all, beta-blockers are an integral part of guideline-directed medical therapy (GDMT), and GDMT saves lives.

Balancing Heart Rate and Stroke Volume Effects

The pulmonologist sees beta-blockers differently. To augment cardiac output and optimize oxygen uptake (VO₂) during exercise, we need the heart rate response. In fact, the heart rate response contributes more to cardiac output than augmenting stroke volume (SV) and more to VO₂ than the increase in arteriovenous (AV) oxygen difference. An inability to increase the heart rate commensurate with physiologic work is called chronotropic incompetence (CI). That’s what beta-blockers do ─ they cause CI.

Physiology dictates that CI will cause activity intolerance. That said, it’s hard to quantify the impact from beta-blockers at the individual patient level. Data suggest the heart rate effect is profound. A study in patients without heart failure found that 22% of participants on beta-blockers had CI, and the investigators used a conservative CI definition (≤ 62% of heart rate reserve used). A recent report published in JAMA Cardiology found that stopping beta-blockers in patients with heart failure allowed for an extra 30 beats/min at max exercise.

Wasserman and Whipp’s textbook, the last word on all things exercise, presents a sample subject who undergoes two separate cardiopulmonary exercise tests (CPETs). Before the first, he’s given a placebo, and before the second, he gets an intravenous beta-blocker. He’s a 23-year-old otherwise healthy male — the perfect test case for isolating beta-blocker impact without confounding by comorbid diseases, other medications, or deconditioning. His max heart rate dropped by 30 beats/min after the beta-blocker, identical to what we saw in the JAMA Cardiology study (with the heart rate increasing by 30 beats/min following withdrawal). Case closed. Stop the beta-blockers on your patients so they can meet their exercise goals and get healthy!

Such pithy enthusiasm discounts physiology’s complexities. When blunting our patient’s heart rate response with beta-blockers, we also increase diastolic filling time, which increases SV. For the 23-year-old in Wasserman and Whipp’s physiology textbook, the beta-blocker increased O₂ pulse (the product of SV and AV difference). Presumably, this is mediated by the increased SV. There was a net reduction in VO₂ peak, but it was nominal, suggesting that the drop in heart rate was largely offset by the increase in O₂ pulse. For the patients in the JAMA Cardiology study, the entire group had a small increase in VO2 peak with beta-blocker withdrawal, but the effect differed by left ventricular function. Across different studies, the beta-blocker effect on heart rate is consistent but the change in overall exercise capacity is not. 

Patient Variability in Beta-Blocker Response

In addition to left ventricular function, there are other factors likely to drive variability at the patient level. We’ve treated the response to beta-blockers as a class effect — an obvious oversimplification. The impact on exercise and the heart will vary by dose and drug (eg, atenolol vs metoprolol vs carvedilol, and so on). Beta-blockers can also affect the lungs, and we’re still debating how cautious to be in the presence of asthma or chronic obstructive pulmonary disease. 

In a world of infinite time, resources, and expertise, we’d CPET everyone before and after beta-blocker use. Our current reality requires the unthinkable: We’ll have to talk to each other and our patients. For example, heart failure guidelines recommend titrating drugs to match the dose from trials that proved efficacy. These doses are quite high. Simple discussion with the cardiologist and the patient may allow for an adjustment back down with careful monitoring and close attention to activity tolerance. With any luck, you’ll preserve the benefits from GDMT while optimizing your patient›s ability to meet their exercise goals.
 

Dr. Holley, professor in the department of medicine, Uniformed Services University, Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center, Washington, disclosed ties with Metapharm, CHEST College, and WebMD.

A version of this article appeared on Medscape.com.

Beta-blockers are excellent drugs. They’re cheap and effective; feature prominently in hypertension guidelines; and remain a sine qua non for coronary artery disease, myocardial infarction, and heart failure treatment. They’ve been around forever, and we know they work. Good luck finding an adult medicine patient who isn’t on one.

Beta-blockers act by slowing resting heart rate (and blunting the heart rate response to exercise. The latter is a pernicious cause of activity intolerance that often goes unchecked. Even when the adverse effects of beta-blockers are appreciated, providers are loath to alter dosing, much less stop the drug. After all, beta-blockers are an integral part of guideline-directed medical therapy (GDMT), and GDMT saves lives.

Balancing Heart Rate and Stroke Volume Effects

The pulmonologist sees beta-blockers differently. To augment cardiac output and optimize oxygen uptake (VO₂) during exercise, we need the heart rate response. In fact, the heart rate response contributes more to cardiac output than augmenting stroke volume (SV) and more to VO₂ than the increase in arteriovenous (AV) oxygen difference. An inability to increase the heart rate commensurate with physiologic work is called chronotropic incompetence (CI). That’s what beta-blockers do ─ they cause CI.

Physiology dictates that CI will cause activity intolerance. That said, it’s hard to quantify the impact from beta-blockers at the individual patient level. Data suggest the heart rate effect is profound. A study in patients without heart failure found that 22% of participants on beta-blockers had CI, and the investigators used a conservative CI definition (≤ 62% of heart rate reserve used). A recent report published in JAMA Cardiology found that stopping beta-blockers in patients with heart failure allowed for an extra 30 beats/min at max exercise.

Wasserman and Whipp’s textbook, the last word on all things exercise, presents a sample subject who undergoes two separate cardiopulmonary exercise tests (CPETs). Before the first, he’s given a placebo, and before the second, he gets an intravenous beta-blocker. He’s a 23-year-old otherwise healthy male — the perfect test case for isolating beta-blocker impact without confounding by comorbid diseases, other medications, or deconditioning. His max heart rate dropped by 30 beats/min after the beta-blocker, identical to what we saw in the JAMA Cardiology study (with the heart rate increasing by 30 beats/min following withdrawal). Case closed. Stop the beta-blockers on your patients so they can meet their exercise goals and get healthy!

Such pithy enthusiasm discounts physiology’s complexities. When blunting our patient’s heart rate response with beta-blockers, we also increase diastolic filling time, which increases SV. For the 23-year-old in Wasserman and Whipp’s physiology textbook, the beta-blocker increased O₂ pulse (the product of SV and AV difference). Presumably, this is mediated by the increased SV. There was a net reduction in VO₂ peak, but it was nominal, suggesting that the drop in heart rate was largely offset by the increase in O₂ pulse. For the patients in the JAMA Cardiology study, the entire group had a small increase in VO2 peak with beta-blocker withdrawal, but the effect differed by left ventricular function. Across different studies, the beta-blocker effect on heart rate is consistent but the change in overall exercise capacity is not. 

Patient Variability in Beta-Blocker Response

In addition to left ventricular function, there are other factors likely to drive variability at the patient level. We’ve treated the response to beta-blockers as a class effect — an obvious oversimplification. The impact on exercise and the heart will vary by dose and drug (eg, atenolol vs metoprolol vs carvedilol, and so on). Beta-blockers can also affect the lungs, and we’re still debating how cautious to be in the presence of asthma or chronic obstructive pulmonary disease. 

In a world of infinite time, resources, and expertise, we’d CPET everyone before and after beta-blocker use. Our current reality requires the unthinkable: We’ll have to talk to each other and our patients. For example, heart failure guidelines recommend titrating drugs to match the dose from trials that proved efficacy. These doses are quite high. Simple discussion with the cardiologist and the patient may allow for an adjustment back down with careful monitoring and close attention to activity tolerance. With any luck, you’ll preserve the benefits from GDMT while optimizing your patient›s ability to meet their exercise goals.
 

Dr. Holley, professor in the department of medicine, Uniformed Services University, Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center, Washington, disclosed ties with Metapharm, CHEST College, and WebMD.

A version of this article appeared on Medscape.com.

Beta-blockers are excellent drugs. They’re cheap and effective; feature prominently in hypertension guidelines; and remain a sine qua non for coronary artery disease, myocardial infarction, and heart failure treatment. They’ve been around forever, and we know they work. Good luck finding an adult medicine patient who isn’t on one.

Beta-blockers act by slowing resting heart rate (and blunting the heart rate response to exercise. The latter is a pernicious cause of activity intolerance that often goes unchecked. Even when the adverse effects of beta-blockers are appreciated, providers are loath to alter dosing, much less stop the drug. After all, beta-blockers are an integral part of guideline-directed medical therapy (GDMT), and GDMT saves lives.

Balancing Heart Rate and Stroke Volume Effects

The pulmonologist sees beta-blockers differently. To augment cardiac output and optimize oxygen uptake (VO₂) during exercise, we need the heart rate response. In fact, the heart rate response contributes more to cardiac output than augmenting stroke volume (SV) and more to VO₂ than the increase in arteriovenous (AV) oxygen difference. An inability to increase the heart rate commensurate with physiologic work is called chronotropic incompetence (CI). That’s what beta-blockers do ─ they cause CI.

Physiology dictates that CI will cause activity intolerance. That said, it’s hard to quantify the impact from beta-blockers at the individual patient level. Data suggest the heart rate effect is profound. A study in patients without heart failure found that 22% of participants on beta-blockers had CI, and the investigators used a conservative CI definition (≤ 62% of heart rate reserve used). A recent report published in JAMA Cardiology found that stopping beta-blockers in patients with heart failure allowed for an extra 30 beats/min at max exercise.

Wasserman and Whipp’s textbook, the last word on all things exercise, presents a sample subject who undergoes two separate cardiopulmonary exercise tests (CPETs). Before the first, he’s given a placebo, and before the second, he gets an intravenous beta-blocker. He’s a 23-year-old otherwise healthy male — the perfect test case for isolating beta-blocker impact without confounding by comorbid diseases, other medications, or deconditioning. His max heart rate dropped by 30 beats/min after the beta-blocker, identical to what we saw in the JAMA Cardiology study (with the heart rate increasing by 30 beats/min following withdrawal). Case closed. Stop the beta-blockers on your patients so they can meet their exercise goals and get healthy!

Such pithy enthusiasm discounts physiology’s complexities. When blunting our patient’s heart rate response with beta-blockers, we also increase diastolic filling time, which increases SV. For the 23-year-old in Wasserman and Whipp’s physiology textbook, the beta-blocker increased O₂ pulse (the product of SV and AV difference). Presumably, this is mediated by the increased SV. There was a net reduction in VO₂ peak, but it was nominal, suggesting that the drop in heart rate was largely offset by the increase in O₂ pulse. For the patients in the JAMA Cardiology study, the entire group had a small increase in VO2 peak with beta-blocker withdrawal, but the effect differed by left ventricular function. Across different studies, the beta-blocker effect on heart rate is consistent but the change in overall exercise capacity is not. 

Patient Variability in Beta-Blocker Response

In addition to left ventricular function, there are other factors likely to drive variability at the patient level. We’ve treated the response to beta-blockers as a class effect — an obvious oversimplification. The impact on exercise and the heart will vary by dose and drug (eg, atenolol vs metoprolol vs carvedilol, and so on). Beta-blockers can also affect the lungs, and we’re still debating how cautious to be in the presence of asthma or chronic obstructive pulmonary disease. 

In a world of infinite time, resources, and expertise, we’d CPET everyone before and after beta-blocker use. Our current reality requires the unthinkable: We’ll have to talk to each other and our patients. For example, heart failure guidelines recommend titrating drugs to match the dose from trials that proved efficacy. These doses are quite high. Simple discussion with the cardiologist and the patient may allow for an adjustment back down with careful monitoring and close attention to activity tolerance. With any luck, you’ll preserve the benefits from GDMT while optimizing your patient›s ability to meet their exercise goals.
 

Dr. Holley, professor in the department of medicine, Uniformed Services University, Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center, Washington, disclosed ties with Metapharm, CHEST College, and WebMD.

A version of this article appeared on Medscape.com.

The ethical imperative in healthcare necessitates equitable delivery of care to all individuals, regardless of their socio-economic status or insurance coverage. This principle is rooted in the concept of justice and is crucial to achieving health equity.

As gastroenterologists, despite our various practice settings, we have seen the harmful effects of economic and social disparities on health outcomes. We must therefore ensure that we acknowledge the existence of these disparities, and then begin to provide a framework that allows us to ethically and successfully navigate these complexities for our patients and our affiliated structures.

McCutchen_Aja_ATLANTA_web.jpg

The following cases illustrate the complexities and ethical dilemmas that gastroenterology and hepatology healthcare professionals encounter in delivering care within the traditional healthcare system.

• Case 1: A 44-year-old male presents to the hospital with intermittent rectal bleeding every few weeks without associated abdominal pain or weight loss and not associated with straining. He has bowel movements every 2-3 days. There is no family history of underlying gastrointestinal disease or associated neoplasm. He is accompanied at the time of the interview by his coworker who offered to drive him to the hospital as he is having personal car trouble. Physical examination reveals normal hemodynamics, abdomen is benign, a digital rectal exam reveals small internal hemorrhoids without pain. Hemoglobin is 10, MCV 85. There is scant blood on the glove. He is uninsured. A GI consult is placed to determine the disposition of the patient. The resident on service suggests outpatient follow-up given low risk of clinical deterioration.
• Case 2: A 28-year-old woman postpartum 6 weeks presents in the office with a history of ulcerative colitis which was diagnosed 2 years prior. She was initially placed on steroid therapy. She underwent a colonoscopy at the time of her diagnosis and was following with a gastroenterologist at which time she was found to have moderate left-sided disease with a modified Mayo score of 9. She complains of urgency and rectal bleeding. She saw a gastroenterologist during her pregnancy and was placed on oral mesalamine, which she remains on at the time of evaluation. Once her physical examination is completed and laboratory values are reviewed, you begin to discuss advanced therapies including biologics as she has failed conventional therapies.
• Case 3: You receive a phone call from an outside hospital about a potential transfer for a 46-year-old male who is an immigrant of unknown citizenship status with fulminant liver failure. He meets all criteria including encephalopathy and coagulopathy. He drinks only socially. His secondary liver workup for extensive disease including ceruloplasmin remains pending. Viral hepatology serologies and autoimmune serologies are negative.

Challenges to the Delivery of Equitable Care

These cases underscore the challenges of delivering equitable care within a system that often fails to address the social determinants of health (SDOH). The disparity in the evaluation and treatment of patients based on insurance status not only affects patient outcomes, but also emphasizes the ethical dilemma of balancing cost with population health management.

jiwriphetuwragopricestubrucanuwruwiphekikithawrelacreborecohithouostoprajoprocolewranowrajiswaspuchihastubrukonevitreuenobujeuobrucriboswefrecrespacraslothupatihanuclochodrishisoposhostipekarahobanimowavespocladritrejochothopehevetujadrigechahera

The introduction of measures SDOH-1 and SDOH-2 by the Centers for Medicare & Medicaid Services in the 2023 IPPS Final Rule is a step towards requiring hospitals to systematically collect patient-level SDOH data, aiming to establish meaningful collaborations between healthcare providers and community-based organizations for whole-person care.¹ The primary goal is to allow ecosystems to collect patient-level social risk factors followed by the creation of meaningful collaboration between healthcare providers and the community-based organizations.

The office settings may or may not implement the SDOH and the current electronic medical record systems. However, from a social history standpoint and certainly from a decision standpoint, the impact of SDOH is realized in all settings.
 

Interplay of SDOH and Ethical Considerations

The recognition of social determinants of health is crucial for ethical healthcare delivery. In the first case, considering the patient’s identified social determinants of health — including lack of insurance and transportation, combined with the rising incidence of colorectal cancer in individuals under 55 — an argument could be made for admitting the patient under observation for inpatient colonoscopy.

Data have shown disparities in treatment and referrals in emergency care setting for Black patients with rectal bleeding.² It is imperative that we recognize these existing disparities in diagnosis and outcomes, along with determining SDOH to appropriately come to a final disposition. This approach aligns with the principle of justice and the imperative to deliver equitable care.

In the third case study, we have a patient facing the life-or-death situation of fulminant liver failure. He requires an expeditious decision to be made about transfer candidacy for liver transplant evaluation by the hepatology team.
 

Impact of Insurance Status on Healthcare Access

Insurance status significantly influences access to healthcare and disparities in treatment outcomes. As seen in case 2 and case 3, our therapies often hinge upon access.

In the inflammatory bowel disease (IBD) case, the therapy that we will choose for our IBD patient may be more influenced by access than efficacy. In a national sample of children with Crohn’s disease, publicly insured children were more likely to receive a biologic within 18 months of diagnosis compared to children with private insurance.³ This would suggest that those with private insurance perhaps experience increased barriers.

In the IBD case that we presented here, we do have a publicly insured woman who will face a potential loss of her Medicaid coverage. Our therapeutic decision will therefore not just rely on risk stratification and individualized approach, but rather the programs that are put in place by our pharmaceutical partners to support a future self-pay patient. This may or may not be favorable to her outcome. This discrepancy points to systemic inequalities in healthcare access and the need for policies that ensure equitable treatment for all, regardless of insurance status.
 

Conclusion

The delivery of care in healthcare is an ethical imperative that demands equity and justice. The cases discussed above illustrate the complex interplay between socioeconomic factors, insurance status, and the ethical challenges in providing equitable care.

Systematic efforts to address social determinants of health, as mandated by recent CMS measures, along with a commitment to ethical principles, are essential steps toward reducing disparities and ensuring that all individuals receive the care they need. As healthcare expenditures continue to rise, particularly in areas like gastrointestinal health, addressing these ethical and systemic challenges becomes even more critical for the sustainability of the healthcare system and the well-being of the population it serves.

Gastrointestinal healthcare expenditures totaled $119.6 billion in 2018. Annually there were more than 36.8 million ambulatory visits for GI symptoms and 43.4 million ambulatory visits with primary GI diagnosis.⁴ The use of higher-acuity settings and lack of continuity of care, and the under-recognition and lack of longitudinal framework to follow those families at risk continue to compromise our healthcare system. We must begin to create a framework to provide equitable care for which the cornerstone should be those identified social determinants of health.

Dr. McCutchen is a gastroenterologist at United Digestive, Atlanta, Georgia. She is vice chair of the AGA Research Foundation. Dr. Boules is vice president of global medical and scientific affairs at Ironwood Pharmaceuticals, Cleveland, Ohio.

References

1. www.govinfo.gov/content/pkg/FR-2022-08-10/pdf/2022-16472.pdf.

2. Shields HM et al. Disparities in evaluation of patients with rectal bleeding 40 years and older. Clin Gastroenterol Hepatol. 2014 Apr. doi: 10.1016/j.cgh.2013.07.008.

3. Quiros JA et al. Insurance type influences access to biologics and healthcare utilization in pediatric Crohn’s disease. Crohns Colitis 360. 2021 Aug. doi: 10.1093/crocol/otab057.

4. Peery AF et al. Burden and cost of gastrointestinal, liver, and pancreatic diseases in the United States: Update 2021. Gastroenterology. 2022 Feb. doi: 10.1053/j.gastro.2021.10.017.

The ethical imperative in healthcare necessitates equitable delivery of care to all individuals, regardless of their socio-economic status or insurance coverage. This principle is rooted in the concept of justice and is crucial to achieving health equity.

As gastroenterologists, despite our various practice settings, we have seen the harmful effects of economic and social disparities on health outcomes. We must therefore ensure that we acknowledge the existence of these disparities, and then begin to provide a framework that allows us to ethically and successfully navigate these complexities for our patients and our affiliated structures.

McCutchen_Aja_ATLANTA_web.jpg

The following cases illustrate the complexities and ethical dilemmas that gastroenterology and hepatology healthcare professionals encounter in delivering care within the traditional healthcare system.

• Case 1: A 44-year-old male presents to the hospital with intermittent rectal bleeding every few weeks without associated abdominal pain or weight loss and not associated with straining. He has bowel movements every 2-3 days. There is no family history of underlying gastrointestinal disease or associated neoplasm. He is accompanied at the time of the interview by his coworker who offered to drive him to the hospital as he is having personal car trouble. Physical examination reveals normal hemodynamics, abdomen is benign, a digital rectal exam reveals small internal hemorrhoids without pain. Hemoglobin is 10, MCV 85. There is scant blood on the glove. He is uninsured. A GI consult is placed to determine the disposition of the patient. The resident on service suggests outpatient follow-up given low risk of clinical deterioration.
• Case 2: A 28-year-old woman postpartum 6 weeks presents in the office with a history of ulcerative colitis which was diagnosed 2 years prior. She was initially placed on steroid therapy. She underwent a colonoscopy at the time of her diagnosis and was following with a gastroenterologist at which time she was found to have moderate left-sided disease with a modified Mayo score of 9. She complains of urgency and rectal bleeding. She saw a gastroenterologist during her pregnancy and was placed on oral mesalamine, which she remains on at the time of evaluation. Once her physical examination is completed and laboratory values are reviewed, you begin to discuss advanced therapies including biologics as she has failed conventional therapies.
• Case 3: You receive a phone call from an outside hospital about a potential transfer for a 46-year-old male who is an immigrant of unknown citizenship status with fulminant liver failure. He meets all criteria including encephalopathy and coagulopathy. He drinks only socially. His secondary liver workup for extensive disease including ceruloplasmin remains pending. Viral hepatology serologies and autoimmune serologies are negative.

Challenges to the Delivery of Equitable Care

These cases underscore the challenges of delivering equitable care within a system that often fails to address the social determinants of health (SDOH). The disparity in the evaluation and treatment of patients based on insurance status not only affects patient outcomes, but also emphasizes the ethical dilemma of balancing cost with population health management.

jiwriphetuwragopricestubrucanuwruwiphekikithawrelacreborecohithouostoprajoprocolewranowrajiswaspuchihastubrukonevitreuenobujeuobrucriboswefrecrespacraslothupatihanuclochodrishisoposhostipekarahobanimowavespocladritrejochothopehevetujadrigechahera

The introduction of measures SDOH-1 and SDOH-2 by the Centers for Medicare & Medicaid Services in the 2023 IPPS Final Rule is a step towards requiring hospitals to systematically collect patient-level SDOH data, aiming to establish meaningful collaborations between healthcare providers and community-based organizations for whole-person care.¹ The primary goal is to allow ecosystems to collect patient-level social risk factors followed by the creation of meaningful collaboration between healthcare providers and the community-based organizations.

The office settings may or may not implement the SDOH and the current electronic medical record systems. However, from a social history standpoint and certainly from a decision standpoint, the impact of SDOH is realized in all settings.
 

Interplay of SDOH and Ethical Considerations

The recognition of social determinants of health is crucial for ethical healthcare delivery. In the first case, considering the patient’s identified social determinants of health — including lack of insurance and transportation, combined with the rising incidence of colorectal cancer in individuals under 55 — an argument could be made for admitting the patient under observation for inpatient colonoscopy.

Data have shown disparities in treatment and referrals in emergency care setting for Black patients with rectal bleeding.² It is imperative that we recognize these existing disparities in diagnosis and outcomes, along with determining SDOH to appropriately come to a final disposition. This approach aligns with the principle of justice and the imperative to deliver equitable care.

In the third case study, we have a patient facing the life-or-death situation of fulminant liver failure. He requires an expeditious decision to be made about transfer candidacy for liver transplant evaluation by the hepatology team.
 

Impact of Insurance Status on Healthcare Access

Insurance status significantly influences access to healthcare and disparities in treatment outcomes. As seen in case 2 and case 3, our therapies often hinge upon access.

In the inflammatory bowel disease (IBD) case, the therapy that we will choose for our IBD patient may be more influenced by access than efficacy. In a national sample of children with Crohn’s disease, publicly insured children were more likely to receive a biologic within 18 months of diagnosis compared to children with private insurance.³ This would suggest that those with private insurance perhaps experience increased barriers.

In the IBD case that we presented here, we do have a publicly insured woman who will face a potential loss of her Medicaid coverage. Our therapeutic decision will therefore not just rely on risk stratification and individualized approach, but rather the programs that are put in place by our pharmaceutical partners to support a future self-pay patient. This may or may not be favorable to her outcome. This discrepancy points to systemic inequalities in healthcare access and the need for policies that ensure equitable treatment for all, regardless of insurance status.
 

Conclusion

The delivery of care in healthcare is an ethical imperative that demands equity and justice. The cases discussed above illustrate the complex interplay between socioeconomic factors, insurance status, and the ethical challenges in providing equitable care.

Systematic efforts to address social determinants of health, as mandated by recent CMS measures, along with a commitment to ethical principles, are essential steps toward reducing disparities and ensuring that all individuals receive the care they need. As healthcare expenditures continue to rise, particularly in areas like gastrointestinal health, addressing these ethical and systemic challenges becomes even more critical for the sustainability of the healthcare system and the well-being of the population it serves.

Gastrointestinal healthcare expenditures totaled $119.6 billion in 2018. Annually there were more than 36.8 million ambulatory visits for GI symptoms and 43.4 million ambulatory visits with primary GI diagnosis.⁴ The use of higher-acuity settings and lack of continuity of care, and the under-recognition and lack of longitudinal framework to follow those families at risk continue to compromise our healthcare system. We must begin to create a framework to provide equitable care for which the cornerstone should be those identified social determinants of health.

Dr. McCutchen is a gastroenterologist at United Digestive, Atlanta, Georgia. She is vice chair of the AGA Research Foundation. Dr. Boules is vice president of global medical and scientific affairs at Ironwood Pharmaceuticals, Cleveland, Ohio.

References

1. www.govinfo.gov/content/pkg/FR-2022-08-10/pdf/2022-16472.pdf.

2. Shields HM et al. Disparities in evaluation of patients with rectal bleeding 40 years and older. Clin Gastroenterol Hepatol. 2014 Apr. doi: 10.1016/j.cgh.2013.07.008.

3. Quiros JA et al. Insurance type influences access to biologics and healthcare utilization in pediatric Crohn’s disease. Crohns Colitis 360. 2021 Aug. doi: 10.1093/crocol/otab057.

4. Peery AF et al. Burden and cost of gastrointestinal, liver, and pancreatic diseases in the United States: Update 2021. Gastroenterology. 2022 Feb. doi: 10.1053/j.gastro.2021.10.017.

The ethical imperative in healthcare necessitates equitable delivery of care to all individuals, regardless of their socio-economic status or insurance coverage. This principle is rooted in the concept of justice and is crucial to achieving health equity.

As gastroenterologists, despite our various practice settings, we have seen the harmful effects of economic and social disparities on health outcomes. We must therefore ensure that we acknowledge the existence of these disparities, and then begin to provide a framework that allows us to ethically and successfully navigate these complexities for our patients and our affiliated structures.

McCutchen_Aja_ATLANTA_web.jpg

The following cases illustrate the complexities and ethical dilemmas that gastroenterology and hepatology healthcare professionals encounter in delivering care within the traditional healthcare system.

• Case 1: A 44-year-old male presents to the hospital with intermittent rectal bleeding every few weeks without associated abdominal pain or weight loss and not associated with straining. He has bowel movements every 2-3 days. There is no family history of underlying gastrointestinal disease or associated neoplasm. He is accompanied at the time of the interview by his coworker who offered to drive him to the hospital as he is having personal car trouble. Physical examination reveals normal hemodynamics, abdomen is benign, a digital rectal exam reveals small internal hemorrhoids without pain. Hemoglobin is 10, MCV 85. There is scant blood on the glove. He is uninsured. A GI consult is placed to determine the disposition of the patient. The resident on service suggests outpatient follow-up given low risk of clinical deterioration.
• Case 2: A 28-year-old woman postpartum 6 weeks presents in the office with a history of ulcerative colitis which was diagnosed 2 years prior. She was initially placed on steroid therapy. She underwent a colonoscopy at the time of her diagnosis and was following with a gastroenterologist at which time she was found to have moderate left-sided disease with a modified Mayo score of 9. She complains of urgency and rectal bleeding. She saw a gastroenterologist during her pregnancy and was placed on oral mesalamine, which she remains on at the time of evaluation. Once her physical examination is completed and laboratory values are reviewed, you begin to discuss advanced therapies including biologics as she has failed conventional therapies.
• Case 3: You receive a phone call from an outside hospital about a potential transfer for a 46-year-old male who is an immigrant of unknown citizenship status with fulminant liver failure. He meets all criteria including encephalopathy and coagulopathy. He drinks only socially. His secondary liver workup for extensive disease including ceruloplasmin remains pending. Viral hepatology serologies and autoimmune serologies are negative.

Challenges to the Delivery of Equitable Care

These cases underscore the challenges of delivering equitable care within a system that often fails to address the social determinants of health (SDOH). The disparity in the evaluation and treatment of patients based on insurance status not only affects patient outcomes, but also emphasizes the ethical dilemma of balancing cost with population health management.

jiwriphetuwragopricestubrucanuwruwiphekikithawrelacreborecohithouostoprajoprocolewranowrajiswaspuchihastubrukonevitreuenobujeuobrucriboswefrecrespacraslothupatihanuclochodrishisoposhostipekarahobanimowavespocladritrejochothopehevetujadrigechahera

The introduction of measures SDOH-1 and SDOH-2 by the Centers for Medicare & Medicaid Services in the 2023 IPPS Final Rule is a step towards requiring hospitals to systematically collect patient-level SDOH data, aiming to establish meaningful collaborations between healthcare providers and community-based organizations for whole-person care.¹ The primary goal is to allow ecosystems to collect patient-level social risk factors followed by the creation of meaningful collaboration between healthcare providers and the community-based organizations.

The office settings may or may not implement the SDOH and the current electronic medical record systems. However, from a social history standpoint and certainly from a decision standpoint, the impact of SDOH is realized in all settings.
 

Interplay of SDOH and Ethical Considerations

The recognition of social determinants of health is crucial for ethical healthcare delivery. In the first case, considering the patient’s identified social determinants of health — including lack of insurance and transportation, combined with the rising incidence of colorectal cancer in individuals under 55 — an argument could be made for admitting the patient under observation for inpatient colonoscopy.

Data have shown disparities in treatment and referrals in emergency care setting for Black patients with rectal bleeding.² It is imperative that we recognize these existing disparities in diagnosis and outcomes, along with determining SDOH to appropriately come to a final disposition. This approach aligns with the principle of justice and the imperative to deliver equitable care.

In the third case study, we have a patient facing the life-or-death situation of fulminant liver failure. He requires an expeditious decision to be made about transfer candidacy for liver transplant evaluation by the hepatology team.
 

Impact of Insurance Status on Healthcare Access

Insurance status significantly influences access to healthcare and disparities in treatment outcomes. As seen in case 2 and case 3, our therapies often hinge upon access.

In the inflammatory bowel disease (IBD) case, the therapy that we will choose for our IBD patient may be more influenced by access than efficacy. In a national sample of children with Crohn’s disease, publicly insured children were more likely to receive a biologic within 18 months of diagnosis compared to children with private insurance.³ This would suggest that those with private insurance perhaps experience increased barriers.

In the IBD case that we presented here, we do have a publicly insured woman who will face a potential loss of her Medicaid coverage. Our therapeutic decision will therefore not just rely on risk stratification and individualized approach, but rather the programs that are put in place by our pharmaceutical partners to support a future self-pay patient. This may or may not be favorable to her outcome. This discrepancy points to systemic inequalities in healthcare access and the need for policies that ensure equitable treatment for all, regardless of insurance status.
 

Conclusion

The delivery of care in healthcare is an ethical imperative that demands equity and justice. The cases discussed above illustrate the complex interplay between socioeconomic factors, insurance status, and the ethical challenges in providing equitable care.

Systematic efforts to address social determinants of health, as mandated by recent CMS measures, along with a commitment to ethical principles, are essential steps toward reducing disparities and ensuring that all individuals receive the care they need. As healthcare expenditures continue to rise, particularly in areas like gastrointestinal health, addressing these ethical and systemic challenges becomes even more critical for the sustainability of the healthcare system and the well-being of the population it serves.

Gastrointestinal healthcare expenditures totaled $119.6 billion in 2018. Annually there were more than 36.8 million ambulatory visits for GI symptoms and 43.4 million ambulatory visits with primary GI diagnosis.⁴ The use of higher-acuity settings and lack of continuity of care, and the under-recognition and lack of longitudinal framework to follow those families at risk continue to compromise our healthcare system. We must begin to create a framework to provide equitable care for which the cornerstone should be those identified social determinants of health.

Dr. McCutchen is a gastroenterologist at United Digestive, Atlanta, Georgia. She is vice chair of the AGA Research Foundation. Dr. Boules is vice president of global medical and scientific affairs at Ironwood Pharmaceuticals, Cleveland, Ohio.

References

1. www.govinfo.gov/content/pkg/FR-2022-08-10/pdf/2022-16472.pdf.

2. Shields HM et al. Disparities in evaluation of patients with rectal bleeding 40 years and older. Clin Gastroenterol Hepatol. 2014 Apr. doi: 10.1016/j.cgh.2013.07.008.

3. Quiros JA et al. Insurance type influences access to biologics and healthcare utilization in pediatric Crohn’s disease. Crohns Colitis 360. 2021 Aug. doi: 10.1093/crocol/otab057.

4. Peery AF et al. Burden and cost of gastrointestinal, liver, and pancreatic diseases in the United States: Update 2021. Gastroenterology. 2022 Feb. doi: 10.1053/j.gastro.2021.10.017.

Humans have used salt for centuries, to preserve or cure food before refrigeration was readily available, and even as currency in some cultures. Though modern food preservation efforts have decreased our reliance on salt, we still heavily incorporate it as a flavor enhancer. 

It’s only relatively recently that we’ve begun limiting salt in our diets, as research has linked high sodium intake with chronic, preventable conditions like hypertension, heart disease, and kidney disease.
 

How to Recommend Restriction in a Helpful Way 

The US Department of Agriculture’s Dietary Guidelines for Americans recommends intake of no more than 2300 mg of sodium daily for adults and children aged 14 years or older. This echoes similar recommendations for people at risk for heart disease, kidney disease, and hypertension. However, the sodium intake of the average American still sits at a whopping 3400 mg daily. 

High sodium intake is primarily the result of modern commercial food processing. Food prepared outside the home accounts for up to 70% of sodium intake in the United States, whereas only about 10% comes from salt that is added to food either during or after cooking. For this reason, I hesitate to recommend withholding salt as a primary focus when counseling on a low-sodium diet. 

To many people, certain foods just taste better with salt. Many of my patients in the southern United States simply will not eat foods like eggs and tomatoes if they cannot salt them. We can spend every moment of patient interaction time explaining why excess sodium is unhealthy, but the fact remains that humans prefer food that tastes good. This is why I try to avoid counseling a “no-added-salt” diet; instead, I recommend a low-sodium diet with a focus on fresh, whole foods and limiting salt to only a few food items. 

Patients should be counseled to slowly restrict their salt intake and be made aware that doing so may increase the time it takes for their sensitivity to the taste of less salty foods to return. But it is also important for them to know that it will return. The surest way to kill progress is for an unprepared patient to believe that their food will taste bland forever. A prepared patient understands that their food may taste different for a couple of weeks, but that the change will not last forever.
 

Types of Salt 

I have often worked with patients who insist that their sodium intake is acceptable because they are using sea salt instead of table salt. This is the result of exceptional marketing and misinformation. 

Specialty salts like sea salt and Himalayan pink salt contain about 560 mg and 590 mg of sodium, respectively, per quarter teaspoon. These products do have a slightly different mineral content, with sea salt typically having a negligible amount of calcium, magnesium, or potassium. The very small amount of these minerals offers no obvious health benefits compared with more affordable table salt. 

The sodium content of iodized table salt is comparable to these products, with about 590 mg of sodium per quarter teaspoon. Though its high sodium content will put some practitioners off, it is also an excellent source of iodine, at about 75 mg per serving. It has been estimated that upward of 35% of the US population has iodine deficiency, most commonly due to pregnancy, avoidance of dairy products, increasing rates of vegetarianism, intake of highly processed foods, and avoidance of added salt. For this reason, and its relative affordability, I find table salt to be far more appropriate for the average American than specialty salts.
 

Salt Substitutes 

Monosodium glutamate (MSG). MSG was previously at the center of public health concern owing to reports of “Chinese restaurant syndrome” that have since been debunked. I often recommend MSG to people trying to decrease sodium intake because the US Food and Drug Administration has designated it as GRAS (“generally recognized as safe”), and it has about one quarter of the sodium content of table salt at 125 mg per quarter teaspoon. Its crystalline structure makes it a lower-sodium salt substitute in savory applications like soups, stews, and gravies. 

Hot sauce. These sauces are generally composed of peppers, vinegar, salt, and sugar. There may be some variation and occasionally added ingredients depending upon the brand. However, I find most hot sauces to be a low-sodium seasoning option that works especially well on proteins like eggs, chicken, and pork. 

Potassium-based substitutes. Salt alternatives such as Nu-Salt and Morton Salt Substitute are sodium-free options with a significant amount of potassium, at 525 mg per quarter-teaspoon serving. These alternatives may not be ideal for patients with kidney problems, but they can be very helpful for those with potassium deficiency. 

Herb-based seasonings. Garlic and onion powder are both sodium-free seasonings that many of my patients have found help to increase palatability while decreasing salt use. Black pepper; lemon and lime juice; salt-free herb mixes like Mrs. Dash; and spices like cumin, paprika, dill, chili powder, and ginger are also sodium-free or low-sodium alternatives that can help to alleviate blandness for someone new to a low-sodium diet. I recommend them often and use them in my own cooking at home.

Plant-based diet. If the goal of care is to improve cardiovascular or kidney health, then I find that working with patients to increase intake of plant foods to be a helpful option. This way of eating encourages replacing highly processed foods that may be high in sodium and sugar with plants that tend to be higher in potassium and calcium. The Dietary Approaches to Stop Hypertension (DASH), Mediterranean, and other plant-based diets have been shown to increase cardiovascular and metabolic health by significantly decreasing serum lipids, blood pressure, and hemoglobin A1c and promoting weight loss. They have also been shown to increase the gut microbiome and promote increased cognitive function. 

I rarely encourage the use of added salt. However, research shows that putting down the salt shaker is probably not the most effective option to restrict sodium intake. For those who can cut back, these options can help keep food flavorful and patients compliant. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Humans have used salt for centuries, to preserve or cure food before refrigeration was readily available, and even as currency in some cultures. Though modern food preservation efforts have decreased our reliance on salt, we still heavily incorporate it as a flavor enhancer. 

It’s only relatively recently that we’ve begun limiting salt in our diets, as research has linked high sodium intake with chronic, preventable conditions like hypertension, heart disease, and kidney disease.
 

How to Recommend Restriction in a Helpful Way 

The US Department of Agriculture’s Dietary Guidelines for Americans recommends intake of no more than 2300 mg of sodium daily for adults and children aged 14 years or older. This echoes similar recommendations for people at risk for heart disease, kidney disease, and hypertension. However, the sodium intake of the average American still sits at a whopping 3400 mg daily. 

High sodium intake is primarily the result of modern commercial food processing. Food prepared outside the home accounts for up to 70% of sodium intake in the United States, whereas only about 10% comes from salt that is added to food either during or after cooking. For this reason, I hesitate to recommend withholding salt as a primary focus when counseling on a low-sodium diet. 

To many people, certain foods just taste better with salt. Many of my patients in the southern United States simply will not eat foods like eggs and tomatoes if they cannot salt them. We can spend every moment of patient interaction time explaining why excess sodium is unhealthy, but the fact remains that humans prefer food that tastes good. This is why I try to avoid counseling a “no-added-salt” diet; instead, I recommend a low-sodium diet with a focus on fresh, whole foods and limiting salt to only a few food items. 

Patients should be counseled to slowly restrict their salt intake and be made aware that doing so may increase the time it takes for their sensitivity to the taste of less salty foods to return. But it is also important for them to know that it will return. The surest way to kill progress is for an unprepared patient to believe that their food will taste bland forever. A prepared patient understands that their food may taste different for a couple of weeks, but that the change will not last forever.
 

Types of Salt 

I have often worked with patients who insist that their sodium intake is acceptable because they are using sea salt instead of table salt. This is the result of exceptional marketing and misinformation. 

Specialty salts like sea salt and Himalayan pink salt contain about 560 mg and 590 mg of sodium, respectively, per quarter teaspoon. These products do have a slightly different mineral content, with sea salt typically having a negligible amount of calcium, magnesium, or potassium. The very small amount of these minerals offers no obvious health benefits compared with more affordable table salt. 

The sodium content of iodized table salt is comparable to these products, with about 590 mg of sodium per quarter teaspoon. Though its high sodium content will put some practitioners off, it is also an excellent source of iodine, at about 75 mg per serving. It has been estimated that upward of 35% of the US population has iodine deficiency, most commonly due to pregnancy, avoidance of dairy products, increasing rates of vegetarianism, intake of highly processed foods, and avoidance of added salt. For this reason, and its relative affordability, I find table salt to be far more appropriate for the average American than specialty salts.
 

Salt Substitutes 

Monosodium glutamate (MSG). MSG was previously at the center of public health concern owing to reports of “Chinese restaurant syndrome” that have since been debunked. I often recommend MSG to people trying to decrease sodium intake because the US Food and Drug Administration has designated it as GRAS (“generally recognized as safe”), and it has about one quarter of the sodium content of table salt at 125 mg per quarter teaspoon. Its crystalline structure makes it a lower-sodium salt substitute in savory applications like soups, stews, and gravies. 

Hot sauce. These sauces are generally composed of peppers, vinegar, salt, and sugar. There may be some variation and occasionally added ingredients depending upon the brand. However, I find most hot sauces to be a low-sodium seasoning option that works especially well on proteins like eggs, chicken, and pork. 

Potassium-based substitutes. Salt alternatives such as Nu-Salt and Morton Salt Substitute are sodium-free options with a significant amount of potassium, at 525 mg per quarter-teaspoon serving. These alternatives may not be ideal for patients with kidney problems, but they can be very helpful for those with potassium deficiency. 

Herb-based seasonings. Garlic and onion powder are both sodium-free seasonings that many of my patients have found help to increase palatability while decreasing salt use. Black pepper; lemon and lime juice; salt-free herb mixes like Mrs. Dash; and spices like cumin, paprika, dill, chili powder, and ginger are also sodium-free or low-sodium alternatives that can help to alleviate blandness for someone new to a low-sodium diet. I recommend them often and use them in my own cooking at home.

Plant-based diet. If the goal of care is to improve cardiovascular or kidney health, then I find that working with patients to increase intake of plant foods to be a helpful option. This way of eating encourages replacing highly processed foods that may be high in sodium and sugar with plants that tend to be higher in potassium and calcium. The Dietary Approaches to Stop Hypertension (DASH), Mediterranean, and other plant-based diets have been shown to increase cardiovascular and metabolic health by significantly decreasing serum lipids, blood pressure, and hemoglobin A1c and promoting weight loss. They have also been shown to increase the gut microbiome and promote increased cognitive function. 

I rarely encourage the use of added salt. However, research shows that putting down the salt shaker is probably not the most effective option to restrict sodium intake. For those who can cut back, these options can help keep food flavorful and patients compliant. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Humans have used salt for centuries, to preserve or cure food before refrigeration was readily available, and even as currency in some cultures. Though modern food preservation efforts have decreased our reliance on salt, we still heavily incorporate it as a flavor enhancer. 

It’s only relatively recently that we’ve begun limiting salt in our diets, as research has linked high sodium intake with chronic, preventable conditions like hypertension, heart disease, and kidney disease.
 

How to Recommend Restriction in a Helpful Way 

The US Department of Agriculture’s Dietary Guidelines for Americans recommends intake of no more than 2300 mg of sodium daily for adults and children aged 14 years or older. This echoes similar recommendations for people at risk for heart disease, kidney disease, and hypertension. However, the sodium intake of the average American still sits at a whopping 3400 mg daily. 

High sodium intake is primarily the result of modern commercial food processing. Food prepared outside the home accounts for up to 70% of sodium intake in the United States, whereas only about 10% comes from salt that is added to food either during or after cooking. For this reason, I hesitate to recommend withholding salt as a primary focus when counseling on a low-sodium diet. 

To many people, certain foods just taste better with salt. Many of my patients in the southern United States simply will not eat foods like eggs and tomatoes if they cannot salt them. We can spend every moment of patient interaction time explaining why excess sodium is unhealthy, but the fact remains that humans prefer food that tastes good. This is why I try to avoid counseling a “no-added-salt” diet; instead, I recommend a low-sodium diet with a focus on fresh, whole foods and limiting salt to only a few food items. 

Patients should be counseled to slowly restrict their salt intake and be made aware that doing so may increase the time it takes for their sensitivity to the taste of less salty foods to return. But it is also important for them to know that it will return. The surest way to kill progress is for an unprepared patient to believe that their food will taste bland forever. A prepared patient understands that their food may taste different for a couple of weeks, but that the change will not last forever.
 

Types of Salt 

I have often worked with patients who insist that their sodium intake is acceptable because they are using sea salt instead of table salt. This is the result of exceptional marketing and misinformation. 

Specialty salts like sea salt and Himalayan pink salt contain about 560 mg and 590 mg of sodium, respectively, per quarter teaspoon. These products do have a slightly different mineral content, with sea salt typically having a negligible amount of calcium, magnesium, or potassium. The very small amount of these minerals offers no obvious health benefits compared with more affordable table salt. 

The sodium content of iodized table salt is comparable to these products, with about 590 mg of sodium per quarter teaspoon. Though its high sodium content will put some practitioners off, it is also an excellent source of iodine, at about 75 mg per serving. It has been estimated that upward of 35% of the US population has iodine deficiency, most commonly due to pregnancy, avoidance of dairy products, increasing rates of vegetarianism, intake of highly processed foods, and avoidance of added salt. For this reason, and its relative affordability, I find table salt to be far more appropriate for the average American than specialty salts.
 

Salt Substitutes 

Monosodium glutamate (MSG). MSG was previously at the center of public health concern owing to reports of “Chinese restaurant syndrome” that have since been debunked. I often recommend MSG to people trying to decrease sodium intake because the US Food and Drug Administration has designated it as GRAS (“generally recognized as safe”), and it has about one quarter of the sodium content of table salt at 125 mg per quarter teaspoon. Its crystalline structure makes it a lower-sodium salt substitute in savory applications like soups, stews, and gravies. 

Hot sauce. These sauces are generally composed of peppers, vinegar, salt, and sugar. There may be some variation and occasionally added ingredients depending upon the brand. However, I find most hot sauces to be a low-sodium seasoning option that works especially well on proteins like eggs, chicken, and pork. 

Potassium-based substitutes. Salt alternatives such as Nu-Salt and Morton Salt Substitute are sodium-free options with a significant amount of potassium, at 525 mg per quarter-teaspoon serving. These alternatives may not be ideal for patients with kidney problems, but they can be very helpful for those with potassium deficiency. 

Herb-based seasonings. Garlic and onion powder are both sodium-free seasonings that many of my patients have found help to increase palatability while decreasing salt use. Black pepper; lemon and lime juice; salt-free herb mixes like Mrs. Dash; and spices like cumin, paprika, dill, chili powder, and ginger are also sodium-free or low-sodium alternatives that can help to alleviate blandness for someone new to a low-sodium diet. I recommend them often and use them in my own cooking at home.

Plant-based diet. If the goal of care is to improve cardiovascular or kidney health, then I find that working with patients to increase intake of plant foods to be a helpful option. This way of eating encourages replacing highly processed foods that may be high in sodium and sugar with plants that tend to be higher in potassium and calcium. The Dietary Approaches to Stop Hypertension (DASH), Mediterranean, and other plant-based diets have been shown to increase cardiovascular and metabolic health by significantly decreasing serum lipids, blood pressure, and hemoglobin A1c and promoting weight loss. They have also been shown to increase the gut microbiome and promote increased cognitive function. 

I rarely encourage the use of added salt. However, research shows that putting down the salt shaker is probably not the most effective option to restrict sodium intake. For those who can cut back, these options can help keep food flavorful and patients compliant. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Molluscum contagiosum (ie, molluscum) is a ubiquitous infection caused by the poxvirus molluscum contagiosum virus (MCV). Although skin deep, molluscum shares many factors with the more virulent poxviridae. Moisture and trauma can cause viral material to be released from the pearly papules through a small opening, which also allows entry of bacteria and medications into the lesion. The MCV is transmitted by direct contact with skin or via fomites.¹

Molluscum can affect children of any age, with MCV type 1 peaking in toddlers and school-aged children and MCV type 2 after the sexual debut. The prevalence of molluscum has increased since the 1980s. It is stressful for children and caregivers and poses challenges in schools as well as sports such as swimming, wrestling, and karate.^1,2

For the first time, we have US Food and Drug Administration (FDA)–approved products to treat MCV infections. Previously, only off-label agents were used. Therefore, we have to contemplate why treatment is important to our patients.

What type of care is required for molluscum?

Counseling is the first and only mandatory treatment, which consists of 3 parts: natural history, risk factors for spread, and options for therapy. The natural history of molluscum in children is early spread, contagion to oneself and others (as high as 60% of sibling co-bathers³), triggering of dermatitis, eventual onset of the beginning-of-the-end (BOTE) sign, and eventually clearance. The natural history in adults is poorly understood.

Early clearance is uncommon; reports have suggested 45.6% to 48.4% of affected patients are clear at 1 year and 69.5% to 72.6% at 1.5 years.⁴ For many children, especially those with atopic dermatitis (AD), lesions linger and often spread, with many experiencing disease for 3 to 4 years. Fomites such as towels, washcloths, and sponges can transfer the virus and spread lesions; therefore, I advise patients to gently pat their skin dry, wash towels frequently, and avoid sharing bathing equipment.^1,3,5 Children and adults with immunosuppression may have a greater number of lesions and more prolonged course of disease, including those with HIV as well as DOC8 and CARD11 mutations.⁶ The American Academy of Pediatrics (AAP) emphasizes that children should not be excluded from attending child care/school or from swimming in public pools but lesions should be covered.⁶ Lesions, especially those in the antecubital region, can trigger new-onset AD or AD flares.³ In response, gentle skin care including fragrance-free cleansers and periodic application of moisturizers may ward off AD. Topical corticosteroids are preferred.

Dermatitis in MCV is a great mimicker and can resemble erythema multiforme, Gianotti-Crosti syndrome, impetigo, and AD.¹ Superinfection recently has been reported; however, in a retrospective analysis of 56 patients with inflamed lesions secondary to molluscum infection, only 7 had positive bacterial cultures, which supports the idea of the swelling and redness of inflammation as a mimic for infection.⁷ When true infection does occur, tender, swollen, pus-filled lesions should be lanced and cultured.^1,7,8

When should we consider therapy?

Therapy is highly dependent on the child, the caregiver, and the social circumstances.¹ More than 80% of parents are anxious about molluscum, and countless children are embarrassed or ashamed.¹ Ultimately, an unhappy child merits care. The AAP cites the following as reasons to treat: “(1) alleviate discomfort, including itching; (2) reduce autoinoculation; (3) limit transmission of the virus to close contacts; (4) reduce cosmetic concerns; and (5) prevent secondary infection.”⁶ For adults, we should consider limitations to intimacy and reduction of sexual transmission risk.⁶

Treatment can be based on the number of lesions. With a few lesions (<3), therapy is worthwhile if they are unsightly; appear on exposed skin causing embarrassment; and/or are itchy, uncomfortable, or large. In a report of 300 children with molluscum treated with cantharidin, most patients choosing therapy had 10 to 20 lesions, but this was over multiple visits.⁸ Looking at a 2018 data set of 50 patients (all-comers) with molluscum,³ the mean number of lesions was 10 (median, 7); 3 lesions were 1 SD below, while 14, 17, and 45 were 1, 2, and 3 SDs above, respectively. This data set shows that patients can develop more lesions rapidly, and most children have many visible lesions (N.B. Silverberg, MD, unpublished data).

Because each lesion contains infectious viral particles and patients scratch, more lesions are equated to greater autoinoculation and contagion. In addition to the AAP criteria, treatment can be considered for households with immunocompromised individuals, children at risk for new-onset AD, or those with AD at risk for flare. For patients with 45 lesions or more (3 SDs), clearance is harder to achieve with 2 sessions of in-office therapy, and multiple methods or the addition of immunomodulatory therapeutics should be considered.

Do we have to clear every lesion?

New molluscum lesions may arise until a patient achieves immunity, and they may appear more than a month after inoculation, making it difficult to keep up with the rapid spread. Latency between exposure and lesion development usually is 2 to 7 weeks but may be as long as 6 months, making it difficult to prevent spread.⁶ Therefore, when we treat, we should not promise full clearance to patients and parents. Rather, we should inform them that new lesions may develop later, and therapy is only effective on visible lesions. In a recent study, a 50% clearance of lesions was the satisfactory threshold for parents, demonstrating that satisfaction is possible with partial clearance.⁹

What is new in therapeutics for molluscum?

Molluscum therapies are either destructive, immunomodulatory, or antiviral. Two agents now are approved by the FDA for the treatment of molluscum infections.

Berdazimer gel 10.3% is approved for patients 1 year or older, but it is not yet available. This agent has both immunomodulatory and antiviral properties.¹⁰ It features a home therapy that is mixed on a small palette, then painted on by the patient or parent once daily for 12 weeks. Study outcomes demonstrated more than 50% lesional clearance.^11,12 Complete clearance was achieved in at least 30% of patients.¹²A proprietary topical version of cantharidin 0.7% in flexible collodion is now FDA approved for patients 2 years and older. This vesicant-triggering iatrogenic is targeted at creating blisters overlying molluscum lesions. It is conceptually similar to older versions but with some enhanced features.^5,13,14 This version was used for therapy every 3 weeks for up to 4 sessions in clinical trials. Safety is similar across all body sites treated (nonmucosal and not near the mucosal surfaces) but not for mucosa, the mid face, or eyelids.¹³ Complete lesion clearance was 46.3% to 54% and statistically greater than placebo (P<.001).¹⁴Both agents are well tolerated in children with AD; adverse effects include blistering with cantharidin and dermatitislike symptoms with berdazimer.^15,16 These therapies have the advantage of being easy to use.

Final Thoughts

We have entered an era of high-quality molluscum therapy. Patient care involves developing a good knowledge of the agents, incorporating shared decision-making with patients and caregivers, and addressing therapy in the context of comorbid diseases such as AD.

Molluscum contagiosum (ie, molluscum) is a ubiquitous infection caused by the poxvirus molluscum contagiosum virus (MCV). Although skin deep, molluscum shares many factors with the more virulent poxviridae. Moisture and trauma can cause viral material to be released from the pearly papules through a small opening, which also allows entry of bacteria and medications into the lesion. The MCV is transmitted by direct contact with skin or via fomites.¹

Molluscum can affect children of any age, with MCV type 1 peaking in toddlers and school-aged children and MCV type 2 after the sexual debut. The prevalence of molluscum has increased since the 1980s. It is stressful for children and caregivers and poses challenges in schools as well as sports such as swimming, wrestling, and karate.^1,2

For the first time, we have US Food and Drug Administration (FDA)–approved products to treat MCV infections. Previously, only off-label agents were used. Therefore, we have to contemplate why treatment is important to our patients.

What type of care is required for molluscum?

Counseling is the first and only mandatory treatment, which consists of 3 parts: natural history, risk factors for spread, and options for therapy. The natural history of molluscum in children is early spread, contagion to oneself and others (as high as 60% of sibling co-bathers³), triggering of dermatitis, eventual onset of the beginning-of-the-end (BOTE) sign, and eventually clearance. The natural history in adults is poorly understood.

Early clearance is uncommon; reports have suggested 45.6% to 48.4% of affected patients are clear at 1 year and 69.5% to 72.6% at 1.5 years.⁴ For many children, especially those with atopic dermatitis (AD), lesions linger and often spread, with many experiencing disease for 3 to 4 years. Fomites such as towels, washcloths, and sponges can transfer the virus and spread lesions; therefore, I advise patients to gently pat their skin dry, wash towels frequently, and avoid sharing bathing equipment.^1,3,5 Children and adults with immunosuppression may have a greater number of lesions and more prolonged course of disease, including those with HIV as well as DOC8 and CARD11 mutations.⁶ The American Academy of Pediatrics (AAP) emphasizes that children should not be excluded from attending child care/school or from swimming in public pools but lesions should be covered.⁶ Lesions, especially those in the antecubital region, can trigger new-onset AD or AD flares.³ In response, gentle skin care including fragrance-free cleansers and periodic application of moisturizers may ward off AD. Topical corticosteroids are preferred.

Dermatitis in MCV is a great mimicker and can resemble erythema multiforme, Gianotti-Crosti syndrome, impetigo, and AD.¹ Superinfection recently has been reported; however, in a retrospective analysis of 56 patients with inflamed lesions secondary to molluscum infection, only 7 had positive bacterial cultures, which supports the idea of the swelling and redness of inflammation as a mimic for infection.⁷ When true infection does occur, tender, swollen, pus-filled lesions should be lanced and cultured.^1,7,8

When should we consider therapy?

Therapy is highly dependent on the child, the caregiver, and the social circumstances.¹ More than 80% of parents are anxious about molluscum, and countless children are embarrassed or ashamed.¹ Ultimately, an unhappy child merits care. The AAP cites the following as reasons to treat: “(1) alleviate discomfort, including itching; (2) reduce autoinoculation; (3) limit transmission of the virus to close contacts; (4) reduce cosmetic concerns; and (5) prevent secondary infection.”⁶ For adults, we should consider limitations to intimacy and reduction of sexual transmission risk.⁶

Treatment can be based on the number of lesions. With a few lesions (<3), therapy is worthwhile if they are unsightly; appear on exposed skin causing embarrassment; and/or are itchy, uncomfortable, or large. In a report of 300 children with molluscum treated with cantharidin, most patients choosing therapy had 10 to 20 lesions, but this was over multiple visits.⁸ Looking at a 2018 data set of 50 patients (all-comers) with molluscum,³ the mean number of lesions was 10 (median, 7); 3 lesions were 1 SD below, while 14, 17, and 45 were 1, 2, and 3 SDs above, respectively. This data set shows that patients can develop more lesions rapidly, and most children have many visible lesions (N.B. Silverberg, MD, unpublished data).

Because each lesion contains infectious viral particles and patients scratch, more lesions are equated to greater autoinoculation and contagion. In addition to the AAP criteria, treatment can be considered for households with immunocompromised individuals, children at risk for new-onset AD, or those with AD at risk for flare. For patients with 45 lesions or more (3 SDs), clearance is harder to achieve with 2 sessions of in-office therapy, and multiple methods or the addition of immunomodulatory therapeutics should be considered.

Do we have to clear every lesion?

New molluscum lesions may arise until a patient achieves immunity, and they may appear more than a month after inoculation, making it difficult to keep up with the rapid spread. Latency between exposure and lesion development usually is 2 to 7 weeks but may be as long as 6 months, making it difficult to prevent spread.⁶ Therefore, when we treat, we should not promise full clearance to patients and parents. Rather, we should inform them that new lesions may develop later, and therapy is only effective on visible lesions. In a recent study, a 50% clearance of lesions was the satisfactory threshold for parents, demonstrating that satisfaction is possible with partial clearance.⁹

What is new in therapeutics for molluscum?

Molluscum therapies are either destructive, immunomodulatory, or antiviral. Two agents now are approved by the FDA for the treatment of molluscum infections.

Berdazimer gel 10.3% is approved for patients 1 year or older, but it is not yet available. This agent has both immunomodulatory and antiviral properties.¹⁰ It features a home therapy that is mixed on a small palette, then painted on by the patient or parent once daily for 12 weeks. Study outcomes demonstrated more than 50% lesional clearance.^11,12 Complete clearance was achieved in at least 30% of patients.¹²A proprietary topical version of cantharidin 0.7% in flexible collodion is now FDA approved for patients 2 years and older. This vesicant-triggering iatrogenic is targeted at creating blisters overlying molluscum lesions. It is conceptually similar to older versions but with some enhanced features.^5,13,14 This version was used for therapy every 3 weeks for up to 4 sessions in clinical trials. Safety is similar across all body sites treated (nonmucosal and not near the mucosal surfaces) but not for mucosa, the mid face, or eyelids.¹³ Complete lesion clearance was 46.3% to 54% and statistically greater than placebo (P<.001).¹⁴Both agents are well tolerated in children with AD; adverse effects include blistering with cantharidin and dermatitislike symptoms with berdazimer.^15,16 These therapies have the advantage of being easy to use.

Final Thoughts

We have entered an era of high-quality molluscum therapy. Patient care involves developing a good knowledge of the agents, incorporating shared decision-making with patients and caregivers, and addressing therapy in the context of comorbid diseases such as AD.

Molluscum contagiosum (ie, molluscum) is a ubiquitous infection caused by the poxvirus molluscum contagiosum virus (MCV). Although skin deep, molluscum shares many factors with the more virulent poxviridae. Moisture and trauma can cause viral material to be released from the pearly papules through a small opening, which also allows entry of bacteria and medications into the lesion. The MCV is transmitted by direct contact with skin or via fomites.¹

Molluscum can affect children of any age, with MCV type 1 peaking in toddlers and school-aged children and MCV type 2 after the sexual debut. The prevalence of molluscum has increased since the 1980s. It is stressful for children and caregivers and poses challenges in schools as well as sports such as swimming, wrestling, and karate.^1,2

For the first time, we have US Food and Drug Administration (FDA)–approved products to treat MCV infections. Previously, only off-label agents were used. Therefore, we have to contemplate why treatment is important to our patients.

What type of care is required for molluscum?

Counseling is the first and only mandatory treatment, which consists of 3 parts: natural history, risk factors for spread, and options for therapy. The natural history of molluscum in children is early spread, contagion to oneself and others (as high as 60% of sibling co-bathers³), triggering of dermatitis, eventual onset of the beginning-of-the-end (BOTE) sign, and eventually clearance. The natural history in adults is poorly understood.

Early clearance is uncommon; reports have suggested 45.6% to 48.4% of affected patients are clear at 1 year and 69.5% to 72.6% at 1.5 years.⁴ For many children, especially those with atopic dermatitis (AD), lesions linger and often spread, with many experiencing disease for 3 to 4 years. Fomites such as towels, washcloths, and sponges can transfer the virus and spread lesions; therefore, I advise patients to gently pat their skin dry, wash towels frequently, and avoid sharing bathing equipment.^1,3,5 Children and adults with immunosuppression may have a greater number of lesions and more prolonged course of disease, including those with HIV as well as DOC8 and CARD11 mutations.⁶ The American Academy of Pediatrics (AAP) emphasizes that children should not be excluded from attending child care/school or from swimming in public pools but lesions should be covered.⁶ Lesions, especially those in the antecubital region, can trigger new-onset AD or AD flares.³ In response, gentle skin care including fragrance-free cleansers and periodic application of moisturizers may ward off AD. Topical corticosteroids are preferred.

Dermatitis in MCV is a great mimicker and can resemble erythema multiforme, Gianotti-Crosti syndrome, impetigo, and AD.¹ Superinfection recently has been reported; however, in a retrospective analysis of 56 patients with inflamed lesions secondary to molluscum infection, only 7 had positive bacterial cultures, which supports the idea of the swelling and redness of inflammation as a mimic for infection.⁷ When true infection does occur, tender, swollen, pus-filled lesions should be lanced and cultured.^1,7,8

When should we consider therapy?

Therapy is highly dependent on the child, the caregiver, and the social circumstances.¹ More than 80% of parents are anxious about molluscum, and countless children are embarrassed or ashamed.¹ Ultimately, an unhappy child merits care. The AAP cites the following as reasons to treat: “(1) alleviate discomfort, including itching; (2) reduce autoinoculation; (3) limit transmission of the virus to close contacts; (4) reduce cosmetic concerns; and (5) prevent secondary infection.”⁶ For adults, we should consider limitations to intimacy and reduction of sexual transmission risk.⁶

Treatment can be based on the number of lesions. With a few lesions (<3), therapy is worthwhile if they are unsightly; appear on exposed skin causing embarrassment; and/or are itchy, uncomfortable, or large. In a report of 300 children with molluscum treated with cantharidin, most patients choosing therapy had 10 to 20 lesions, but this was over multiple visits.⁸ Looking at a 2018 data set of 50 patients (all-comers) with molluscum,³ the mean number of lesions was 10 (median, 7); 3 lesions were 1 SD below, while 14, 17, and 45 were 1, 2, and 3 SDs above, respectively. This data set shows that patients can develop more lesions rapidly, and most children have many visible lesions (N.B. Silverberg, MD, unpublished data).

Because each lesion contains infectious viral particles and patients scratch, more lesions are equated to greater autoinoculation and contagion. In addition to the AAP criteria, treatment can be considered for households with immunocompromised individuals, children at risk for new-onset AD, or those with AD at risk for flare. For patients with 45 lesions or more (3 SDs), clearance is harder to achieve with 2 sessions of in-office therapy, and multiple methods or the addition of immunomodulatory therapeutics should be considered.

Do we have to clear every lesion?

New molluscum lesions may arise until a patient achieves immunity, and they may appear more than a month after inoculation, making it difficult to keep up with the rapid spread. Latency between exposure and lesion development usually is 2 to 7 weeks but may be as long as 6 months, making it difficult to prevent spread.⁶ Therefore, when we treat, we should not promise full clearance to patients and parents. Rather, we should inform them that new lesions may develop later, and therapy is only effective on visible lesions. In a recent study, a 50% clearance of lesions was the satisfactory threshold for parents, demonstrating that satisfaction is possible with partial clearance.⁹

What is new in therapeutics for molluscum?

Molluscum therapies are either destructive, immunomodulatory, or antiviral. Two agents now are approved by the FDA for the treatment of molluscum infections.

Berdazimer gel 10.3% is approved for patients 1 year or older, but it is not yet available. This agent has both immunomodulatory and antiviral properties.¹⁰ It features a home therapy that is mixed on a small palette, then painted on by the patient or parent once daily for 12 weeks. Study outcomes demonstrated more than 50% lesional clearance.^11,12 Complete clearance was achieved in at least 30% of patients.¹²A proprietary topical version of cantharidin 0.7% in flexible collodion is now FDA approved for patients 2 years and older. This vesicant-triggering iatrogenic is targeted at creating blisters overlying molluscum lesions. It is conceptually similar to older versions but with some enhanced features.^5,13,14 This version was used for therapy every 3 weeks for up to 4 sessions in clinical trials. Safety is similar across all body sites treated (nonmucosal and not near the mucosal surfaces) but not for mucosa, the mid face, or eyelids.¹³ Complete lesion clearance was 46.3% to 54% and statistically greater than placebo (P<.001).¹⁴Both agents are well tolerated in children with AD; adverse effects include blistering with cantharidin and dermatitislike symptoms with berdazimer.^15,16 These therapies have the advantage of being easy to use.

Final Thoughts

We have entered an era of high-quality molluscum therapy. Patient care involves developing a good knowledge of the agents, incorporating shared decision-making with patients and caregivers, and addressing therapy in the context of comorbid diseases such as AD.

Richard* was a master-of-the-universe type. He went to Wharton, ran a large hedge fund, and lived in Greenwich, Connecticut. His three children attended Ivy League schools. He played golf on the weekends and ate three healthy meals per day. There was just one issue: He had gained 90 pounds since the 1990s from consuming six to seven alcoholic beverages per day. He already had one DUI under his belt, and his marriage was on shaky ground. He had tried to address his alcohol abuse disorder on multiple occasions: He went to a yearlong class on alcoholism, saw a psychologist for cognitive-behavioral therapy, and joined Alcoholics Anonymous, all to no avail. 

When I met him in December 2023, he had hit rock bottom and was willing to try anything.

At our first visit, I prescribed him weekly tirzepatide (Zepbound) off label, along with a small dose of naltrexone. 

Richard shared some feedback after his first 2 weeks:

The naltrexone works great and is strong ... small dose for me effective ... I haven’t wanted to drink and when I do I can’t finish a glass over 2 hours … went from 25 drinks a week to about 4 … don’t notice other side effects … sleeping better too.

And after 6 weeks:

Some more feedback … on week 6-7 and all going well ... drinking very little alcohol and still on half tab of naltrexone ... that works well and have no side effects ... the Zepbound works well too. I do get hungry a few days after the shot but still don’t crave sugar or bad snacks … weight down 21 pounds since started … 292 to 271.

And finally, after 8 weeks:

Looking at my last text to you I see the progress … been incredible ... now down 35 pounds and at 257 … continue to feel excellent with plenty of energy … want to exercise more ... and no temptation to eat or drink unhealthy stuff ... I’m very happy this has surpassed my expectations on how fast it’s worked and I don’t feel any side effects. Marriage has never been better … all thanks to you. 

Tirzepatide contains two hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), that are naturally produced by our bodies after meals. Scientists recently learned that the GLP-1 system contributes to the feedback loop of addictive behaviors. Increasing synthetic GLP-1, through medications like tirzepatide, appears to minimize addictive behaviors by limiting their ability to upregulate the brain’s production of dopamine. 

Dopamine is a neurotransmitter produced in the brain’s reward center, which regulates how people experience pleasure and control impulses. Dopamine reinforces the pleasure experienced by certain behaviors like drinking, smoking, and eating sweets. These new medications reduce the amount of dopamine released after these activities and thereby lower the motivation to repeat these behaviors. 

Contrary to some reports in the news, the vast majority of my male patients using these medications for alcohol abuse disorder experience concurrent increases in testosterone, for two reasons: (1) testosterone increases as body mass index decreases and (2) chronic alcohol use can damage the cells in the testicles that produce testosterone and also decrease the brain’s ability to stimulate the testicles to produce testosterone. 

At his most recent checkup last month, Richard’s testosterone had risen from borderline to robust levels, his libido and sleep had improved, and he reported never having felt so healthy or confident. Fingers crossed that the US Food and Drug Administration won’t wait too long before approving this class of medications for more than just diabetes, heart disease, and obesity. 

*Patient’s name has been changed.
 

Dr. Messer is clinical assistant professor, Icahn School of Medicine at Mount Sinai, New York, and associate professor, Zucker School of Medicine at Hofstra University, Hempstead, New York. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Richard* was a master-of-the-universe type. He went to Wharton, ran a large hedge fund, and lived in Greenwich, Connecticut. His three children attended Ivy League schools. He played golf on the weekends and ate three healthy meals per day. There was just one issue: He had gained 90 pounds since the 1990s from consuming six to seven alcoholic beverages per day. He already had one DUI under his belt, and his marriage was on shaky ground. He had tried to address his alcohol abuse disorder on multiple occasions: He went to a yearlong class on alcoholism, saw a psychologist for cognitive-behavioral therapy, and joined Alcoholics Anonymous, all to no avail. 

When I met him in December 2023, he had hit rock bottom and was willing to try anything.

At our first visit, I prescribed him weekly tirzepatide (Zepbound) off label, along with a small dose of naltrexone. 

Richard shared some feedback after his first 2 weeks:

The naltrexone works great and is strong ... small dose for me effective ... I haven’t wanted to drink and when I do I can’t finish a glass over 2 hours … went from 25 drinks a week to about 4 … don’t notice other side effects … sleeping better too.

And after 6 weeks:

Some more feedback … on week 6-7 and all going well ... drinking very little alcohol and still on half tab of naltrexone ... that works well and have no side effects ... the Zepbound works well too. I do get hungry a few days after the shot but still don’t crave sugar or bad snacks … weight down 21 pounds since started … 292 to 271.

And finally, after 8 weeks:

Looking at my last text to you I see the progress … been incredible ... now down 35 pounds and at 257 … continue to feel excellent with plenty of energy … want to exercise more ... and no temptation to eat or drink unhealthy stuff ... I’m very happy this has surpassed my expectations on how fast it’s worked and I don’t feel any side effects. Marriage has never been better … all thanks to you. 

Tirzepatide contains two hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), that are naturally produced by our bodies after meals. Scientists recently learned that the GLP-1 system contributes to the feedback loop of addictive behaviors. Increasing synthetic GLP-1, through medications like tirzepatide, appears to minimize addictive behaviors by limiting their ability to upregulate the brain’s production of dopamine. 

Dopamine is a neurotransmitter produced in the brain’s reward center, which regulates how people experience pleasure and control impulses. Dopamine reinforces the pleasure experienced by certain behaviors like drinking, smoking, and eating sweets. These new medications reduce the amount of dopamine released after these activities and thereby lower the motivation to repeat these behaviors. 

Contrary to some reports in the news, the vast majority of my male patients using these medications for alcohol abuse disorder experience concurrent increases in testosterone, for two reasons: (1) testosterone increases as body mass index decreases and (2) chronic alcohol use can damage the cells in the testicles that produce testosterone and also decrease the brain’s ability to stimulate the testicles to produce testosterone. 

At his most recent checkup last month, Richard’s testosterone had risen from borderline to robust levels, his libido and sleep had improved, and he reported never having felt so healthy or confident. Fingers crossed that the US Food and Drug Administration won’t wait too long before approving this class of medications for more than just diabetes, heart disease, and obesity. 

*Patient’s name has been changed.
 

Dr. Messer is clinical assistant professor, Icahn School of Medicine at Mount Sinai, New York, and associate professor, Zucker School of Medicine at Hofstra University, Hempstead, New York. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Richard* was a master-of-the-universe type. He went to Wharton, ran a large hedge fund, and lived in Greenwich, Connecticut. His three children attended Ivy League schools. He played golf on the weekends and ate three healthy meals per day. There was just one issue: He had gained 90 pounds since the 1990s from consuming six to seven alcoholic beverages per day. He already had one DUI under his belt, and his marriage was on shaky ground. He had tried to address his alcohol abuse disorder on multiple occasions: He went to a yearlong class on alcoholism, saw a psychologist for cognitive-behavioral therapy, and joined Alcoholics Anonymous, all to no avail. 

When I met him in December 2023, he had hit rock bottom and was willing to try anything.

At our first visit, I prescribed him weekly tirzepatide (Zepbound) off label, along with a small dose of naltrexone. 

Richard shared some feedback after his first 2 weeks:

The naltrexone works great and is strong ... small dose for me effective ... I haven’t wanted to drink and when I do I can’t finish a glass over 2 hours … went from 25 drinks a week to about 4 … don’t notice other side effects … sleeping better too.

And after 6 weeks:

Some more feedback … on week 6-7 and all going well ... drinking very little alcohol and still on half tab of naltrexone ... that works well and have no side effects ... the Zepbound works well too. I do get hungry a few days after the shot but still don’t crave sugar or bad snacks … weight down 21 pounds since started … 292 to 271.

And finally, after 8 weeks:

Looking at my last text to you I see the progress … been incredible ... now down 35 pounds and at 257 … continue to feel excellent with plenty of energy … want to exercise more ... and no temptation to eat or drink unhealthy stuff ... I’m very happy this has surpassed my expectations on how fast it’s worked and I don’t feel any side effects. Marriage has never been better … all thanks to you. 

Tirzepatide contains two hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), that are naturally produced by our bodies after meals. Scientists recently learned that the GLP-1 system contributes to the feedback loop of addictive behaviors. Increasing synthetic GLP-1, through medications like tirzepatide, appears to minimize addictive behaviors by limiting their ability to upregulate the brain’s production of dopamine. 

Dopamine is a neurotransmitter produced in the brain’s reward center, which regulates how people experience pleasure and control impulses. Dopamine reinforces the pleasure experienced by certain behaviors like drinking, smoking, and eating sweets. These new medications reduce the amount of dopamine released after these activities and thereby lower the motivation to repeat these behaviors. 

Contrary to some reports in the news, the vast majority of my male patients using these medications for alcohol abuse disorder experience concurrent increases in testosterone, for two reasons: (1) testosterone increases as body mass index decreases and (2) chronic alcohol use can damage the cells in the testicles that produce testosterone and also decrease the brain’s ability to stimulate the testicles to produce testosterone. 

At his most recent checkup last month, Richard’s testosterone had risen from borderline to robust levels, his libido and sleep had improved, and he reported never having felt so healthy or confident. Fingers crossed that the US Food and Drug Administration won’t wait too long before approving this class of medications for more than just diabetes, heart disease, and obesity. 

*Patient’s name has been changed.
 

Dr. Messer is clinical assistant professor, Icahn School of Medicine at Mount Sinai, New York, and associate professor, Zucker School of Medicine at Hofstra University, Hempstead, New York. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.