Clinician Reviews

Clinicians are using dupilumab off label to treat a wider range of allergic conditions in adults and children.

The drug, marketed as Dupixent, is currently approved in the United States to treat atopic dermatitis, asthma, chronic rhinosinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis in adults. Dupilumab is also approved to treat eosinophilic esophagitis in patients aged 12 years and older and atopic dermatitis and asthma in some patients as young as age 6 months.

As the roster of approved and off-label indications grows, skin specialists said, pediatricians and other primary care providers should become familiar with the drug – given the increasing likelihood that their patients may be taking the medication.

The U.S. Food and Drug Administration first approved dupilumab in 2017 for eczema and has continued to add new treatment indications, the most recent being for prurigo nodularis, in 2022. Sanofi, which markets the drug with Regeneron, announced in April 2022 that some 430,000 patients worldwide were taking the drug – a figure it hoped to raise by 1.5 million by 2025.
 

A well-tolerated – if expensive – drug

Dupilumab, an interleukin-4 (IL-4) receptor alpha-antagonist biologic, blocks both IL-4 and IL-13 signaling, Marlys Fassett, MD, PhD, associate professor of dermatology at the University of California, San Francisco, told this news organization.

Dr. Fassett said she prescribes the drug off label for chronic idiopathic urticaria, including in older patients, and finds that the side effects in older patients are similar to those in younger people. The medication costs $36,000 per year, although some patients can get it more cheaply.

“Dupixent is a super-safe drug because it doesn’t immunosuppress any other part of the immune system, so you still have good antibacterial, antiviral, and antifungal immunity,” she added. “That makes perfect sense as a biological mechanism, and it’s been found safe in clinical trials.”

Case reports of potential adverse reactions to dupilumab have included ocular surface disease, lichen planus, and rash on the face and neck.

“We’re still learning about complications and are watching patients carefully,” said Marissa J. Perman, MD, section chief of dermatology at Children’s Hospital of Philadelphia.

Many people with atopic dermatitis also have other allergic conditions, such as contact dermatitis, asthma, prurigo nodularis, allergic rhinitis, and seasonal allergies. Each of these conditions has a pathway that depends on IL-4 receptors, Dr. Fassett said.

“It’s amazing how many conditions Dupixent improves. Sometimes we prescribe on-label Dupixent for atopic dermatitis, and inadvertently, the drug also improves that patient’s other, off-label conditions,” Dr. Fassett said. “I think that’s the best evidence that Dupixent works in these off-label cases.”

Lindsay C. Strowd, MD, associate professor of dermatology at Wake Forest University, Winston-Salem, N.C., said she uses off-label dupilumab to treat bullous pemphigoid and intense pruritus of unknown etiology.

“And several times I have treated drug reaction with eosinophilia and systemic symptoms, a rare adverse drug reaction that causes a rash and eosinophilia,” Dr. Strowd added.

Tissa Hata, MD, professor of medicine and clinical service chief at the University of California, San Diego, mainly treats elderly patients. She uses dupilumab to treat bullous pemphigoid and chronic pruritus. “There have been reports of using Dupixent to treat adult alopecia areata, chronic urticaria, localized scleroderma, and even keloids,” she told this news organization.

As a pediatric dermatologist, Dr. Perman treats children with atopic dermatitis as young as 3 months of age. She also uses dupilumab for alopecia areata, graft vs. host disease, and pruritus not otherwise specified.

Conjunctivitis and facial redness are two side effects Dr. Fassett sometimes sees with dupilumab. They occur similarly with all conditions and in all age groups. “We don’t know why they occur, and we don’t always know how to alleviate them,” she said. “So a small number of patients stop using Dupixent because they can’t tolerate those two side effects.

“We’re not worried about infection risk,” Dr. Fassett said. “Your patients may have heard of dupilumab as an immunosuppressant, but its immunosuppression is very focused. You can reassure them that they’re not at increased risk for viral or bacterial infections when they’re on this drug.”

“I don’t think there are any different safety signals to watch for with on-label vs. off-label Dupixent use,” Dr. Strowd added. “In general, the medicine is very safe.”

Dr. Hata said she is impressed with dupilumab’s safety in her elderly patients. All her patients older than 85 years who have taken the drug for bullous pemphigoid have tolerated it well, she said.

“Dupixent seems to be a safe alternative for elderly patients with pruritus because they often cannot tolerate sedating antihistamines due to the risk of falling,” Dr. Hata said. “And UV therapy may be difficult for elderly patients due to problems with transport.”

Although some of Dr. Hata’s elderly patients with atopic dermatitis have discontinued use of the drug after developing conjunctivitis, none taking the drug off label have discontinued it because of side effects, she noted.

“Dupixent manages the condition, but it is not a cure,” Dr. Fassett noted. “Based on the current data, we think it’s safe and effective to take long term, potentially for life.”

Making injections less bothersome

Dupilumab is injected subcutaneously from a single-dose prefilled syringe or a prefilled pen (syringe hidden in an opaque sheath), typically in the thigh, arm, abdomen, or buttocks. According to Sanofi and Regeneron, patients receive dupilumab injections every 2 to 4 weeks in doses based on their age and weight.

“The medication is somewhat viscous, so taking the syringe or pen out of the refrigerator ahead of time to warm it up can make the experience less painful,” Dr. Strowd advised. “For pediatric patients, I sometimes prescribe topical lidocaine applied 30 minutes before injection.”

Dr. Hata suggested icing the skin prior to injecting or distracting the patient by tapping a different area of the skin.

For her pediatric patients, Dr. Perman said she uses “lots of distraction, EMLA cream, and having one person hold the child while a second person injects.”

Clinic and pharmacy staff may show patients how to inject properly, Dr. Fassett added; and the product website provides injection tutorials.
 

Off-label dupixent can be expensive, difficult to obtain

The list price per injection, regardless of dose, is around $1,800. But according to the company’s website, most patients have health insurance or qualify for other assistance, so “very few patients pay the list price.”

Even so, “due to cost and insurance coverage hurdles, obtaining Dupixent for off-label use can be difficult,” Dr. Strowd said.

“In academic medicine, we can obtain drugs for our patients that community doctors may not get approval for,” Dr. Fassett added. “Community doctors can use information in the medical literature and in news articles to press insurance companies to spend money to provide their patients with Dupixent.”

The experts who commented have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Clinicians are using dupilumab off label to treat a wider range of allergic conditions in adults and children.

The drug, marketed as Dupixent, is currently approved in the United States to treat atopic dermatitis, asthma, chronic rhinosinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis in adults. Dupilumab is also approved to treat eosinophilic esophagitis in patients aged 12 years and older and atopic dermatitis and asthma in some patients as young as age 6 months.

As the roster of approved and off-label indications grows, skin specialists said, pediatricians and other primary care providers should become familiar with the drug – given the increasing likelihood that their patients may be taking the medication.

The U.S. Food and Drug Administration first approved dupilumab in 2017 for eczema and has continued to add new treatment indications, the most recent being for prurigo nodularis, in 2022. Sanofi, which markets the drug with Regeneron, announced in April 2022 that some 430,000 patients worldwide were taking the drug – a figure it hoped to raise by 1.5 million by 2025.
 

A well-tolerated – if expensive – drug

Dupilumab, an interleukin-4 (IL-4) receptor alpha-antagonist biologic, blocks both IL-4 and IL-13 signaling, Marlys Fassett, MD, PhD, associate professor of dermatology at the University of California, San Francisco, told this news organization.

Dr. Fassett said she prescribes the drug off label for chronic idiopathic urticaria, including in older patients, and finds that the side effects in older patients are similar to those in younger people. The medication costs $36,000 per year, although some patients can get it more cheaply.

“Dupixent is a super-safe drug because it doesn’t immunosuppress any other part of the immune system, so you still have good antibacterial, antiviral, and antifungal immunity,” she added. “That makes perfect sense as a biological mechanism, and it’s been found safe in clinical trials.”

Case reports of potential adverse reactions to dupilumab have included ocular surface disease, lichen planus, and rash on the face and neck.

“We’re still learning about complications and are watching patients carefully,” said Marissa J. Perman, MD, section chief of dermatology at Children’s Hospital of Philadelphia.

Many people with atopic dermatitis also have other allergic conditions, such as contact dermatitis, asthma, prurigo nodularis, allergic rhinitis, and seasonal allergies. Each of these conditions has a pathway that depends on IL-4 receptors, Dr. Fassett said.

“It’s amazing how many conditions Dupixent improves. Sometimes we prescribe on-label Dupixent for atopic dermatitis, and inadvertently, the drug also improves that patient’s other, off-label conditions,” Dr. Fassett said. “I think that’s the best evidence that Dupixent works in these off-label cases.”

Lindsay C. Strowd, MD, associate professor of dermatology at Wake Forest University, Winston-Salem, N.C., said she uses off-label dupilumab to treat bullous pemphigoid and intense pruritus of unknown etiology.

“And several times I have treated drug reaction with eosinophilia and systemic symptoms, a rare adverse drug reaction that causes a rash and eosinophilia,” Dr. Strowd added.

Tissa Hata, MD, professor of medicine and clinical service chief at the University of California, San Diego, mainly treats elderly patients. She uses dupilumab to treat bullous pemphigoid and chronic pruritus. “There have been reports of using Dupixent to treat adult alopecia areata, chronic urticaria, localized scleroderma, and even keloids,” she told this news organization.

As a pediatric dermatologist, Dr. Perman treats children with atopic dermatitis as young as 3 months of age. She also uses dupilumab for alopecia areata, graft vs. host disease, and pruritus not otherwise specified.

Conjunctivitis and facial redness are two side effects Dr. Fassett sometimes sees with dupilumab. They occur similarly with all conditions and in all age groups. “We don’t know why they occur, and we don’t always know how to alleviate them,” she said. “So a small number of patients stop using Dupixent because they can’t tolerate those two side effects.

“We’re not worried about infection risk,” Dr. Fassett said. “Your patients may have heard of dupilumab as an immunosuppressant, but its immunosuppression is very focused. You can reassure them that they’re not at increased risk for viral or bacterial infections when they’re on this drug.”

“I don’t think there are any different safety signals to watch for with on-label vs. off-label Dupixent use,” Dr. Strowd added. “In general, the medicine is very safe.”

Dr. Hata said she is impressed with dupilumab’s safety in her elderly patients. All her patients older than 85 years who have taken the drug for bullous pemphigoid have tolerated it well, she said.

“Dupixent seems to be a safe alternative for elderly patients with pruritus because they often cannot tolerate sedating antihistamines due to the risk of falling,” Dr. Hata said. “And UV therapy may be difficult for elderly patients due to problems with transport.”

Although some of Dr. Hata’s elderly patients with atopic dermatitis have discontinued use of the drug after developing conjunctivitis, none taking the drug off label have discontinued it because of side effects, she noted.

“Dupixent manages the condition, but it is not a cure,” Dr. Fassett noted. “Based on the current data, we think it’s safe and effective to take long term, potentially for life.”

Making injections less bothersome

Dupilumab is injected subcutaneously from a single-dose prefilled syringe or a prefilled pen (syringe hidden in an opaque sheath), typically in the thigh, arm, abdomen, or buttocks. According to Sanofi and Regeneron, patients receive dupilumab injections every 2 to 4 weeks in doses based on their age and weight.

“The medication is somewhat viscous, so taking the syringe or pen out of the refrigerator ahead of time to warm it up can make the experience less painful,” Dr. Strowd advised. “For pediatric patients, I sometimes prescribe topical lidocaine applied 30 minutes before injection.”

Dr. Hata suggested icing the skin prior to injecting or distracting the patient by tapping a different area of the skin.

For her pediatric patients, Dr. Perman said she uses “lots of distraction, EMLA cream, and having one person hold the child while a second person injects.”

Clinic and pharmacy staff may show patients how to inject properly, Dr. Fassett added; and the product website provides injection tutorials.
 

Off-label dupixent can be expensive, difficult to obtain

The list price per injection, regardless of dose, is around $1,800. But according to the company’s website, most patients have health insurance or qualify for other assistance, so “very few patients pay the list price.”

Even so, “due to cost and insurance coverage hurdles, obtaining Dupixent for off-label use can be difficult,” Dr. Strowd said.

“In academic medicine, we can obtain drugs for our patients that community doctors may not get approval for,” Dr. Fassett added. “Community doctors can use information in the medical literature and in news articles to press insurance companies to spend money to provide their patients with Dupixent.”

The experts who commented have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Clinicians are using dupilumab off label to treat a wider range of allergic conditions in adults and children.

The drug, marketed as Dupixent, is currently approved in the United States to treat atopic dermatitis, asthma, chronic rhinosinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis in adults. Dupilumab is also approved to treat eosinophilic esophagitis in patients aged 12 years and older and atopic dermatitis and asthma in some patients as young as age 6 months.

As the roster of approved and off-label indications grows, skin specialists said, pediatricians and other primary care providers should become familiar with the drug – given the increasing likelihood that their patients may be taking the medication.

The U.S. Food and Drug Administration first approved dupilumab in 2017 for eczema and has continued to add new treatment indications, the most recent being for prurigo nodularis, in 2022. Sanofi, which markets the drug with Regeneron, announced in April 2022 that some 430,000 patients worldwide were taking the drug – a figure it hoped to raise by 1.5 million by 2025.
 

A well-tolerated – if expensive – drug

Dupilumab, an interleukin-4 (IL-4) receptor alpha-antagonist biologic, blocks both IL-4 and IL-13 signaling, Marlys Fassett, MD, PhD, associate professor of dermatology at the University of California, San Francisco, told this news organization.

Dr. Fassett said she prescribes the drug off label for chronic idiopathic urticaria, including in older patients, and finds that the side effects in older patients are similar to those in younger people. The medication costs $36,000 per year, although some patients can get it more cheaply.

“Dupixent is a super-safe drug because it doesn’t immunosuppress any other part of the immune system, so you still have good antibacterial, antiviral, and antifungal immunity,” she added. “That makes perfect sense as a biological mechanism, and it’s been found safe in clinical trials.”

Case reports of potential adverse reactions to dupilumab have included ocular surface disease, lichen planus, and rash on the face and neck.

“We’re still learning about complications and are watching patients carefully,” said Marissa J. Perman, MD, section chief of dermatology at Children’s Hospital of Philadelphia.

Many people with atopic dermatitis also have other allergic conditions, such as contact dermatitis, asthma, prurigo nodularis, allergic rhinitis, and seasonal allergies. Each of these conditions has a pathway that depends on IL-4 receptors, Dr. Fassett said.

“It’s amazing how many conditions Dupixent improves. Sometimes we prescribe on-label Dupixent for atopic dermatitis, and inadvertently, the drug also improves that patient’s other, off-label conditions,” Dr. Fassett said. “I think that’s the best evidence that Dupixent works in these off-label cases.”

Lindsay C. Strowd, MD, associate professor of dermatology at Wake Forest University, Winston-Salem, N.C., said she uses off-label dupilumab to treat bullous pemphigoid and intense pruritus of unknown etiology.

“And several times I have treated drug reaction with eosinophilia and systemic symptoms, a rare adverse drug reaction that causes a rash and eosinophilia,” Dr. Strowd added.

Tissa Hata, MD, professor of medicine and clinical service chief at the University of California, San Diego, mainly treats elderly patients. She uses dupilumab to treat bullous pemphigoid and chronic pruritus. “There have been reports of using Dupixent to treat adult alopecia areata, chronic urticaria, localized scleroderma, and even keloids,” she told this news organization.

As a pediatric dermatologist, Dr. Perman treats children with atopic dermatitis as young as 3 months of age. She also uses dupilumab for alopecia areata, graft vs. host disease, and pruritus not otherwise specified.

Conjunctivitis and facial redness are two side effects Dr. Fassett sometimes sees with dupilumab. They occur similarly with all conditions and in all age groups. “We don’t know why they occur, and we don’t always know how to alleviate them,” she said. “So a small number of patients stop using Dupixent because they can’t tolerate those two side effects.

“We’re not worried about infection risk,” Dr. Fassett said. “Your patients may have heard of dupilumab as an immunosuppressant, but its immunosuppression is very focused. You can reassure them that they’re not at increased risk for viral or bacterial infections when they’re on this drug.”

“I don’t think there are any different safety signals to watch for with on-label vs. off-label Dupixent use,” Dr. Strowd added. “In general, the medicine is very safe.”

Dr. Hata said she is impressed with dupilumab’s safety in her elderly patients. All her patients older than 85 years who have taken the drug for bullous pemphigoid have tolerated it well, she said.

“Dupixent seems to be a safe alternative for elderly patients with pruritus because they often cannot tolerate sedating antihistamines due to the risk of falling,” Dr. Hata said. “And UV therapy may be difficult for elderly patients due to problems with transport.”

Although some of Dr. Hata’s elderly patients with atopic dermatitis have discontinued use of the drug after developing conjunctivitis, none taking the drug off label have discontinued it because of side effects, she noted.

“Dupixent manages the condition, but it is not a cure,” Dr. Fassett noted. “Based on the current data, we think it’s safe and effective to take long term, potentially for life.”

Making injections less bothersome

Dupilumab is injected subcutaneously from a single-dose prefilled syringe or a prefilled pen (syringe hidden in an opaque sheath), typically in the thigh, arm, abdomen, or buttocks. According to Sanofi and Regeneron, patients receive dupilumab injections every 2 to 4 weeks in doses based on their age and weight.

“The medication is somewhat viscous, so taking the syringe or pen out of the refrigerator ahead of time to warm it up can make the experience less painful,” Dr. Strowd advised. “For pediatric patients, I sometimes prescribe topical lidocaine applied 30 minutes before injection.”

Dr. Hata suggested icing the skin prior to injecting or distracting the patient by tapping a different area of the skin.

For her pediatric patients, Dr. Perman said she uses “lots of distraction, EMLA cream, and having one person hold the child while a second person injects.”

Clinic and pharmacy staff may show patients how to inject properly, Dr. Fassett added; and the product website provides injection tutorials.
 

Off-label dupixent can be expensive, difficult to obtain

The list price per injection, regardless of dose, is around $1,800. But according to the company’s website, most patients have health insurance or qualify for other assistance, so “very few patients pay the list price.”

Even so, “due to cost and insurance coverage hurdles, obtaining Dupixent for off-label use can be difficult,” Dr. Strowd said.

“In academic medicine, we can obtain drugs for our patients that community doctors may not get approval for,” Dr. Fassett added. “Community doctors can use information in the medical literature and in news articles to press insurance companies to spend money to provide their patients with Dupixent.”

The experts who commented have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

People may get more protection against COVID-19 if they get their vaccinations and boosters in the same arm, a new study says.

Scientists in Germany looked at health data for 303 people who got the mRNA vaccine and then a booster shot. Their antibody levels were measured two weeks after the second shot. None of the people had had COVID before the vaccinations.

Scientists found that the number of protective “killer T cells” was higher in the 147 study participants who got both shots in the same arm, said the study published in EBioMedicine.

The killer cells were found in 67% of cases in which both shots went into the same arm, compared with 43% of cases with different arms.

“That may suggest that that ipsilateral vaccination (in the same arm) is more likely to provide better protection should the vaccinated person become infected with the SARS-CoV-2 virus,” Laura Ziegler, a doctoral student at Saarland University, Germany, said in a news release.

William Schaffner, MD, a professor in the Division of Infectious Diseases at Vanderbilt University Medical Center, Nashville, Tenn., told CBS News that same-arm vaccinations may work better because the cells that provide the immune response are in local lymph nodes.

There’s greater immunological response if the immune cells in the lymph nodes are restimulated in the same place, said Dr. Schaffner, who was not involved in the German study.

The scientists from Saarland University said more research is needed before they can be certain that having vaccinations in the same arm is actually more effective for COVID shots and sequential vaccinations against diseases such as the flu.

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

People may get more protection against COVID-19 if they get their vaccinations and boosters in the same arm, a new study says.

Scientists in Germany looked at health data for 303 people who got the mRNA vaccine and then a booster shot. Their antibody levels were measured two weeks after the second shot. None of the people had had COVID before the vaccinations.

Scientists found that the number of protective “killer T cells” was higher in the 147 study participants who got both shots in the same arm, said the study published in EBioMedicine.

The killer cells were found in 67% of cases in which both shots went into the same arm, compared with 43% of cases with different arms.

“That may suggest that that ipsilateral vaccination (in the same arm) is more likely to provide better protection should the vaccinated person become infected with the SARS-CoV-2 virus,” Laura Ziegler, a doctoral student at Saarland University, Germany, said in a news release.

William Schaffner, MD, a professor in the Division of Infectious Diseases at Vanderbilt University Medical Center, Nashville, Tenn., told CBS News that same-arm vaccinations may work better because the cells that provide the immune response are in local lymph nodes.

There’s greater immunological response if the immune cells in the lymph nodes are restimulated in the same place, said Dr. Schaffner, who was not involved in the German study.

The scientists from Saarland University said more research is needed before they can be certain that having vaccinations in the same arm is actually more effective for COVID shots and sequential vaccinations against diseases such as the flu.

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

People may get more protection against COVID-19 if they get their vaccinations and boosters in the same arm, a new study says.

Scientists in Germany looked at health data for 303 people who got the mRNA vaccine and then a booster shot. Their antibody levels were measured two weeks after the second shot. None of the people had had COVID before the vaccinations.

Scientists found that the number of protective “killer T cells” was higher in the 147 study participants who got both shots in the same arm, said the study published in EBioMedicine.

The killer cells were found in 67% of cases in which both shots went into the same arm, compared with 43% of cases with different arms.

“That may suggest that that ipsilateral vaccination (in the same arm) is more likely to provide better protection should the vaccinated person become infected with the SARS-CoV-2 virus,” Laura Ziegler, a doctoral student at Saarland University, Germany, said in a news release.

William Schaffner, MD, a professor in the Division of Infectious Diseases at Vanderbilt University Medical Center, Nashville, Tenn., told CBS News that same-arm vaccinations may work better because the cells that provide the immune response are in local lymph nodes.

There’s greater immunological response if the immune cells in the lymph nodes are restimulated in the same place, said Dr. Schaffner, who was not involved in the German study.

The scientists from Saarland University said more research is needed before they can be certain that having vaccinations in the same arm is actually more effective for COVID shots and sequential vaccinations against diseases such as the flu.

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

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

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

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

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

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

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

The European Medicines Agency has validated the marketing authorization application for delgocitinib cream, for the treatment of adults with chronic moderate to severe hand eczema, which marks the beginning of the review process for the treatment by the EMA’s Committee for Medicinal Products for Human Use.

Delgocitinib is an investigational topical pan–Janus kinase inhibitor that inhibits activation of the JAK-STAT pathway.

The development follows results reported from two phase 3 clinical trials known as DELTA 1 and DELTA 2, which evaluated the safety and efficacy of delgocitinib cream applications twice per day compared with a vehicle cream in adults with mild to severe chronic hand eczema. Results of DELTA 1 were presented at the 2023 annual meeting of the American Academy of Dermatology. A multisite, open-label extension trial known as DELTA 3 is still in progress.

According to a press release from LEO Pharma, which is developing the product, the efficacy and safety of delgocitinib cream have not been evaluated by any regulatory authority. In 2020, the drug was granted fast-track designation by the Food and Drug Administration for the potential treatment of adults with moderate to severe chronic hand eczema. There are currently no treatment options available in the United States specifically approved for treating the condition.



 

The European Medicines Agency has validated the marketing authorization application for delgocitinib cream, for the treatment of adults with chronic moderate to severe hand eczema, which marks the beginning of the review process for the treatment by the EMA’s Committee for Medicinal Products for Human Use.

Delgocitinib is an investigational topical pan–Janus kinase inhibitor that inhibits activation of the JAK-STAT pathway.

The development follows results reported from two phase 3 clinical trials known as DELTA 1 and DELTA 2, which evaluated the safety and efficacy of delgocitinib cream applications twice per day compared with a vehicle cream in adults with mild to severe chronic hand eczema. Results of DELTA 1 were presented at the 2023 annual meeting of the American Academy of Dermatology. A multisite, open-label extension trial known as DELTA 3 is still in progress.

According to a press release from LEO Pharma, which is developing the product, the efficacy and safety of delgocitinib cream have not been evaluated by any regulatory authority. In 2020, the drug was granted fast-track designation by the Food and Drug Administration for the potential treatment of adults with moderate to severe chronic hand eczema. There are currently no treatment options available in the United States specifically approved for treating the condition.



 

The European Medicines Agency has validated the marketing authorization application for delgocitinib cream, for the treatment of adults with chronic moderate to severe hand eczema, which marks the beginning of the review process for the treatment by the EMA’s Committee for Medicinal Products for Human Use.

Delgocitinib is an investigational topical pan–Janus kinase inhibitor that inhibits activation of the JAK-STAT pathway.

The development follows results reported from two phase 3 clinical trials known as DELTA 1 and DELTA 2, which evaluated the safety and efficacy of delgocitinib cream applications twice per day compared with a vehicle cream in adults with mild to severe chronic hand eczema. Results of DELTA 1 were presented at the 2023 annual meeting of the American Academy of Dermatology. A multisite, open-label extension trial known as DELTA 3 is still in progress.

According to a press release from LEO Pharma, which is developing the product, the efficacy and safety of delgocitinib cream have not been evaluated by any regulatory authority. In 2020, the drug was granted fast-track designation by the Food and Drug Administration for the potential treatment of adults with moderate to severe chronic hand eczema. There are currently no treatment options available in the United States specifically approved for treating the condition.



 

Physicians may be missing opportunities to reduce harmful polypharmacy in elderly patients with newly diagnosed dementia, investigators for a large study of Medicare beneficiaries reported.

They found that those with an incident dementia diagnosis were somewhat more likely to initiate central nervous system–active medications and slightly more likely to discontinue cardiometabolic and anticholinergic medications, compared with controls.

According to the authors, time of diagnosis can be a potential inflexion point for deprescribing long-term medications with high safety risks, limited likelihood of benefit, or possible association with impaired cognition.

“Understanding the chronology of medication changes following a first dementia diagnosis may identify targets for deprescribing interventions to reduce preventable medication-related harms, said Timothy S. Anderson, MD, MAS, of the division of general medicine at Beth Israel Deaconess Medical Center, Boston, and colleagues in JAMA Internal Medicine.

“Our results provide a baseline to inform efforts to rethink the clinical approach to medication use at the time of a new dementia diagnosis.”

Hundreds of thousands of Americans are diagnosed annually with Alzheimer’s and related dementias, the authors pointed out, and the majority have multiple other chronic conditions. Worsening cognitive impairment may alter the risk-benefit balance of medications taken for these conditions.

Matched cohort study

The sample consisted of adults 67 years or older enrolled in traditional Medicare and Medicare Part D. Patients with an initial incident dementia diagnosis between January 2012 and December 2018 were matched with controls (as of last doctor’s office visit) based on demographics, geographic location, and baseline medication count. Data were analyzed from 2021 to June 2023.

The study included 266,675 adults with incident dementia and 266,675 controls. In both groups, 65.1% were 80 years or older (mean age, 82.2) and 67.8% were female. At baseline, patients with incident dementia were more likely than controls to use CNS-active medications (54.32% vs. 48.39%) and anticholinergic medications (17.79% vs. 15.96%) and less likely to use most cardiometabolic medications (for example, antidiabetics, 31.19% vs. 36.45%).

Immediately following the index diagnosis, the dementia cohort had greater increases in the mean number of medications used: 0.41 vs. –0.06 (95% confidence interval, 0.27-0.66) and in the proportion using CNS-active medications (absolute change, 3.44% vs. 0.79%; 95% CI, 0.85%-4.45%). The rise was because of an increased use of antipsychotics, antidepressants, and antiepileptics.

The affected cohort showed a modestly greater decline in anticholinergic medications: quarterly change in use: −0.53% vs. −0.21% (95% CI, −0.55% to −0.08%); and in most cardiometabolic medications: for example, quarterly change in antihypertensive use: –0.84% vs. –0.40% (95% CI, –0.64% to –0.25%). Still, a year post diagnosis, 75.2% of dementia patients were using five or more medications, for a 2.8% increase.

The drug classes with the steepest rate of discontinuation – such as lipid-lowering and antihypertensive medications – had low risks for adverse drug events, while higher-risk classes – such as insulins and antiplatelet and anticoagulant agents – had smaller or no reductions in use.

While the findings point to opportunities to reduce polypharmacy by deprescribing long-term medications of dubious benefit, interventions to reduce polypharmacy and inappropriate medications have been modestly successful for patients without dementia, the authors said. But the recent OPTIMIZE trial, an educational effort aimed at primary care clinicians and patients with cognitive impairment, reduced neither polypharmacy nor potentially inappropriate medications.

Luke D. Kim, MD, a geriatrician at the Cleveland Clinic in Ohio, agreed that seniors with dementia can benefit from reassessment of their pharmacologic therapies. “Older adults in general are more prone to have side effects from medications as their renal and hepatic clearance and metabolism are different and lower than those of younger individuals. But they tend to take multiple medications owing to more comorbidities,” said Dr. Kim, who was not involved in the study. “While all older adults need to be more careful about medication management, those with dementia need an even more careful approach as they have diminished cognitive reserve and risk more potential harm from medications.” 

The authors noted that since decision-making models aligned with patient priorities for older adults without dementia led to reductions in overall medication use, that may be a path forward in populations with dementia.

The study was supported by grants from the National Institute on Aging, National Institutes of Health. The authors had no competing interests to disclose. Dr. Kim disclosed no competing interests relevant to his comments.

Physicians may be missing opportunities to reduce harmful polypharmacy in elderly patients with newly diagnosed dementia, investigators for a large study of Medicare beneficiaries reported.

They found that those with an incident dementia diagnosis were somewhat more likely to initiate central nervous system–active medications and slightly more likely to discontinue cardiometabolic and anticholinergic medications, compared with controls.

According to the authors, time of diagnosis can be a potential inflexion point for deprescribing long-term medications with high safety risks, limited likelihood of benefit, or possible association with impaired cognition.

“Understanding the chronology of medication changes following a first dementia diagnosis may identify targets for deprescribing interventions to reduce preventable medication-related harms, said Timothy S. Anderson, MD, MAS, of the division of general medicine at Beth Israel Deaconess Medical Center, Boston, and colleagues in JAMA Internal Medicine.

“Our results provide a baseline to inform efforts to rethink the clinical approach to medication use at the time of a new dementia diagnosis.”

Hundreds of thousands of Americans are diagnosed annually with Alzheimer’s and related dementias, the authors pointed out, and the majority have multiple other chronic conditions. Worsening cognitive impairment may alter the risk-benefit balance of medications taken for these conditions.

Matched cohort study

The sample consisted of adults 67 years or older enrolled in traditional Medicare and Medicare Part D. Patients with an initial incident dementia diagnosis between January 2012 and December 2018 were matched with controls (as of last doctor’s office visit) based on demographics, geographic location, and baseline medication count. Data were analyzed from 2021 to June 2023.

The study included 266,675 adults with incident dementia and 266,675 controls. In both groups, 65.1% were 80 years or older (mean age, 82.2) and 67.8% were female. At baseline, patients with incident dementia were more likely than controls to use CNS-active medications (54.32% vs. 48.39%) and anticholinergic medications (17.79% vs. 15.96%) and less likely to use most cardiometabolic medications (for example, antidiabetics, 31.19% vs. 36.45%).

Immediately following the index diagnosis, the dementia cohort had greater increases in the mean number of medications used: 0.41 vs. –0.06 (95% confidence interval, 0.27-0.66) and in the proportion using CNS-active medications (absolute change, 3.44% vs. 0.79%; 95% CI, 0.85%-4.45%). The rise was because of an increased use of antipsychotics, antidepressants, and antiepileptics.

The affected cohort showed a modestly greater decline in anticholinergic medications: quarterly change in use: −0.53% vs. −0.21% (95% CI, −0.55% to −0.08%); and in most cardiometabolic medications: for example, quarterly change in antihypertensive use: –0.84% vs. –0.40% (95% CI, –0.64% to –0.25%). Still, a year post diagnosis, 75.2% of dementia patients were using five or more medications, for a 2.8% increase.

The drug classes with the steepest rate of discontinuation – such as lipid-lowering and antihypertensive medications – had low risks for adverse drug events, while higher-risk classes – such as insulins and antiplatelet and anticoagulant agents – had smaller or no reductions in use.

While the findings point to opportunities to reduce polypharmacy by deprescribing long-term medications of dubious benefit, interventions to reduce polypharmacy and inappropriate medications have been modestly successful for patients without dementia, the authors said. But the recent OPTIMIZE trial, an educational effort aimed at primary care clinicians and patients with cognitive impairment, reduced neither polypharmacy nor potentially inappropriate medications.

Luke D. Kim, MD, a geriatrician at the Cleveland Clinic in Ohio, agreed that seniors with dementia can benefit from reassessment of their pharmacologic therapies. “Older adults in general are more prone to have side effects from medications as their renal and hepatic clearance and metabolism are different and lower than those of younger individuals. But they tend to take multiple medications owing to more comorbidities,” said Dr. Kim, who was not involved in the study. “While all older adults need to be more careful about medication management, those with dementia need an even more careful approach as they have diminished cognitive reserve and risk more potential harm from medications.” 

The authors noted that since decision-making models aligned with patient priorities for older adults without dementia led to reductions in overall medication use, that may be a path forward in populations with dementia.

The study was supported by grants from the National Institute on Aging, National Institutes of Health. The authors had no competing interests to disclose. Dr. Kim disclosed no competing interests relevant to his comments.

Physicians may be missing opportunities to reduce harmful polypharmacy in elderly patients with newly diagnosed dementia, investigators for a large study of Medicare beneficiaries reported.

They found that those with an incident dementia diagnosis were somewhat more likely to initiate central nervous system–active medications and slightly more likely to discontinue cardiometabolic and anticholinergic medications, compared with controls.

According to the authors, time of diagnosis can be a potential inflexion point for deprescribing long-term medications with high safety risks, limited likelihood of benefit, or possible association with impaired cognition.

“Understanding the chronology of medication changes following a first dementia diagnosis may identify targets for deprescribing interventions to reduce preventable medication-related harms, said Timothy S. Anderson, MD, MAS, of the division of general medicine at Beth Israel Deaconess Medical Center, Boston, and colleagues in JAMA Internal Medicine.

“Our results provide a baseline to inform efforts to rethink the clinical approach to medication use at the time of a new dementia diagnosis.”

Hundreds of thousands of Americans are diagnosed annually with Alzheimer’s and related dementias, the authors pointed out, and the majority have multiple other chronic conditions. Worsening cognitive impairment may alter the risk-benefit balance of medications taken for these conditions.

Matched cohort study

The sample consisted of adults 67 years or older enrolled in traditional Medicare and Medicare Part D. Patients with an initial incident dementia diagnosis between January 2012 and December 2018 were matched with controls (as of last doctor’s office visit) based on demographics, geographic location, and baseline medication count. Data were analyzed from 2021 to June 2023.

The study included 266,675 adults with incident dementia and 266,675 controls. In both groups, 65.1% were 80 years or older (mean age, 82.2) and 67.8% were female. At baseline, patients with incident dementia were more likely than controls to use CNS-active medications (54.32% vs. 48.39%) and anticholinergic medications (17.79% vs. 15.96%) and less likely to use most cardiometabolic medications (for example, antidiabetics, 31.19% vs. 36.45%).

Immediately following the index diagnosis, the dementia cohort had greater increases in the mean number of medications used: 0.41 vs. –0.06 (95% confidence interval, 0.27-0.66) and in the proportion using CNS-active medications (absolute change, 3.44% vs. 0.79%; 95% CI, 0.85%-4.45%). The rise was because of an increased use of antipsychotics, antidepressants, and antiepileptics.

The affected cohort showed a modestly greater decline in anticholinergic medications: quarterly change in use: −0.53% vs. −0.21% (95% CI, −0.55% to −0.08%); and in most cardiometabolic medications: for example, quarterly change in antihypertensive use: –0.84% vs. –0.40% (95% CI, –0.64% to –0.25%). Still, a year post diagnosis, 75.2% of dementia patients were using five or more medications, for a 2.8% increase.

The drug classes with the steepest rate of discontinuation – such as lipid-lowering and antihypertensive medications – had low risks for adverse drug events, while higher-risk classes – such as insulins and antiplatelet and anticoagulant agents – had smaller or no reductions in use.

While the findings point to opportunities to reduce polypharmacy by deprescribing long-term medications of dubious benefit, interventions to reduce polypharmacy and inappropriate medications have been modestly successful for patients without dementia, the authors said. But the recent OPTIMIZE trial, an educational effort aimed at primary care clinicians and patients with cognitive impairment, reduced neither polypharmacy nor potentially inappropriate medications.

Luke D. Kim, MD, a geriatrician at the Cleveland Clinic in Ohio, agreed that seniors with dementia can benefit from reassessment of their pharmacologic therapies. “Older adults in general are more prone to have side effects from medications as their renal and hepatic clearance and metabolism are different and lower than those of younger individuals. But they tend to take multiple medications owing to more comorbidities,” said Dr. Kim, who was not involved in the study. “While all older adults need to be more careful about medication management, those with dementia need an even more careful approach as they have diminished cognitive reserve and risk more potential harm from medications.” 

The authors noted that since decision-making models aligned with patient priorities for older adults without dementia led to reductions in overall medication use, that may be a path forward in populations with dementia.

The study was supported by grants from the National Institute on Aging, National Institutes of Health. The authors had no competing interests to disclose. Dr. Kim disclosed no competing interests relevant to his comments.

By now, concerns about COVID-related lawsuits have faded into the rear view mirror for most physicians.

But just when COVID lawsuits appear to be dwindling out, legal experts see a new lawsuit risk on the horizon – long COVID claims. While some say it’s doubtful the claims will succeed, the lawsuits could still create legal headaches for doctors in the form of time and money.

Long COVID claims are defined as complaints that allege that a diagnosis of long COVID was missed or delayed and that caused harm or injury. Lawsuits may also include claims in which patients allege that they were misdiagnosed as having long COVID when they were really suffering from another condition.

So far, a handful of long COVID claims have come down the pipeline, said Peter A. Kolbert, JD, senior vice president of claims and litigation services for Healthcare Risk Advisors, part of TDC Group.

“This is an area that is emerging as we speak,” Mr. Kolbert said. “We are starting to see these claims trickle in.”

In a recent case, for example, a patient sued her primary care physician for negligence, alleging her original SARS-CoV-2 infection was mismanaged and that this led to permanent neuropathy from long COVID. Had the patient been treated appropriately, the patient contends, she would not have developed long COVID or the resulting neuropathy, said Mr. Kolbert. An outcome in the case has not yet been reached, added Mr. Kolbert, who heard about the claim from a colleague.

The increase in the number of lawsuits raises concerns about how courts and juries might decide long COVID claims when so much about the condition is still unknown and best treatment practices are still developing. Research shows that long COVID occurs in at least 10% of cases of SARS-CoV-2 infection, and more than 200 symptoms have been identified. A Kaiser Family Foundation study found that 15% of the U.S. population believe they have experienced the symptoms of long COVID at some point, and 6% of people believe they currently have long COVID.

The risk of long COVID lawsuits underscores the importance of physicians taking proactive steps to protect themselves from liability when treating patients who might have the condition, say legal experts.

“There are legal standards that say new, unestablished scientific principles shouldn’t be first tested by a jury, they should be recognized and established within their [professional] area,” Mr. Kolbert said. “While we are seeing lawsuits related to long COVID, I think it is truly putting the cart before the horse, because there needs to be societal recognition that we’re still learning how to define and treat long COVID.”
 

What are patients alleging?

In the few long COVID claims that have arisen, some complaints have alleged delay in the recognition and treatment of long COVID, according to Mr. Kolbert. There have also been claims that physicians failed to refer a patient with long COVID to a specialist in a timely way and that this results in the patient’s experiencing chronic fatigue or a neuropathy.

Fatigue is one of the most common symptoms associated with long COVID, according to recent studies. Other symptoms include postexertional malaise, brain fog, and gastrointestinal problems.

Another rising legal theme is failure to adequately communicate with patients about what long COVID is and what it entails.

Whether plaintiffs who bring long COVID claims will be successful in court remains a question.

Andrew D. DeSimone, JD, a Lexington, Ky.–based medical malpractice defense attorney, said he has not seen any claims involving long COVID. He added that a long COVID claim would be challenging to prove, considering the standard of care for treating the condition is still evolving. Plaintiffs in a medical malpractice action must prove that physicians owed a duty of care to the patient, that the doctor breached that duty by failing to conform to the standard of care, and that the breach caused an injury that harmed the patient.

Mr. DeSimone also doubts whether juries would be very sympathetic to such plaintiffs.

“There’s a lot of fatigue around COVID still,” he said. “I don’t know if a jury would buy into someone claiming long COVID. I think the claim would have a hard time gaining traction. Not that it’s impossible.”

Another unanswered question is whether legal protections enacted by states during the pandemic might apply to long COVID claims.

Shortly after the pandemic started, most states enacted laws or executive orders that shielded physicians from liability claims relating to the prevention and treatment of COVID-19, unless gross negligence or willful misconduct is proved. The U.S. Department of Health and Human Services published a declaration under the Public Readiness and Emergency Preparedness Act (PREP Act) that provided liability immunity to health care professionals for any activity related to medical countermeasures against COVID-19.

Some of these state immunities have since expired. Other states have extended their legal protections for short periods. In Indiana, for example, physicians and businesses are protected until Dec. 31, 2024, from civil tort actions that allege damages arising from COVID-19.

It’s possible that in long COVID lawsuits, physicians would be protected by the immunities unless the cases come after the protections expire, said J. Richard Moore, a medical liability defense attorney based in Indianapolis.

“I could foresee long COVID claims that don’t accrue until after December 2024, meaning it only becomes clear that a patient is struggling with long COVID–related symptoms after that date,” he said. “That could result in COVID claims that do not fall under the immunities.”

Mr. Moore said that if long COVID claims become truly problematic, the legislature could extend the immunities.

Other states, such as Washington, have statutes in place that increase the burden of proof for plaintiffs in cases in which care is affected by COVID and/or the treating of COVID. Elizabeth A. Leedom, a Seattle-based medical liability defense attorney, said the law would likely encompass long COVID claims if the care and treatment at issue occurred during the COVID state of emergency.

Compliance with current treatment guidelines is likely to be a good defense against any claim of delay/failure to diagnose COVID, including long COVID, she said.

Mr. Kolbert, however, doubts that the state immunities would protect against the claims.

“Courts are enforcing qualified immunities as to [traditional] COVID claims. However, I suspect that long COVID claims will fall into a category of traditional medical malpractice claim, such as delay in or failure to diagnose,” he said. In such cases, physicians “may not be able to take advantage of state-qualified immunities. Of course, this will depend upon the language of each state’s qualified immunity provisions.”

As for the statute of limitations, the clock generally starts running either when the alleged negligent conduct occurred or when the patient knew or, in the exercise of ordinary diligence, should have known, that they had been harmed by the alleged negligence, Mr. Moore said. Statutes of limitations are state specific, but the majority of states mandate a 2- to 3-year limit between the injury and the filing of a claim.

So, while the statute of limitations may be soon expiring for alleged harm that occurred during the pandemic, for patients newly diagnosed with long COVID or who have just discovered associated injuries, the clock may have just started ticking.
 

How to protect yourself against suits

Avoiding liability associated with long COVID involves the traditional legal guidance physicians are used to hearing, but with an added factor, Mr. Kolbert said.

There always needs to be communication with patients regarding the disease process, but in this area, there needs to be strong communication as to whether patients have had COVID in the past and what symptoms they are experiencing, he said. Physicians should ensure that patients know that long COVID may present in a variety of ways and that there is no definitive test for long COVID.

Physicians should document when the patient has been instructed to follow up and should take necessary steps to ensure the patient returns for follow-up care, he added.

On the opposite side of the spectrum is making sure not to assume a condition or symptom is the result of long COVID, he said. Care should be taken not to diagnose long COVID without excluding traditional causes.

“Ensure that patients know that COVID is not over, per se, and that science supports vaccination,” Mr. Kolbert said. “The best defense here is a strong communicative offense, engaging with the patient and thoughtfully charting about this.”

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

By now, concerns about COVID-related lawsuits have faded into the rear view mirror for most physicians.

But just when COVID lawsuits appear to be dwindling out, legal experts see a new lawsuit risk on the horizon – long COVID claims. While some say it’s doubtful the claims will succeed, the lawsuits could still create legal headaches for doctors in the form of time and money.

Long COVID claims are defined as complaints that allege that a diagnosis of long COVID was missed or delayed and that caused harm or injury. Lawsuits may also include claims in which patients allege that they were misdiagnosed as having long COVID when they were really suffering from another condition.

So far, a handful of long COVID claims have come down the pipeline, said Peter A. Kolbert, JD, senior vice president of claims and litigation services for Healthcare Risk Advisors, part of TDC Group.

“This is an area that is emerging as we speak,” Mr. Kolbert said. “We are starting to see these claims trickle in.”

In a recent case, for example, a patient sued her primary care physician for negligence, alleging her original SARS-CoV-2 infection was mismanaged and that this led to permanent neuropathy from long COVID. Had the patient been treated appropriately, the patient contends, she would not have developed long COVID or the resulting neuropathy, said Mr. Kolbert. An outcome in the case has not yet been reached, added Mr. Kolbert, who heard about the claim from a colleague.

The increase in the number of lawsuits raises concerns about how courts and juries might decide long COVID claims when so much about the condition is still unknown and best treatment practices are still developing. Research shows that long COVID occurs in at least 10% of cases of SARS-CoV-2 infection, and more than 200 symptoms have been identified. A Kaiser Family Foundation study found that 15% of the U.S. population believe they have experienced the symptoms of long COVID at some point, and 6% of people believe they currently have long COVID.

The risk of long COVID lawsuits underscores the importance of physicians taking proactive steps to protect themselves from liability when treating patients who might have the condition, say legal experts.

“There are legal standards that say new, unestablished scientific principles shouldn’t be first tested by a jury, they should be recognized and established within their [professional] area,” Mr. Kolbert said. “While we are seeing lawsuits related to long COVID, I think it is truly putting the cart before the horse, because there needs to be societal recognition that we’re still learning how to define and treat long COVID.”
 

What are patients alleging?

In the few long COVID claims that have arisen, some complaints have alleged delay in the recognition and treatment of long COVID, according to Mr. Kolbert. There have also been claims that physicians failed to refer a patient with long COVID to a specialist in a timely way and that this results in the patient’s experiencing chronic fatigue or a neuropathy.

Fatigue is one of the most common symptoms associated with long COVID, according to recent studies. Other symptoms include postexertional malaise, brain fog, and gastrointestinal problems.

Another rising legal theme is failure to adequately communicate with patients about what long COVID is and what it entails.

Whether plaintiffs who bring long COVID claims will be successful in court remains a question.

Andrew D. DeSimone, JD, a Lexington, Ky.–based medical malpractice defense attorney, said he has not seen any claims involving long COVID. He added that a long COVID claim would be challenging to prove, considering the standard of care for treating the condition is still evolving. Plaintiffs in a medical malpractice action must prove that physicians owed a duty of care to the patient, that the doctor breached that duty by failing to conform to the standard of care, and that the breach caused an injury that harmed the patient.

Mr. DeSimone also doubts whether juries would be very sympathetic to such plaintiffs.

“There’s a lot of fatigue around COVID still,” he said. “I don’t know if a jury would buy into someone claiming long COVID. I think the claim would have a hard time gaining traction. Not that it’s impossible.”

Another unanswered question is whether legal protections enacted by states during the pandemic might apply to long COVID claims.

Shortly after the pandemic started, most states enacted laws or executive orders that shielded physicians from liability claims relating to the prevention and treatment of COVID-19, unless gross negligence or willful misconduct is proved. The U.S. Department of Health and Human Services published a declaration under the Public Readiness and Emergency Preparedness Act (PREP Act) that provided liability immunity to health care professionals for any activity related to medical countermeasures against COVID-19.

Some of these state immunities have since expired. Other states have extended their legal protections for short periods. In Indiana, for example, physicians and businesses are protected until Dec. 31, 2024, from civil tort actions that allege damages arising from COVID-19.

It’s possible that in long COVID lawsuits, physicians would be protected by the immunities unless the cases come after the protections expire, said J. Richard Moore, a medical liability defense attorney based in Indianapolis.

“I could foresee long COVID claims that don’t accrue until after December 2024, meaning it only becomes clear that a patient is struggling with long COVID–related symptoms after that date,” he said. “That could result in COVID claims that do not fall under the immunities.”

Mr. Moore said that if long COVID claims become truly problematic, the legislature could extend the immunities.

Other states, such as Washington, have statutes in place that increase the burden of proof for plaintiffs in cases in which care is affected by COVID and/or the treating of COVID. Elizabeth A. Leedom, a Seattle-based medical liability defense attorney, said the law would likely encompass long COVID claims if the care and treatment at issue occurred during the COVID state of emergency.

Compliance with current treatment guidelines is likely to be a good defense against any claim of delay/failure to diagnose COVID, including long COVID, she said.

Mr. Kolbert, however, doubts that the state immunities would protect against the claims.

“Courts are enforcing qualified immunities as to [traditional] COVID claims. However, I suspect that long COVID claims will fall into a category of traditional medical malpractice claim, such as delay in or failure to diagnose,” he said. In such cases, physicians “may not be able to take advantage of state-qualified immunities. Of course, this will depend upon the language of each state’s qualified immunity provisions.”

As for the statute of limitations, the clock generally starts running either when the alleged negligent conduct occurred or when the patient knew or, in the exercise of ordinary diligence, should have known, that they had been harmed by the alleged negligence, Mr. Moore said. Statutes of limitations are state specific, but the majority of states mandate a 2- to 3-year limit between the injury and the filing of a claim.

So, while the statute of limitations may be soon expiring for alleged harm that occurred during the pandemic, for patients newly diagnosed with long COVID or who have just discovered associated injuries, the clock may have just started ticking.
 

How to protect yourself against suits

Avoiding liability associated with long COVID involves the traditional legal guidance physicians are used to hearing, but with an added factor, Mr. Kolbert said.

There always needs to be communication with patients regarding the disease process, but in this area, there needs to be strong communication as to whether patients have had COVID in the past and what symptoms they are experiencing, he said. Physicians should ensure that patients know that long COVID may present in a variety of ways and that there is no definitive test for long COVID.

Physicians should document when the patient has been instructed to follow up and should take necessary steps to ensure the patient returns for follow-up care, he added.

On the opposite side of the spectrum is making sure not to assume a condition or symptom is the result of long COVID, he said. Care should be taken not to diagnose long COVID without excluding traditional causes.

“Ensure that patients know that COVID is not over, per se, and that science supports vaccination,” Mr. Kolbert said. “The best defense here is a strong communicative offense, engaging with the patient and thoughtfully charting about this.”

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

By now, concerns about COVID-related lawsuits have faded into the rear view mirror for most physicians.

But just when COVID lawsuits appear to be dwindling out, legal experts see a new lawsuit risk on the horizon – long COVID claims. While some say it’s doubtful the claims will succeed, the lawsuits could still create legal headaches for doctors in the form of time and money.

Long COVID claims are defined as complaints that allege that a diagnosis of long COVID was missed or delayed and that caused harm or injury. Lawsuits may also include claims in which patients allege that they were misdiagnosed as having long COVID when they were really suffering from another condition.

So far, a handful of long COVID claims have come down the pipeline, said Peter A. Kolbert, JD, senior vice president of claims and litigation services for Healthcare Risk Advisors, part of TDC Group.

“This is an area that is emerging as we speak,” Mr. Kolbert said. “We are starting to see these claims trickle in.”

In a recent case, for example, a patient sued her primary care physician for negligence, alleging her original SARS-CoV-2 infection was mismanaged and that this led to permanent neuropathy from long COVID. Had the patient been treated appropriately, the patient contends, she would not have developed long COVID or the resulting neuropathy, said Mr. Kolbert. An outcome in the case has not yet been reached, added Mr. Kolbert, who heard about the claim from a colleague.

The increase in the number of lawsuits raises concerns about how courts and juries might decide long COVID claims when so much about the condition is still unknown and best treatment practices are still developing. Research shows that long COVID occurs in at least 10% of cases of SARS-CoV-2 infection, and more than 200 symptoms have been identified. A Kaiser Family Foundation study found that 15% of the U.S. population believe they have experienced the symptoms of long COVID at some point, and 6% of people believe they currently have long COVID.

The risk of long COVID lawsuits underscores the importance of physicians taking proactive steps to protect themselves from liability when treating patients who might have the condition, say legal experts.

“There are legal standards that say new, unestablished scientific principles shouldn’t be first tested by a jury, they should be recognized and established within their [professional] area,” Mr. Kolbert said. “While we are seeing lawsuits related to long COVID, I think it is truly putting the cart before the horse, because there needs to be societal recognition that we’re still learning how to define and treat long COVID.”
 

What are patients alleging?

In the few long COVID claims that have arisen, some complaints have alleged delay in the recognition and treatment of long COVID, according to Mr. Kolbert. There have also been claims that physicians failed to refer a patient with long COVID to a specialist in a timely way and that this results in the patient’s experiencing chronic fatigue or a neuropathy.

Fatigue is one of the most common symptoms associated with long COVID, according to recent studies. Other symptoms include postexertional malaise, brain fog, and gastrointestinal problems.

Another rising legal theme is failure to adequately communicate with patients about what long COVID is and what it entails.

Whether plaintiffs who bring long COVID claims will be successful in court remains a question.

Andrew D. DeSimone, JD, a Lexington, Ky.–based medical malpractice defense attorney, said he has not seen any claims involving long COVID. He added that a long COVID claim would be challenging to prove, considering the standard of care for treating the condition is still evolving. Plaintiffs in a medical malpractice action must prove that physicians owed a duty of care to the patient, that the doctor breached that duty by failing to conform to the standard of care, and that the breach caused an injury that harmed the patient.

Mr. DeSimone also doubts whether juries would be very sympathetic to such plaintiffs.

“There’s a lot of fatigue around COVID still,” he said. “I don’t know if a jury would buy into someone claiming long COVID. I think the claim would have a hard time gaining traction. Not that it’s impossible.”

Another unanswered question is whether legal protections enacted by states during the pandemic might apply to long COVID claims.

Shortly after the pandemic started, most states enacted laws or executive orders that shielded physicians from liability claims relating to the prevention and treatment of COVID-19, unless gross negligence or willful misconduct is proved. The U.S. Department of Health and Human Services published a declaration under the Public Readiness and Emergency Preparedness Act (PREP Act) that provided liability immunity to health care professionals for any activity related to medical countermeasures against COVID-19.

Some of these state immunities have since expired. Other states have extended their legal protections for short periods. In Indiana, for example, physicians and businesses are protected until Dec. 31, 2024, from civil tort actions that allege damages arising from COVID-19.

It’s possible that in long COVID lawsuits, physicians would be protected by the immunities unless the cases come after the protections expire, said J. Richard Moore, a medical liability defense attorney based in Indianapolis.

“I could foresee long COVID claims that don’t accrue until after December 2024, meaning it only becomes clear that a patient is struggling with long COVID–related symptoms after that date,” he said. “That could result in COVID claims that do not fall under the immunities.”

Mr. Moore said that if long COVID claims become truly problematic, the legislature could extend the immunities.

Other states, such as Washington, have statutes in place that increase the burden of proof for plaintiffs in cases in which care is affected by COVID and/or the treating of COVID. Elizabeth A. Leedom, a Seattle-based medical liability defense attorney, said the law would likely encompass long COVID claims if the care and treatment at issue occurred during the COVID state of emergency.

Compliance with current treatment guidelines is likely to be a good defense against any claim of delay/failure to diagnose COVID, including long COVID, she said.

Mr. Kolbert, however, doubts that the state immunities would protect against the claims.

“Courts are enforcing qualified immunities as to [traditional] COVID claims. However, I suspect that long COVID claims will fall into a category of traditional medical malpractice claim, such as delay in or failure to diagnose,” he said. In such cases, physicians “may not be able to take advantage of state-qualified immunities. Of course, this will depend upon the language of each state’s qualified immunity provisions.”

As for the statute of limitations, the clock generally starts running either when the alleged negligent conduct occurred or when the patient knew or, in the exercise of ordinary diligence, should have known, that they had been harmed by the alleged negligence, Mr. Moore said. Statutes of limitations are state specific, but the majority of states mandate a 2- to 3-year limit between the injury and the filing of a claim.

So, while the statute of limitations may be soon expiring for alleged harm that occurred during the pandemic, for patients newly diagnosed with long COVID or who have just discovered associated injuries, the clock may have just started ticking.
 

How to protect yourself against suits

Avoiding liability associated with long COVID involves the traditional legal guidance physicians are used to hearing, but with an added factor, Mr. Kolbert said.

There always needs to be communication with patients regarding the disease process, but in this area, there needs to be strong communication as to whether patients have had COVID in the past and what symptoms they are experiencing, he said. Physicians should ensure that patients know that long COVID may present in a variety of ways and that there is no definitive test for long COVID.

Physicians should document when the patient has been instructed to follow up and should take necessary steps to ensure the patient returns for follow-up care, he added.

On the opposite side of the spectrum is making sure not to assume a condition or symptom is the result of long COVID, he said. Care should be taken not to diagnose long COVID without excluding traditional causes.

“Ensure that patients know that COVID is not over, per se, and that science supports vaccination,” Mr. Kolbert said. “The best defense here is a strong communicative offense, engaging with the patient and thoughtfully charting about this.”

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

Despite claims by their makers, blue light glasses probably don’t reduce eyestrain for people who spend a lot of time looking at computer screens or their phones, a new study says. The glasses probably don’t improve wearers’ sleep habits either, according to the study. 

Blue light glasses are usually marketed as being able to filter out the potentially harmful effects of blue light from screens, such as eyestrain, dry eye, and sleep problems. Interest in blue light glasses increased during the COVID-19 pandemic as more people stayed home and looked at their computers and phones. They’re often prescribed by optometrists.

The study, published in the Cochrane Database of Systematic Reviews, looked at data collected from 17 clinical trials in six countries that recruited 619 people. 

“We found there may be no short-term advantages with using blue light–filtering spectacle lenses to reduce visual fatigue associated with computer use, compared to non–blue-light–filtering lenses,” senior author Laura Downie, PhD, an associate professor of optometry and vision sciences at the University of Melbourne, said in a statement.

“It is also currently unclear whether these lenses affect vision quality or sleep-related outcomes, and no conclusions could be drawn about any potential effects on retinal health in the longer term. People should be aware of these findings when deciding whether to purchase these spectacles.”

Researchers noted that one reason the glasses don’t help is that the amount of blue light received from computer screens and other artificial sources is only about a thousandth of what people get from natural daylight. On top of that, blue light lenses usually filter out only about 10%-25% of blue light.

“Our findings do not support the prescription of blue light–filtering lenses to the general population,” Dr. Downie said. 

Eye experts say people can cut down on eyestrain by simply cutting down on the amount of time they look at screens, or by taking regular breaks. To improve sleep, stop looking at screens for a few hours before bedtime.

The researchers noted limitations in their analysis. None of the studies investigated contrast sensitivity, color discrimination, discomfort glare, macular health, serum melatonin levels, or overall patient visual satisfaction.

Also, the length of the different studies varied. More studies of the use of blue light–filtering glasses is needed, the researchers said.

The study received funding from Australia’s National Health and Medical Research Council, the Public Health Agency in the United Kingdom, and Queen’s University Belfast. Two coauthors reported receiving payment from the College of Optometrists.

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

Despite claims by their makers, blue light glasses probably don’t reduce eyestrain for people who spend a lot of time looking at computer screens or their phones, a new study says. The glasses probably don’t improve wearers’ sleep habits either, according to the study. 

Blue light glasses are usually marketed as being able to filter out the potentially harmful effects of blue light from screens, such as eyestrain, dry eye, and sleep problems. Interest in blue light glasses increased during the COVID-19 pandemic as more people stayed home and looked at their computers and phones. They’re often prescribed by optometrists.

The study, published in the Cochrane Database of Systematic Reviews, looked at data collected from 17 clinical trials in six countries that recruited 619 people. 

“We found there may be no short-term advantages with using blue light–filtering spectacle lenses to reduce visual fatigue associated with computer use, compared to non–blue-light–filtering lenses,” senior author Laura Downie, PhD, an associate professor of optometry and vision sciences at the University of Melbourne, said in a statement.

“It is also currently unclear whether these lenses affect vision quality or sleep-related outcomes, and no conclusions could be drawn about any potential effects on retinal health in the longer term. People should be aware of these findings when deciding whether to purchase these spectacles.”

Researchers noted that one reason the glasses don’t help is that the amount of blue light received from computer screens and other artificial sources is only about a thousandth of what people get from natural daylight. On top of that, blue light lenses usually filter out only about 10%-25% of blue light.

“Our findings do not support the prescription of blue light–filtering lenses to the general population,” Dr. Downie said. 

Eye experts say people can cut down on eyestrain by simply cutting down on the amount of time they look at screens, or by taking regular breaks. To improve sleep, stop looking at screens for a few hours before bedtime.

The researchers noted limitations in their analysis. None of the studies investigated contrast sensitivity, color discrimination, discomfort glare, macular health, serum melatonin levels, or overall patient visual satisfaction.

Also, the length of the different studies varied. More studies of the use of blue light–filtering glasses is needed, the researchers said.

The study received funding from Australia’s National Health and Medical Research Council, the Public Health Agency in the United Kingdom, and Queen’s University Belfast. Two coauthors reported receiving payment from the College of Optometrists.

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

Despite claims by their makers, blue light glasses probably don’t reduce eyestrain for people who spend a lot of time looking at computer screens or their phones, a new study says. The glasses probably don’t improve wearers’ sleep habits either, according to the study. 

Blue light glasses are usually marketed as being able to filter out the potentially harmful effects of blue light from screens, such as eyestrain, dry eye, and sleep problems. Interest in blue light glasses increased during the COVID-19 pandemic as more people stayed home and looked at their computers and phones. They’re often prescribed by optometrists.

The study, published in the Cochrane Database of Systematic Reviews, looked at data collected from 17 clinical trials in six countries that recruited 619 people. 

“We found there may be no short-term advantages with using blue light–filtering spectacle lenses to reduce visual fatigue associated with computer use, compared to non–blue-light–filtering lenses,” senior author Laura Downie, PhD, an associate professor of optometry and vision sciences at the University of Melbourne, said in a statement.

“It is also currently unclear whether these lenses affect vision quality or sleep-related outcomes, and no conclusions could be drawn about any potential effects on retinal health in the longer term. People should be aware of these findings when deciding whether to purchase these spectacles.”

Researchers noted that one reason the glasses don’t help is that the amount of blue light received from computer screens and other artificial sources is only about a thousandth of what people get from natural daylight. On top of that, blue light lenses usually filter out only about 10%-25% of blue light.

“Our findings do not support the prescription of blue light–filtering lenses to the general population,” Dr. Downie said. 

Eye experts say people can cut down on eyestrain by simply cutting down on the amount of time they look at screens, or by taking regular breaks. To improve sleep, stop looking at screens for a few hours before bedtime.

The researchers noted limitations in their analysis. None of the studies investigated contrast sensitivity, color discrimination, discomfort glare, macular health, serum melatonin levels, or overall patient visual satisfaction.

Also, the length of the different studies varied. More studies of the use of blue light–filtering glasses is needed, the researchers said.

The study received funding from Australia’s National Health and Medical Research Council, the Public Health Agency in the United Kingdom, and Queen’s University Belfast. Two coauthors reported receiving payment from the College of Optometrists.

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

Measuring four circulating biomarkers through a simple blood test in patients with type 2 diabetes and kidney disease may predict their risk of heart and kidney disease progression, suggests an analysis of the CREDENCE trial.

The research, published online in the journal Circulation, also revealed that patients treated with the sodium-glucose cotransporter-2 inhibitor canagliflozin (Invokana, Invokamet) had lower levels of the biomarkers after 1 year compared with those given placebo.

Examination of biomarker levels in more than 2,600 patients from CREDENCE showed that high baseline concentrations of the individual biomarkers were able to predict the future risk for a composite endpoint of renal and heart outcomes.

The combination of all four biomarkers into a single panel revealed that patients with the highest levels were more than four times as likely to experience the composite endpoint than were those with the lowest levels.

As two of the biomarkers used in the study have yet to have established prognostic thresholds, the results remain exploratory.

Lead author James L. Januzzi, MD, director of the Heart Failure and Biomarker Trials at the Baim Institute for Clinical Research, Boston, said that further study will help refine the predictive value of the panel.

“Given that the American Heart Association/American College of Cardiology and the American Diabetes Association now all recommend measurement of biomarkers to enhance the ability to predict risk in persons with type 2 diabetes, these results may considerably extend the reach of biomarker-based testing, refining accuracy even further,” he said in a press release.

In an interview, Dr. Januzzi said that “three out of the four biomarkers are already clinically and commercially available,” while the fourth, for insulin-like growth factor binding protein 7 (IGFBP7), is “on the near horizon.”

He stressed that the “future for multiple biomarker testing, however, will be less about ordering each individual test, and ultimately will revolve around panels of blood work that are ordered as a single test.”

Dr. Januzzi added that “rather than using the rather primitive approach that we took” of looking at the individual biomarkers in adjusted models, the next stage “will be to utilize algorithms to combine the results into a single value.

“A clinician will not have to struggle with looking at individual results but will just receive one aggregated test result that informs them whether a patient is at low, medium or higher risk,” he explained.

However, this will require determining the relative importance of each biomarker and weighting them in the final model.

Consequently, the current results “set the foundation for identifying some very powerful individual tests that may ultimately, in aggregate, help us to help our patients with diabetes avoid a major complication,” Dr. Januzzi said.

By revealing that some individuals with both type 2 diabetes and kidney disease are at higher risk than others, he also hopes the findings can be leveraged to treat patients with “varying degrees of intensity with proven therapies, including weight loss, dietary adjustment, and pharmacologic intervention.”

Dr. Januzzi added: “Diabetes affects a dramatic, and growing, percentage of our population, and this type of personalized strategy to reduce the major complications of this rather common disease is an important step forward.”

The authors noted that there is a “bidirectional relationship” between cardiovascular disease and chronic kidney disease (CKD), such that either diagnosis may increase the risk of, or exacerbate, the other. 

Individuals with type 2 diabetes and CKD albuminuria, they added, are at particularly high risk for major cardiovascular events, and studies have shown that several circulating cardiorenal stress biomarkers may predict the onset and progression of CKD in type 2 diabetes, as well as predict cardiovascular events.
 

Several biomarkers associated with myocardial stress and necrosis

The recent CANVAS trial revealed that, among individuals with type 2 diabetes with and without CKD, several biomarkers were associated with myocardial stress and necrosis, and renal tubular injury, predicting the progression of CKD with albuminuria, and the risk for heart failure events.

Taking inspiration from those findings, the current researchers studied a panel of similar cardiac and renal biomarkers among participants from the CREDENCE trial, for which 4,401 patients with type 2 diabetes and CKD at high risk of progression were randomly assigned to canagliflozin or placebo.

The current analysis involved 2,627 participants who had baseline plasma samples available for analysis of four circulating biomarkers: N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hs-cTnT), growth differentiation factor-15 (GDF-15), and IGFBP7.

Among those, 2,385 participants also had year 1 plasma samples available for analysis, while year 3 plasma samples were available for 895 individuals.

The results showed that, in general, median baseline concentrations of each biomarker in both treatment groups were elevated compared with healthy reference populations.

Baseline log-transformed concentrations of each biomarker were also strongly predictive of cardiac and renal outcomes, including heart failure and progression of CKD.

For example, each unit increase in baseline NT-proBNP concentrations was associated with a hazard ratio of 1.35 for the primary composite endpoint of end-stage kidney disease, doubling of serum creatinine levels, renal death, or cardiovascular disease (P < .001).

For each unit increase in hs-cTnT levels, the hazard ratio for the primary composite was 1.73 (P < .001), for GDF-15 it was 1.84 (P < .0001), and for IGFBP7 the hazard ratio was 3.14 (P < .001).

Combining the four biomarkers into a single multimarker panel revealed that, compared with individuals with a low-risk score, those with a high-risk score had a hazard ratio for the primary outcome of 4.01, whereas those with a moderate risk score had a hazard ratio of 2.39 (P < .001 for both).

For the individual outcome of heart failure hospitalization, the effect was even greater. A high-risk score was associated with a hazard ratio vs. a low-risk score of 6.04 (P < .001), whereas patients with a moderate risk score had a hazard ratio of 2.45 (P = .04).

The researchers also reported that, between baseline and year 1, concentrations of all four biomarkers rose from 6% to 29% in the placebo group, but from 3% to just 10% in those treated with canagliflozin.

“It was reassuring to discover that canagliflozin helped reduce risks the most in people with the highest chances for complications,” said Dr. Januzzi.

The CREDENCE trial and the current analysis were funded by Janssen Research & Development LLC. NT-proBNP, hs-cTnT, GDF-15, and IGFBP7 reagents were provided by Roche Diagnostics. Dr. Januzzi is funded in part by the Hutter Family Professorship. Dr. Januzzi declared relationships with Imbria Pharmaceuticals, Jana Care, Abbott, Applied Therapeutics, HeartFlow, Innolife, Roche Diagnostics, Beckman, Boehringer Ingelheim, Bristol-Myers Squibb, Janssen, Merck, Novartis, Pfizer, Siemens, Abbott, AbbVie, CVRx, Intercept, and Takeda.


 

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

Measuring four circulating biomarkers through a simple blood test in patients with type 2 diabetes and kidney disease may predict their risk of heart and kidney disease progression, suggests an analysis of the CREDENCE trial.

The research, published online in the journal Circulation, also revealed that patients treated with the sodium-glucose cotransporter-2 inhibitor canagliflozin (Invokana, Invokamet) had lower levels of the biomarkers after 1 year compared with those given placebo.

Examination of biomarker levels in more than 2,600 patients from CREDENCE showed that high baseline concentrations of the individual biomarkers were able to predict the future risk for a composite endpoint of renal and heart outcomes.

The combination of all four biomarkers into a single panel revealed that patients with the highest levels were more than four times as likely to experience the composite endpoint than were those with the lowest levels.

As two of the biomarkers used in the study have yet to have established prognostic thresholds, the results remain exploratory.

Lead author James L. Januzzi, MD, director of the Heart Failure and Biomarker Trials at the Baim Institute for Clinical Research, Boston, said that further study will help refine the predictive value of the panel.

“Given that the American Heart Association/American College of Cardiology and the American Diabetes Association now all recommend measurement of biomarkers to enhance the ability to predict risk in persons with type 2 diabetes, these results may considerably extend the reach of biomarker-based testing, refining accuracy even further,” he said in a press release.

In an interview, Dr. Januzzi said that “three out of the four biomarkers are already clinically and commercially available,” while the fourth, for insulin-like growth factor binding protein 7 (IGFBP7), is “on the near horizon.”

He stressed that the “future for multiple biomarker testing, however, will be less about ordering each individual test, and ultimately will revolve around panels of blood work that are ordered as a single test.”

Dr. Januzzi added that “rather than using the rather primitive approach that we took” of looking at the individual biomarkers in adjusted models, the next stage “will be to utilize algorithms to combine the results into a single value.

“A clinician will not have to struggle with looking at individual results but will just receive one aggregated test result that informs them whether a patient is at low, medium or higher risk,” he explained.

However, this will require determining the relative importance of each biomarker and weighting them in the final model.

Consequently, the current results “set the foundation for identifying some very powerful individual tests that may ultimately, in aggregate, help us to help our patients with diabetes avoid a major complication,” Dr. Januzzi said.

By revealing that some individuals with both type 2 diabetes and kidney disease are at higher risk than others, he also hopes the findings can be leveraged to treat patients with “varying degrees of intensity with proven therapies, including weight loss, dietary adjustment, and pharmacologic intervention.”

Dr. Januzzi added: “Diabetes affects a dramatic, and growing, percentage of our population, and this type of personalized strategy to reduce the major complications of this rather common disease is an important step forward.”

The authors noted that there is a “bidirectional relationship” between cardiovascular disease and chronic kidney disease (CKD), such that either diagnosis may increase the risk of, or exacerbate, the other. 

Individuals with type 2 diabetes and CKD albuminuria, they added, are at particularly high risk for major cardiovascular events, and studies have shown that several circulating cardiorenal stress biomarkers may predict the onset and progression of CKD in type 2 diabetes, as well as predict cardiovascular events.
 

Several biomarkers associated with myocardial stress and necrosis

The recent CANVAS trial revealed that, among individuals with type 2 diabetes with and without CKD, several biomarkers were associated with myocardial stress and necrosis, and renal tubular injury, predicting the progression of CKD with albuminuria, and the risk for heart failure events.

Taking inspiration from those findings, the current researchers studied a panel of similar cardiac and renal biomarkers among participants from the CREDENCE trial, for which 4,401 patients with type 2 diabetes and CKD at high risk of progression were randomly assigned to canagliflozin or placebo.

The current analysis involved 2,627 participants who had baseline plasma samples available for analysis of four circulating biomarkers: N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hs-cTnT), growth differentiation factor-15 (GDF-15), and IGFBP7.

Among those, 2,385 participants also had year 1 plasma samples available for analysis, while year 3 plasma samples were available for 895 individuals.

The results showed that, in general, median baseline concentrations of each biomarker in both treatment groups were elevated compared with healthy reference populations.

Baseline log-transformed concentrations of each biomarker were also strongly predictive of cardiac and renal outcomes, including heart failure and progression of CKD.

For example, each unit increase in baseline NT-proBNP concentrations was associated with a hazard ratio of 1.35 for the primary composite endpoint of end-stage kidney disease, doubling of serum creatinine levels, renal death, or cardiovascular disease (P < .001).

For each unit increase in hs-cTnT levels, the hazard ratio for the primary composite was 1.73 (P < .001), for GDF-15 it was 1.84 (P < .0001), and for IGFBP7 the hazard ratio was 3.14 (P < .001).

Combining the four biomarkers into a single multimarker panel revealed that, compared with individuals with a low-risk score, those with a high-risk score had a hazard ratio for the primary outcome of 4.01, whereas those with a moderate risk score had a hazard ratio of 2.39 (P < .001 for both).

For the individual outcome of heart failure hospitalization, the effect was even greater. A high-risk score was associated with a hazard ratio vs. a low-risk score of 6.04 (P < .001), whereas patients with a moderate risk score had a hazard ratio of 2.45 (P = .04).

The researchers also reported that, between baseline and year 1, concentrations of all four biomarkers rose from 6% to 29% in the placebo group, but from 3% to just 10% in those treated with canagliflozin.

“It was reassuring to discover that canagliflozin helped reduce risks the most in people with the highest chances for complications,” said Dr. Januzzi.

The CREDENCE trial and the current analysis were funded by Janssen Research & Development LLC. NT-proBNP, hs-cTnT, GDF-15, and IGFBP7 reagents were provided by Roche Diagnostics. Dr. Januzzi is funded in part by the Hutter Family Professorship. Dr. Januzzi declared relationships with Imbria Pharmaceuticals, Jana Care, Abbott, Applied Therapeutics, HeartFlow, Innolife, Roche Diagnostics, Beckman, Boehringer Ingelheim, Bristol-Myers Squibb, Janssen, Merck, Novartis, Pfizer, Siemens, Abbott, AbbVie, CVRx, Intercept, and Takeda.


 

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

Measuring four circulating biomarkers through a simple blood test in patients with type 2 diabetes and kidney disease may predict their risk of heart and kidney disease progression, suggests an analysis of the CREDENCE trial.

The research, published online in the journal Circulation, also revealed that patients treated with the sodium-glucose cotransporter-2 inhibitor canagliflozin (Invokana, Invokamet) had lower levels of the biomarkers after 1 year compared with those given placebo.

Examination of biomarker levels in more than 2,600 patients from CREDENCE showed that high baseline concentrations of the individual biomarkers were able to predict the future risk for a composite endpoint of renal and heart outcomes.

The combination of all four biomarkers into a single panel revealed that patients with the highest levels were more than four times as likely to experience the composite endpoint than were those with the lowest levels.

As two of the biomarkers used in the study have yet to have established prognostic thresholds, the results remain exploratory.

Lead author James L. Januzzi, MD, director of the Heart Failure and Biomarker Trials at the Baim Institute for Clinical Research, Boston, said that further study will help refine the predictive value of the panel.

“Given that the American Heart Association/American College of Cardiology and the American Diabetes Association now all recommend measurement of biomarkers to enhance the ability to predict risk in persons with type 2 diabetes, these results may considerably extend the reach of biomarker-based testing, refining accuracy even further,” he said in a press release.

In an interview, Dr. Januzzi said that “three out of the four biomarkers are already clinically and commercially available,” while the fourth, for insulin-like growth factor binding protein 7 (IGFBP7), is “on the near horizon.”

He stressed that the “future for multiple biomarker testing, however, will be less about ordering each individual test, and ultimately will revolve around panels of blood work that are ordered as a single test.”

Dr. Januzzi added that “rather than using the rather primitive approach that we took” of looking at the individual biomarkers in adjusted models, the next stage “will be to utilize algorithms to combine the results into a single value.

“A clinician will not have to struggle with looking at individual results but will just receive one aggregated test result that informs them whether a patient is at low, medium or higher risk,” he explained.

However, this will require determining the relative importance of each biomarker and weighting them in the final model.

Consequently, the current results “set the foundation for identifying some very powerful individual tests that may ultimately, in aggregate, help us to help our patients with diabetes avoid a major complication,” Dr. Januzzi said.

By revealing that some individuals with both type 2 diabetes and kidney disease are at higher risk than others, he also hopes the findings can be leveraged to treat patients with “varying degrees of intensity with proven therapies, including weight loss, dietary adjustment, and pharmacologic intervention.”

Dr. Januzzi added: “Diabetes affects a dramatic, and growing, percentage of our population, and this type of personalized strategy to reduce the major complications of this rather common disease is an important step forward.”

The authors noted that there is a “bidirectional relationship” between cardiovascular disease and chronic kidney disease (CKD), such that either diagnosis may increase the risk of, or exacerbate, the other. 

Individuals with type 2 diabetes and CKD albuminuria, they added, are at particularly high risk for major cardiovascular events, and studies have shown that several circulating cardiorenal stress biomarkers may predict the onset and progression of CKD in type 2 diabetes, as well as predict cardiovascular events.
 

Several biomarkers associated with myocardial stress and necrosis

The recent CANVAS trial revealed that, among individuals with type 2 diabetes with and without CKD, several biomarkers were associated with myocardial stress and necrosis, and renal tubular injury, predicting the progression of CKD with albuminuria, and the risk for heart failure events.

Taking inspiration from those findings, the current researchers studied a panel of similar cardiac and renal biomarkers among participants from the CREDENCE trial, for which 4,401 patients with type 2 diabetes and CKD at high risk of progression were randomly assigned to canagliflozin or placebo.

The current analysis involved 2,627 participants who had baseline plasma samples available for analysis of four circulating biomarkers: N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hs-cTnT), growth differentiation factor-15 (GDF-15), and IGFBP7.

Among those, 2,385 participants also had year 1 plasma samples available for analysis, while year 3 plasma samples were available for 895 individuals.

The results showed that, in general, median baseline concentrations of each biomarker in both treatment groups were elevated compared with healthy reference populations.

Baseline log-transformed concentrations of each biomarker were also strongly predictive of cardiac and renal outcomes, including heart failure and progression of CKD.

For example, each unit increase in baseline NT-proBNP concentrations was associated with a hazard ratio of 1.35 for the primary composite endpoint of end-stage kidney disease, doubling of serum creatinine levels, renal death, or cardiovascular disease (P < .001).

For each unit increase in hs-cTnT levels, the hazard ratio for the primary composite was 1.73 (P < .001), for GDF-15 it was 1.84 (P < .0001), and for IGFBP7 the hazard ratio was 3.14 (P < .001).

Combining the four biomarkers into a single multimarker panel revealed that, compared with individuals with a low-risk score, those with a high-risk score had a hazard ratio for the primary outcome of 4.01, whereas those with a moderate risk score had a hazard ratio of 2.39 (P < .001 for both).

For the individual outcome of heart failure hospitalization, the effect was even greater. A high-risk score was associated with a hazard ratio vs. a low-risk score of 6.04 (P < .001), whereas patients with a moderate risk score had a hazard ratio of 2.45 (P = .04).

The researchers also reported that, between baseline and year 1, concentrations of all four biomarkers rose from 6% to 29% in the placebo group, but from 3% to just 10% in those treated with canagliflozin.

“It was reassuring to discover that canagliflozin helped reduce risks the most in people with the highest chances for complications,” said Dr. Januzzi.

The CREDENCE trial and the current analysis were funded by Janssen Research & Development LLC. NT-proBNP, hs-cTnT, GDF-15, and IGFBP7 reagents were provided by Roche Diagnostics. Dr. Januzzi is funded in part by the Hutter Family Professorship. Dr. Januzzi declared relationships with Imbria Pharmaceuticals, Jana Care, Abbott, Applied Therapeutics, HeartFlow, Innolife, Roche Diagnostics, Beckman, Boehringer Ingelheim, Bristol-Myers Squibb, Janssen, Merck, Novartis, Pfizer, Siemens, Abbott, AbbVie, CVRx, Intercept, and Takeda.


 

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

Among patients with female pattern hair loss taking low-dose oral minoxidil (LDOM) for at least 4 months, minimal changes from baseline were observed in systolic blood pressure, diastolic blood pressure, and heart rate, results from a small retrospective analysis showed.

“Additionally, few patients experienced hair loss progression while slightly over a third experienced hair regrowth,” the study’s first author, Reese Imhof, MD, a third-year resident in the department of dermatology at Mayo Clinic, Rochester, Minn., said in an interview. The results were published online in JAAD International.

At low doses, oral minoxidil, approved as an antihypertensive over 40 years ago, has become an increasingly popular treatment for hair loss, particularly since an article about its use for hair loss was published in the New York Times in August 2022. (Oral minoxidil is not approved for treating alopecia, and is used off label for this purpose.)

To evaluate the effects of LDOM in female patients with female pattern hair loss, Dr. Imhof, along with colleagues Beija Villalpando, MD, of the department of medicine and Rochelle R. Torgerson, MD, PhD, of the department of dermatology at the Mayo Clinic, reviewed the records of 25 adult women who were evaluated for female pattern hair loss at the Mayo Clinic over a 5-year period that ended on Nov. 27, 2022. Previous studies have looked at the cardiovascular effects of treatment with oral minoxidil and impact on BP in men, but “few studies have reported on female patients receiving LDOM as monotherapy for female pattern hair loss,” the authors noted.

The mean age of the women in their study was 61 years, and they took LDOM for a mean of 6.2 months. Slightly more than half (52%) took a dose of 1.25 mg daily, while 40% took 2.5 mg daily and 8% took 0.625 mg daily.

Of the 25 patients, 10 (40%) had previously tried topical minoxidil but had discontinued it because of local side effects or challenges with adherence. Also, three patients (12%) had previously tried finasteride and spironolactone but discontinued those medications because of adverse side effects.

The researchers noted disease improvement and hair regrowth was observed in nine patients who were treated with LDOM (36%), while three patients (12%) had “unaltered disease progression.” Adverse side effects observed in the cohort included four patients with facial hypertrichosis (16%) and one patient with fluid retention/lower limb edema (4%).

The patients who developed hypertrichosis did not discontinue LDOM, but the patient who developed edema did stop treatment.

At baseline, systolic BP (SBP) ranged from 107-161 mm Hg, diastolic BP (DBP) ranged from 58-88 mm Hg, and heart rate ranged from 54-114 beats per minute. Post treatment, SBP ranged from 102-152 mm Hg, DBP ranged from 63-90 mm Hg, and heart rate ranged from 56 to 105 bpm. “It was surprising how little ambulatory blood pressure and heart rate changed after an average of 6 months of treatment,” Dr. Imhof said in an interview. “On average, SBP decreased by 2.8 mm HG while DBP decreased by 1.4 mm Hg. Heart rate increased an average of 4.4 beats per minute.”

He acknowledged certain limitations of the study, including its small sample size and lack of inclusion of patients who were being treated for hypertension with concomitant antihypertensive medications. “Some unique aspects of our study are that we focused on women, and we had a slightly older cohort than prior studies (61 years old on average) as well as exposure to higher doses of LDOM, with most patients on either 1.25 mg daily or 2.5 mg daily,” Dr. Imhof said.

The researchers reported having no relevant disclosures, and there was no funding source for the study.

Among patients with female pattern hair loss taking low-dose oral minoxidil (LDOM) for at least 4 months, minimal changes from baseline were observed in systolic blood pressure, diastolic blood pressure, and heart rate, results from a small retrospective analysis showed.

“Additionally, few patients experienced hair loss progression while slightly over a third experienced hair regrowth,” the study’s first author, Reese Imhof, MD, a third-year resident in the department of dermatology at Mayo Clinic, Rochester, Minn., said in an interview. The results were published online in JAAD International.

At low doses, oral minoxidil, approved as an antihypertensive over 40 years ago, has become an increasingly popular treatment for hair loss, particularly since an article about its use for hair loss was published in the New York Times in August 2022. (Oral minoxidil is not approved for treating alopecia, and is used off label for this purpose.)

To evaluate the effects of LDOM in female patients with female pattern hair loss, Dr. Imhof, along with colleagues Beija Villalpando, MD, of the department of medicine and Rochelle R. Torgerson, MD, PhD, of the department of dermatology at the Mayo Clinic, reviewed the records of 25 adult women who were evaluated for female pattern hair loss at the Mayo Clinic over a 5-year period that ended on Nov. 27, 2022. Previous studies have looked at the cardiovascular effects of treatment with oral minoxidil and impact on BP in men, but “few studies have reported on female patients receiving LDOM as monotherapy for female pattern hair loss,” the authors noted.

The mean age of the women in their study was 61 years, and they took LDOM for a mean of 6.2 months. Slightly more than half (52%) took a dose of 1.25 mg daily, while 40% took 2.5 mg daily and 8% took 0.625 mg daily.

Of the 25 patients, 10 (40%) had previously tried topical minoxidil but had discontinued it because of local side effects or challenges with adherence. Also, three patients (12%) had previously tried finasteride and spironolactone but discontinued those medications because of adverse side effects.

The researchers noted disease improvement and hair regrowth was observed in nine patients who were treated with LDOM (36%), while three patients (12%) had “unaltered disease progression.” Adverse side effects observed in the cohort included four patients with facial hypertrichosis (16%) and one patient with fluid retention/lower limb edema (4%).

The patients who developed hypertrichosis did not discontinue LDOM, but the patient who developed edema did stop treatment.

At baseline, systolic BP (SBP) ranged from 107-161 mm Hg, diastolic BP (DBP) ranged from 58-88 mm Hg, and heart rate ranged from 54-114 beats per minute. Post treatment, SBP ranged from 102-152 mm Hg, DBP ranged from 63-90 mm Hg, and heart rate ranged from 56 to 105 bpm. “It was surprising how little ambulatory blood pressure and heart rate changed after an average of 6 months of treatment,” Dr. Imhof said in an interview. “On average, SBP decreased by 2.8 mm HG while DBP decreased by 1.4 mm Hg. Heart rate increased an average of 4.4 beats per minute.”

He acknowledged certain limitations of the study, including its small sample size and lack of inclusion of patients who were being treated for hypertension with concomitant antihypertensive medications. “Some unique aspects of our study are that we focused on women, and we had a slightly older cohort than prior studies (61 years old on average) as well as exposure to higher doses of LDOM, with most patients on either 1.25 mg daily or 2.5 mg daily,” Dr. Imhof said.

The researchers reported having no relevant disclosures, and there was no funding source for the study.

Among patients with female pattern hair loss taking low-dose oral minoxidil (LDOM) for at least 4 months, minimal changes from baseline were observed in systolic blood pressure, diastolic blood pressure, and heart rate, results from a small retrospective analysis showed.

“Additionally, few patients experienced hair loss progression while slightly over a third experienced hair regrowth,” the study’s first author, Reese Imhof, MD, a third-year resident in the department of dermatology at Mayo Clinic, Rochester, Minn., said in an interview. The results were published online in JAAD International.

At low doses, oral minoxidil, approved as an antihypertensive over 40 years ago, has become an increasingly popular treatment for hair loss, particularly since an article about its use for hair loss was published in the New York Times in August 2022. (Oral minoxidil is not approved for treating alopecia, and is used off label for this purpose.)

To evaluate the effects of LDOM in female patients with female pattern hair loss, Dr. Imhof, along with colleagues Beija Villalpando, MD, of the department of medicine and Rochelle R. Torgerson, MD, PhD, of the department of dermatology at the Mayo Clinic, reviewed the records of 25 adult women who were evaluated for female pattern hair loss at the Mayo Clinic over a 5-year period that ended on Nov. 27, 2022. Previous studies have looked at the cardiovascular effects of treatment with oral minoxidil and impact on BP in men, but “few studies have reported on female patients receiving LDOM as monotherapy for female pattern hair loss,” the authors noted.

The mean age of the women in their study was 61 years, and they took LDOM for a mean of 6.2 months. Slightly more than half (52%) took a dose of 1.25 mg daily, while 40% took 2.5 mg daily and 8% took 0.625 mg daily.

Of the 25 patients, 10 (40%) had previously tried topical minoxidil but had discontinued it because of local side effects or challenges with adherence. Also, three patients (12%) had previously tried finasteride and spironolactone but discontinued those medications because of adverse side effects.

The researchers noted disease improvement and hair regrowth was observed in nine patients who were treated with LDOM (36%), while three patients (12%) had “unaltered disease progression.” Adverse side effects observed in the cohort included four patients with facial hypertrichosis (16%) and one patient with fluid retention/lower limb edema (4%).

The patients who developed hypertrichosis did not discontinue LDOM, but the patient who developed edema did stop treatment.

At baseline, systolic BP (SBP) ranged from 107-161 mm Hg, diastolic BP (DBP) ranged from 58-88 mm Hg, and heart rate ranged from 54-114 beats per minute. Post treatment, SBP ranged from 102-152 mm Hg, DBP ranged from 63-90 mm Hg, and heart rate ranged from 56 to 105 bpm. “It was surprising how little ambulatory blood pressure and heart rate changed after an average of 6 months of treatment,” Dr. Imhof said in an interview. “On average, SBP decreased by 2.8 mm HG while DBP decreased by 1.4 mm Hg. Heart rate increased an average of 4.4 beats per minute.”

He acknowledged certain limitations of the study, including its small sample size and lack of inclusion of patients who were being treated for hypertension with concomitant antihypertensive medications. “Some unique aspects of our study are that we focused on women, and we had a slightly older cohort than prior studies (61 years old on average) as well as exposure to higher doses of LDOM, with most patients on either 1.25 mg daily or 2.5 mg daily,” Dr. Imhof said.

The researchers reported having no relevant disclosures, and there was no funding source for the study.