Clinician Reviews

Obesity, in and of itself, and independent of other cardiovascular risk factors, may cause changes to the heart that can lead to sudden cardiac death, a new case-control study suggests.

Researchers who analyzed hearts taken at autopsy from people who had died from sudden cardiac death found that a number of the hearts obtained from obese decedents were heavier than those from normal-weight decedents and that the hazard ratio of unexplained cardiomegaly in this cohort was 5.3, compared with normal-weight individuals.

“Even when we ruled out any conditions that could potentially cause enlargement of the heart, including hypertension, heart valve problems, diabetes, and other cardiovascular risk factors, the association with obesity cardiomyopathy, or OCM, and sudden cardiac death remained,” lead author Joseph Westaby, PhD, from the Cardiac Risk in the Young (CRY) Cardiovascular Pathology Laboratories at St George’s University of London, said in an interview.

The study was published online in JACC: Advances.

Intrigued by this finding, Dr. Westaby and associates sought to characterize the clinical and pathological features of OCM associated with sudden cardiac death by comparing this population to two control groups: sudden cardiac death patients who were either obese or of normal weight, and had morphologically normal hearts.

Their group is uniquely positioned to do such research, Dr. Westaby explained.

“Here at St George’s University of London, we have a specialized cardiovascular pathology service. ... All hearts obtained at autopsy from individuals who have died from sudden cardiac death, or who were suspected to have had a cardiovascular cause of death, anywhere in the U.K., are referred to the CRY Centre for further analysis,” he said.

Patients were divided into two groups according to body mass index: an obesity group (BMI > 30 kg/m²) and a normal-weight group (BMI, 18.5-24.9).

An increased heart weight above 550 g in men and 450 g in women in the absence of coronary artery disease, hypertension, diabetes, or valvular disease was classified as unexplained cardiomegaly, and individuals with obesity and cardiomegaly were defined as obesity cardiomyopathy.

Age- and sex-matched controls with obesity (n = 106) were selected based on a BMI greater than 30, with a morphologically normal heart weighing less than 550 g in men and than 450 g in women. 

Age- and sex-matched normal weight controls (n = 106) were selected based on a BMI of 18.5-24.9 and a morphologically normal heart weighing less than 550 g in men and less than 450 g in women. 

The researchers identified 53 OCM cases from a cohort of more than 4,500 sudden cardiac death cases that had BMI measurements. In normal-weight patients, there were 14 cases of unexplained cardiomegaly.

The mean age at death of individuals with OCM was 42 years (range, 30-54 years). Most of the deaths occurred in men (n = 34; 64%), who also died younger than women (40 ± 13 years vs. 45 ± 10 years; P = .036).

The average heart weight in OCM patients was 598 ± 93 g. Risk of sudden cardiac death increased when BMI reached 35.

Compared with matched controls, there were increases in right and left ventricular wall thickness (all P < .05) in OCM cases. Right ventricular epicardial fat was increased in OCM cases, compared with normal-weight controls only.

Left ventricular fibrosis was identified in seven (13%) OCM cases.
 

Role of genetics to be explored

“This study highlights the need for further investigation into these individuals because, at the moment, we can’t be sure that the only contributing factor to this is the obesity,” said Dr. Westaby.

In the works are plans to see if there may be an underlying genetic predisposition in obese individuals that may have contributed to the development of an enlarged heart. The group also plans to study the families of the deceased individuals to determine if they are at risk of developing cardiomegaly, he said.

“This paper makes an important contribution to the literature that raises many important questions for future research,” Timothy P. Fitzgibbons, MD, PhD, from the University of Massachusetts, Worcester, wrote in an accompanying editorial.

Being able to access so many autopsy samples gives the current study considerable heft, Dr. Fitzgibbons said in an interview.

“A lot has been made of the obesity paradox and the perhaps benign nature of obesity but this paper suggests the opposite, that it is a very serious problem and can, in fact, in and of itself, cause heart abnormalities that could cause sudden death,” he noted.

The fact that only 13% of OCM cases had fibrosis on histology suggests that fibrosis was not the main cause of sudden cardiac death, he said.

“Often we will do MRIs to look for areas of fibrosis within the heart because those areas make patients prone to re-entry arrhythmias, in particular, ventricular tachycardia. But the authors suggest that the enlarged myocytes may themselves be predisposing to arrhythmias, rather than fibrosis,” Dr. Fitzgibbons said.

The study was supported by Cardiac Risk in the Young. Dr. Westaby and Dr. Fitzgibbons have reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Obesity, in and of itself, and independent of other cardiovascular risk factors, may cause changes to the heart that can lead to sudden cardiac death, a new case-control study suggests.

Researchers who analyzed hearts taken at autopsy from people who had died from sudden cardiac death found that a number of the hearts obtained from obese decedents were heavier than those from normal-weight decedents and that the hazard ratio of unexplained cardiomegaly in this cohort was 5.3, compared with normal-weight individuals.

“Even when we ruled out any conditions that could potentially cause enlargement of the heart, including hypertension, heart valve problems, diabetes, and other cardiovascular risk factors, the association with obesity cardiomyopathy, or OCM, and sudden cardiac death remained,” lead author Joseph Westaby, PhD, from the Cardiac Risk in the Young (CRY) Cardiovascular Pathology Laboratories at St George’s University of London, said in an interview.

The study was published online in JACC: Advances.

Intrigued by this finding, Dr. Westaby and associates sought to characterize the clinical and pathological features of OCM associated with sudden cardiac death by comparing this population to two control groups: sudden cardiac death patients who were either obese or of normal weight, and had morphologically normal hearts.

Their group is uniquely positioned to do such research, Dr. Westaby explained.

“Here at St George’s University of London, we have a specialized cardiovascular pathology service. ... All hearts obtained at autopsy from individuals who have died from sudden cardiac death, or who were suspected to have had a cardiovascular cause of death, anywhere in the U.K., are referred to the CRY Centre for further analysis,” he said.

Patients were divided into two groups according to body mass index: an obesity group (BMI > 30 kg/m²) and a normal-weight group (BMI, 18.5-24.9).

An increased heart weight above 550 g in men and 450 g in women in the absence of coronary artery disease, hypertension, diabetes, or valvular disease was classified as unexplained cardiomegaly, and individuals with obesity and cardiomegaly were defined as obesity cardiomyopathy.

Age- and sex-matched controls with obesity (n = 106) were selected based on a BMI greater than 30, with a morphologically normal heart weighing less than 550 g in men and than 450 g in women. 

Age- and sex-matched normal weight controls (n = 106) were selected based on a BMI of 18.5-24.9 and a morphologically normal heart weighing less than 550 g in men and less than 450 g in women. 

The researchers identified 53 OCM cases from a cohort of more than 4,500 sudden cardiac death cases that had BMI measurements. In normal-weight patients, there were 14 cases of unexplained cardiomegaly.

The mean age at death of individuals with OCM was 42 years (range, 30-54 years). Most of the deaths occurred in men (n = 34; 64%), who also died younger than women (40 ± 13 years vs. 45 ± 10 years; P = .036).

The average heart weight in OCM patients was 598 ± 93 g. Risk of sudden cardiac death increased when BMI reached 35.

Compared with matched controls, there were increases in right and left ventricular wall thickness (all P < .05) in OCM cases. Right ventricular epicardial fat was increased in OCM cases, compared with normal-weight controls only.

Left ventricular fibrosis was identified in seven (13%) OCM cases.
 

Role of genetics to be explored

“This study highlights the need for further investigation into these individuals because, at the moment, we can’t be sure that the only contributing factor to this is the obesity,” said Dr. Westaby.

In the works are plans to see if there may be an underlying genetic predisposition in obese individuals that may have contributed to the development of an enlarged heart. The group also plans to study the families of the deceased individuals to determine if they are at risk of developing cardiomegaly, he said.

“This paper makes an important contribution to the literature that raises many important questions for future research,” Timothy P. Fitzgibbons, MD, PhD, from the University of Massachusetts, Worcester, wrote in an accompanying editorial.

Being able to access so many autopsy samples gives the current study considerable heft, Dr. Fitzgibbons said in an interview.

“A lot has been made of the obesity paradox and the perhaps benign nature of obesity but this paper suggests the opposite, that it is a very serious problem and can, in fact, in and of itself, cause heart abnormalities that could cause sudden death,” he noted.

The fact that only 13% of OCM cases had fibrosis on histology suggests that fibrosis was not the main cause of sudden cardiac death, he said.

“Often we will do MRIs to look for areas of fibrosis within the heart because those areas make patients prone to re-entry arrhythmias, in particular, ventricular tachycardia. But the authors suggest that the enlarged myocytes may themselves be predisposing to arrhythmias, rather than fibrosis,” Dr. Fitzgibbons said.

The study was supported by Cardiac Risk in the Young. Dr. Westaby and Dr. Fitzgibbons have reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Obesity, in and of itself, and independent of other cardiovascular risk factors, may cause changes to the heart that can lead to sudden cardiac death, a new case-control study suggests.

Researchers who analyzed hearts taken at autopsy from people who had died from sudden cardiac death found that a number of the hearts obtained from obese decedents were heavier than those from normal-weight decedents and that the hazard ratio of unexplained cardiomegaly in this cohort was 5.3, compared with normal-weight individuals.

“Even when we ruled out any conditions that could potentially cause enlargement of the heart, including hypertension, heart valve problems, diabetes, and other cardiovascular risk factors, the association with obesity cardiomyopathy, or OCM, and sudden cardiac death remained,” lead author Joseph Westaby, PhD, from the Cardiac Risk in the Young (CRY) Cardiovascular Pathology Laboratories at St George’s University of London, said in an interview.

The study was published online in JACC: Advances.

Intrigued by this finding, Dr. Westaby and associates sought to characterize the clinical and pathological features of OCM associated with sudden cardiac death by comparing this population to two control groups: sudden cardiac death patients who were either obese or of normal weight, and had morphologically normal hearts.

Their group is uniquely positioned to do such research, Dr. Westaby explained.

“Here at St George’s University of London, we have a specialized cardiovascular pathology service. ... All hearts obtained at autopsy from individuals who have died from sudden cardiac death, or who were suspected to have had a cardiovascular cause of death, anywhere in the U.K., are referred to the CRY Centre for further analysis,” he said.

Patients were divided into two groups according to body mass index: an obesity group (BMI > 30 kg/m²) and a normal-weight group (BMI, 18.5-24.9).

An increased heart weight above 550 g in men and 450 g in women in the absence of coronary artery disease, hypertension, diabetes, or valvular disease was classified as unexplained cardiomegaly, and individuals with obesity and cardiomegaly were defined as obesity cardiomyopathy.

Age- and sex-matched controls with obesity (n = 106) were selected based on a BMI greater than 30, with a morphologically normal heart weighing less than 550 g in men and than 450 g in women. 

Age- and sex-matched normal weight controls (n = 106) were selected based on a BMI of 18.5-24.9 and a morphologically normal heart weighing less than 550 g in men and less than 450 g in women. 

The researchers identified 53 OCM cases from a cohort of more than 4,500 sudden cardiac death cases that had BMI measurements. In normal-weight patients, there were 14 cases of unexplained cardiomegaly.

The mean age at death of individuals with OCM was 42 years (range, 30-54 years). Most of the deaths occurred in men (n = 34; 64%), who also died younger than women (40 ± 13 years vs. 45 ± 10 years; P = .036).

The average heart weight in OCM patients was 598 ± 93 g. Risk of sudden cardiac death increased when BMI reached 35.

Compared with matched controls, there were increases in right and left ventricular wall thickness (all P < .05) in OCM cases. Right ventricular epicardial fat was increased in OCM cases, compared with normal-weight controls only.

Left ventricular fibrosis was identified in seven (13%) OCM cases.
 

Role of genetics to be explored

“This study highlights the need for further investigation into these individuals because, at the moment, we can’t be sure that the only contributing factor to this is the obesity,” said Dr. Westaby.

In the works are plans to see if there may be an underlying genetic predisposition in obese individuals that may have contributed to the development of an enlarged heart. The group also plans to study the families of the deceased individuals to determine if they are at risk of developing cardiomegaly, he said.

“This paper makes an important contribution to the literature that raises many important questions for future research,” Timothy P. Fitzgibbons, MD, PhD, from the University of Massachusetts, Worcester, wrote in an accompanying editorial.

Being able to access so many autopsy samples gives the current study considerable heft, Dr. Fitzgibbons said in an interview.

“A lot has been made of the obesity paradox and the perhaps benign nature of obesity but this paper suggests the opposite, that it is a very serious problem and can, in fact, in and of itself, cause heart abnormalities that could cause sudden death,” he noted.

The fact that only 13% of OCM cases had fibrosis on histology suggests that fibrosis was not the main cause of sudden cardiac death, he said.

“Often we will do MRIs to look for areas of fibrosis within the heart because those areas make patients prone to re-entry arrhythmias, in particular, ventricular tachycardia. But the authors suggest that the enlarged myocytes may themselves be predisposing to arrhythmias, rather than fibrosis,” Dr. Fitzgibbons said.

The study was supported by Cardiac Risk in the Young. Dr. Westaby and Dr. Fitzgibbons have reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Left atrial appendage occlusion (LAAO) is associated with fewer injuries and less bleeding from falls than anticoagulant medications in patients with atrial fibrillation (AF) and a previous stroke, a new cohort study suggests.

Investigators prospectively followed more than 1,250 patients with AF and a previous ischemic stroke. Approximately half underwent LAAO, while the other half were treated with direct oral anticoagulants (DOACs). Patients were followed for close to 2 years.

Slightly more than 20% of patients fell during that period in each group, and after their falls, patients on DOACs had significantly more severe injuries and longer hospital stays, compared with those treated by LAAO, who were not taking anticoagulants. The risk for a major bleed, including an intracranial bleed, was 70% lower in the LAAO group.

LAAO has previously been considered for people at risk of bleeding events – for example, those with gastrointestinal (GI) bleeds, bruising, or intracranial bleeding – but had not yet been studied in those at risk for falls, coauthor Moussa Mansour, MD, professor of medicine, Harvard Medical School, and director of the Atrial Fibrillation Program at Massachusetts General Hospital, Boston, said in an interview.

This is the first study to focus on LAAO specifically for those at risk for falling and demonstrated that the LAAO has utility in this population as well, which is important because the U.S. population is an aging population, and at advanced ages, “people’s balance becomes unsteady and they are at high risk of falling,” he said.

The findings were published online as a research letter in the Journal of the American College of Cardiology.
 

Multidisciplinary collaboration

“More than one in five of our neurology patients with AF fall – many with devastating consequences – making stroke prevention extremely challenging,” senior author MingMing Ning, MD, MMsc, associate professor of neurology, Harvard Medical School, and director of the Cardio-Neurology and the Clinical Proteomics Research Center at Massachusetts General Hospital, Boston, said in an interview.

“There is a dire need to tailor treatment to keep our patients safe while preventing future strokes,” she said.

Anticoagulants are effective in stroke prevention in these patients but are associated with a higher risk for major bleeding, especially after a fall.

The current prospective observational study recruited 1,266 stroke patients who were treated either with LAAO or DOACs (n = 570 and 696, respectively). Patients were followed for a median of 1.8 years (IQR: 0.9-3.0).

During the follow-up period, 22.6% of LAAO-treated patients and 22.7% of DOAC-treated patients sustained a fall (mean age 78.9 years, 57.4% male and 79.1 years, 52.5% male respectively).

Fall severity, evaluated via the Injury Severity Score, was less in the LAAO vs. the DOAC group, with ISS scores of 1 (IQR 1-4) vs. 4 (IQR 1.75-9).

LAAO was associated with significantly reduced severity of fall-related injuries (OR, –1.09, 95% confidence interval [CI], –1.52 to –0.66; P < .001) – a finding that remained statistically significant after adjustment for confounders such as age, sex, and comorbidities contributing to fall risk, such as hypertension, hyperlipidemia, and diabetes.

The incidence of major trauma (defined as ISS >15) was lower in the LAAO group, compared to the DOAC group (0.8% vs. 6.3%, respectively, P = .026), and LAAO-treated patients had a shorter length of hospital stay, with fewer LAAO patients compared with DOAC patients staying in the hospital for more than 3 days (17% vs. 29.1%, respectively, P = .018).

The risk for major post-fall bleeding was lower in the LAAO vs. the DOAC group (4.7% vs. 15.2%, AOR, 0.29; 95% CI, 0.11-0.73; P = .009) – a finding that included intracranial bleeding (3.1% vs. 9.5%; AOR, 0.29; 95% CI, 0.09-0.90; P = .033).

“Many people are living to advanced ages, where their balance becomes unsteady, and in addition, we have an increase in the prevalence of AF because people are living longer and it’s a disease of the elderly, because we have more hypertension, and we also have more tools to diagnose AF. It’s almost a ‘perfect storm’ situation, and we need effective interventions in this population,” said Dr. Mansour.

Before the study, people at risk for falling were not being considered for LAAO; but now, “we believe they should be considered,” he added. “And although people in the current study had all experienced an ischemic stroke, any patient at risk of a fall will potentially benefit.”

Beyond demonstrating the role of LAAO in reducing the risk of post-fall bleeding injuries, the study – which was conducted by specialists in neurology and cardiology among other fields – highlights the importance of multidisciplinary collaboration, which is “key” for effective stroke prevention, Dr. Ning said.

She emphasized that “we need to learn from our patients and tailor treatment to their needs. A patient’s risk of falling, lifestyle, and medication adherence are all important for individualizing care and improving quality of life.”
 

Better option

Commenting for this article, Andrea Natale, MD, executive medical director, Texas Cardiac Arrhythmia Institute at St. David’s Medical Center, Austin, said the authors “should be commended for this prospective study on real-world patients that has yielded highly meaningful data from a clinical standpoint.”

Dr. Natale, who was not involved with the study, said it has “several strong points,” such as a fairly large sample size, exclusive population with a history of AF-related stroke, long follow-up duration, evaluation of fall incidents by blinded experts, and severity of fall assessed by a validated questionnaire.

“This is the first study that directly compared the outcomes of traumatic fall in patients receiving LAAO vs. DOAC,” he said. “Given that history of fall is an independent predictor of bleeding and death, the study findings by Deng et al. offer the hope for a safer life with the LAAO option in the aging, fall-prone AF population.”

The take-home message is that, in patients with history of stroke, LAAO “is a better option, in terms of significantly reduced injury severity and shortened hospital length of stay after traumatic falls,” Dr. Natale said.

This study was supported in part by research grants from Boston Scientific, the Leducq Foundation, and the National Institutes of Health. The authors reported no relevant financial relationships. Dr. Natale is a consultant for Abbott, Baylis, Biosense Webster, Biotronik, Boston Scientific, and Medtronic.
 

A version of this article appeared on Medscape.com.

Left atrial appendage occlusion (LAAO) is associated with fewer injuries and less bleeding from falls than anticoagulant medications in patients with atrial fibrillation (AF) and a previous stroke, a new cohort study suggests.

Investigators prospectively followed more than 1,250 patients with AF and a previous ischemic stroke. Approximately half underwent LAAO, while the other half were treated with direct oral anticoagulants (DOACs). Patients were followed for close to 2 years.

Slightly more than 20% of patients fell during that period in each group, and after their falls, patients on DOACs had significantly more severe injuries and longer hospital stays, compared with those treated by LAAO, who were not taking anticoagulants. The risk for a major bleed, including an intracranial bleed, was 70% lower in the LAAO group.

LAAO has previously been considered for people at risk of bleeding events – for example, those with gastrointestinal (GI) bleeds, bruising, or intracranial bleeding – but had not yet been studied in those at risk for falls, coauthor Moussa Mansour, MD, professor of medicine, Harvard Medical School, and director of the Atrial Fibrillation Program at Massachusetts General Hospital, Boston, said in an interview.

This is the first study to focus on LAAO specifically for those at risk for falling and demonstrated that the LAAO has utility in this population as well, which is important because the U.S. population is an aging population, and at advanced ages, “people’s balance becomes unsteady and they are at high risk of falling,” he said.

The findings were published online as a research letter in the Journal of the American College of Cardiology.
 

Multidisciplinary collaboration

“More than one in five of our neurology patients with AF fall – many with devastating consequences – making stroke prevention extremely challenging,” senior author MingMing Ning, MD, MMsc, associate professor of neurology, Harvard Medical School, and director of the Cardio-Neurology and the Clinical Proteomics Research Center at Massachusetts General Hospital, Boston, said in an interview.

“There is a dire need to tailor treatment to keep our patients safe while preventing future strokes,” she said.

Anticoagulants are effective in stroke prevention in these patients but are associated with a higher risk for major bleeding, especially after a fall.

The current prospective observational study recruited 1,266 stroke patients who were treated either with LAAO or DOACs (n = 570 and 696, respectively). Patients were followed for a median of 1.8 years (IQR: 0.9-3.0).

During the follow-up period, 22.6% of LAAO-treated patients and 22.7% of DOAC-treated patients sustained a fall (mean age 78.9 years, 57.4% male and 79.1 years, 52.5% male respectively).

Fall severity, evaluated via the Injury Severity Score, was less in the LAAO vs. the DOAC group, with ISS scores of 1 (IQR 1-4) vs. 4 (IQR 1.75-9).

LAAO was associated with significantly reduced severity of fall-related injuries (OR, –1.09, 95% confidence interval [CI], –1.52 to –0.66; P < .001) – a finding that remained statistically significant after adjustment for confounders such as age, sex, and comorbidities contributing to fall risk, such as hypertension, hyperlipidemia, and diabetes.

The incidence of major trauma (defined as ISS >15) was lower in the LAAO group, compared to the DOAC group (0.8% vs. 6.3%, respectively, P = .026), and LAAO-treated patients had a shorter length of hospital stay, with fewer LAAO patients compared with DOAC patients staying in the hospital for more than 3 days (17% vs. 29.1%, respectively, P = .018).

The risk for major post-fall bleeding was lower in the LAAO vs. the DOAC group (4.7% vs. 15.2%, AOR, 0.29; 95% CI, 0.11-0.73; P = .009) – a finding that included intracranial bleeding (3.1% vs. 9.5%; AOR, 0.29; 95% CI, 0.09-0.90; P = .033).

“Many people are living to advanced ages, where their balance becomes unsteady, and in addition, we have an increase in the prevalence of AF because people are living longer and it’s a disease of the elderly, because we have more hypertension, and we also have more tools to diagnose AF. It’s almost a ‘perfect storm’ situation, and we need effective interventions in this population,” said Dr. Mansour.

Before the study, people at risk for falling were not being considered for LAAO; but now, “we believe they should be considered,” he added. “And although people in the current study had all experienced an ischemic stroke, any patient at risk of a fall will potentially benefit.”

Beyond demonstrating the role of LAAO in reducing the risk of post-fall bleeding injuries, the study – which was conducted by specialists in neurology and cardiology among other fields – highlights the importance of multidisciplinary collaboration, which is “key” for effective stroke prevention, Dr. Ning said.

She emphasized that “we need to learn from our patients and tailor treatment to their needs. A patient’s risk of falling, lifestyle, and medication adherence are all important for individualizing care and improving quality of life.”
 

Better option

Commenting for this article, Andrea Natale, MD, executive medical director, Texas Cardiac Arrhythmia Institute at St. David’s Medical Center, Austin, said the authors “should be commended for this prospective study on real-world patients that has yielded highly meaningful data from a clinical standpoint.”

Dr. Natale, who was not involved with the study, said it has “several strong points,” such as a fairly large sample size, exclusive population with a history of AF-related stroke, long follow-up duration, evaluation of fall incidents by blinded experts, and severity of fall assessed by a validated questionnaire.

“This is the first study that directly compared the outcomes of traumatic fall in patients receiving LAAO vs. DOAC,” he said. “Given that history of fall is an independent predictor of bleeding and death, the study findings by Deng et al. offer the hope for a safer life with the LAAO option in the aging, fall-prone AF population.”

The take-home message is that, in patients with history of stroke, LAAO “is a better option, in terms of significantly reduced injury severity and shortened hospital length of stay after traumatic falls,” Dr. Natale said.

This study was supported in part by research grants from Boston Scientific, the Leducq Foundation, and the National Institutes of Health. The authors reported no relevant financial relationships. Dr. Natale is a consultant for Abbott, Baylis, Biosense Webster, Biotronik, Boston Scientific, and Medtronic.
 

A version of this article appeared on Medscape.com.

Left atrial appendage occlusion (LAAO) is associated with fewer injuries and less bleeding from falls than anticoagulant medications in patients with atrial fibrillation (AF) and a previous stroke, a new cohort study suggests.

Investigators prospectively followed more than 1,250 patients with AF and a previous ischemic stroke. Approximately half underwent LAAO, while the other half were treated with direct oral anticoagulants (DOACs). Patients were followed for close to 2 years.

Slightly more than 20% of patients fell during that period in each group, and after their falls, patients on DOACs had significantly more severe injuries and longer hospital stays, compared with those treated by LAAO, who were not taking anticoagulants. The risk for a major bleed, including an intracranial bleed, was 70% lower in the LAAO group.

LAAO has previously been considered for people at risk of bleeding events – for example, those with gastrointestinal (GI) bleeds, bruising, or intracranial bleeding – but had not yet been studied in those at risk for falls, coauthor Moussa Mansour, MD, professor of medicine, Harvard Medical School, and director of the Atrial Fibrillation Program at Massachusetts General Hospital, Boston, said in an interview.

This is the first study to focus on LAAO specifically for those at risk for falling and demonstrated that the LAAO has utility in this population as well, which is important because the U.S. population is an aging population, and at advanced ages, “people’s balance becomes unsteady and they are at high risk of falling,” he said.

The findings were published online as a research letter in the Journal of the American College of Cardiology.
 

Multidisciplinary collaboration

“More than one in five of our neurology patients with AF fall – many with devastating consequences – making stroke prevention extremely challenging,” senior author MingMing Ning, MD, MMsc, associate professor of neurology, Harvard Medical School, and director of the Cardio-Neurology and the Clinical Proteomics Research Center at Massachusetts General Hospital, Boston, said in an interview.

“There is a dire need to tailor treatment to keep our patients safe while preventing future strokes,” she said.

Anticoagulants are effective in stroke prevention in these patients but are associated with a higher risk for major bleeding, especially after a fall.

The current prospective observational study recruited 1,266 stroke patients who were treated either with LAAO or DOACs (n = 570 and 696, respectively). Patients were followed for a median of 1.8 years (IQR: 0.9-3.0).

During the follow-up period, 22.6% of LAAO-treated patients and 22.7% of DOAC-treated patients sustained a fall (mean age 78.9 years, 57.4% male and 79.1 years, 52.5% male respectively).

Fall severity, evaluated via the Injury Severity Score, was less in the LAAO vs. the DOAC group, with ISS scores of 1 (IQR 1-4) vs. 4 (IQR 1.75-9).

LAAO was associated with significantly reduced severity of fall-related injuries (OR, –1.09, 95% confidence interval [CI], –1.52 to –0.66; P < .001) – a finding that remained statistically significant after adjustment for confounders such as age, sex, and comorbidities contributing to fall risk, such as hypertension, hyperlipidemia, and diabetes.

The incidence of major trauma (defined as ISS >15) was lower in the LAAO group, compared to the DOAC group (0.8% vs. 6.3%, respectively, P = .026), and LAAO-treated patients had a shorter length of hospital stay, with fewer LAAO patients compared with DOAC patients staying in the hospital for more than 3 days (17% vs. 29.1%, respectively, P = .018).

The risk for major post-fall bleeding was lower in the LAAO vs. the DOAC group (4.7% vs. 15.2%, AOR, 0.29; 95% CI, 0.11-0.73; P = .009) – a finding that included intracranial bleeding (3.1% vs. 9.5%; AOR, 0.29; 95% CI, 0.09-0.90; P = .033).

“Many people are living to advanced ages, where their balance becomes unsteady, and in addition, we have an increase in the prevalence of AF because people are living longer and it’s a disease of the elderly, because we have more hypertension, and we also have more tools to diagnose AF. It’s almost a ‘perfect storm’ situation, and we need effective interventions in this population,” said Dr. Mansour.

Before the study, people at risk for falling were not being considered for LAAO; but now, “we believe they should be considered,” he added. “And although people in the current study had all experienced an ischemic stroke, any patient at risk of a fall will potentially benefit.”

Beyond demonstrating the role of LAAO in reducing the risk of post-fall bleeding injuries, the study – which was conducted by specialists in neurology and cardiology among other fields – highlights the importance of multidisciplinary collaboration, which is “key” for effective stroke prevention, Dr. Ning said.

She emphasized that “we need to learn from our patients and tailor treatment to their needs. A patient’s risk of falling, lifestyle, and medication adherence are all important for individualizing care and improving quality of life.”
 

Better option

Commenting for this article, Andrea Natale, MD, executive medical director, Texas Cardiac Arrhythmia Institute at St. David’s Medical Center, Austin, said the authors “should be commended for this prospective study on real-world patients that has yielded highly meaningful data from a clinical standpoint.”

Dr. Natale, who was not involved with the study, said it has “several strong points,” such as a fairly large sample size, exclusive population with a history of AF-related stroke, long follow-up duration, evaluation of fall incidents by blinded experts, and severity of fall assessed by a validated questionnaire.

“This is the first study that directly compared the outcomes of traumatic fall in patients receiving LAAO vs. DOAC,” he said. “Given that history of fall is an independent predictor of bleeding and death, the study findings by Deng et al. offer the hope for a safer life with the LAAO option in the aging, fall-prone AF population.”

The take-home message is that, in patients with history of stroke, LAAO “is a better option, in terms of significantly reduced injury severity and shortened hospital length of stay after traumatic falls,” Dr. Natale said.

This study was supported in part by research grants from Boston Scientific, the Leducq Foundation, and the National Institutes of Health. The authors reported no relevant financial relationships. Dr. Natale is a consultant for Abbott, Baylis, Biosense Webster, Biotronik, Boston Scientific, and Medtronic.
 

A version of this article appeared on Medscape.com.

SEATTLE – A family of blockbuster drugs for managing blood glucose – and now for promoting weight loss – has been linked to exacerbation of macular disease that frequently accompanies diabetes, new data show.

Two studies presented at the annual meeting of the American Society of Retina Specialists (ASRS) have found that use of injectable agonists of glucagonlike peptide-1 (GLP1) appears to hasten the progression of diabetic retinopathy and diabetic macular edema (DME).

Clinicians should be aware of these effects of GLP-1 inhibitors to ensure appropriate monitoring of patients for the possibility that retinopathy may accelerate, according to Ehsan Rahimy, MD, an adjunct clinical professor at Stanford (Calif.) University, and colleagues.

Dr. Rahimy presented results of a retrospective study of retinopathy progression in patients taking either GLP-1 agonists or sodium-glucose transporter-2 (SGLT-2) inhibitors, also known as gliflozins. “When we looked at the conversion to proliferative disease, you can see it was statistically higher in the GLP-1 group at all time points,” he said.

GLP-1 agonists can promote considerable weight loss in patients with and without diabetes. Moreover, the finding that gliflozins improve cardiovascular and renal function in patients with type 2 diabetes has accelerated the use of these agents for blood glucose control.

Using a repository of data from more than 13,500 people taking either of the two kinds of medication, the researchers looked for conversion of diabetic eye disease to proliferative diabetic retinopathy (PDR) or DME. Secondary outcomes were the need for intravitreal injections, panretinal photocoagulation (PRP), or pars plana vitrectomy (PPV).

Propensity score matching for age, sex, race, ethnicity, and baseline hemoglobin A1c resulted in the inclusion of 5,446 participants in each treatment group. After matching, the mean age of participants in either group was 64 years, and the mean A1c was 8.5%. Slightly more than half the participants were insulin-dependent.

Patients taking GLP-1 inhibitors had higher rates of conversion to PDR than those taking gliflozins at 3 years (6% vs. 4%; P < .01), the researchers found. Nearly 25% of those taking a GLP-1 agonist had progressed to DME after 3 years, compared with 18% of those taking a gliflozin.

People in the group taking GLP-1 inhibitors also had a greater need for interventions than those on a gliflozin; 8% vs. roughly 6%, respectively, required intravitreal injections, Dr. Rahimy reported. Similar trends were noted for need for PRP and PPV, he added, although the absolute numbers of patients were small.
 

Albiglutide the key culprit?

In other research reported at the meeting, a meta-analysis of data collected in 93 randomized clinical trials of the seven currently available GLP-1 agonists found only albiglutide was associated with diabetic retinopathy to a statistically significant degree. Compared with placebo, albiglutide more than doubled the risk for early-stage diabetic retinopathy (relative risk 2.18; 95% confidence interval, 1.01-4.67; P = .05).

Other GLP-1 agonists evaluated in the meta-analysis included semaglutide, tirzepatide, dulaglutide, exenatide, liraglutide, and lixisenatide. These findings were reported in a poster presented at the meeting by Ishani Kapoor, MD candidate, Drexel University, Philadelphia.

“The strength of these effects depends on the specific GLP-1 receptor agonist used, patient-specific clinical characteristics, and demographics,” Ms. Kapoor and coauthors reported. “Further studies are needed to clarify the patient populations that would benefit from GLP-1 receptor agonists and those at risk for [the] development of additional ocular damage.”
 

What causes progression?

Whether worsening of retinopathy stems from rapid weight loss and acute reductions in concentrations of blood glucose or is a direct effect of GLP-1 agonists on the eye is unclear.

“That rapid reduction is thought to play some role,” Dr. Rahimy said. “But if you actually look out there in the basic science literature, it’s suggested that there are direct effects of these medications on the retina too. That being said, it’s suggested that they may be protective to the retina. And I think that’s where we’ve gotten a lot of mixed signals in our community between what we’ve seen on the basic science side vs. what we’re seeing on the real-world side.”

The study was independently funded. Dr. Rahimy reports consultancies or speakerships with AbbVie, Allergan, Apellis, Carl Zeiss, Genentech, and Google, and research support from Regeneron. Ms. Kapoor reports no relevant financial relationships.

A version of this article appeared on Medscape.com.

SEATTLE – A family of blockbuster drugs for managing blood glucose – and now for promoting weight loss – has been linked to exacerbation of macular disease that frequently accompanies diabetes, new data show.

Two studies presented at the annual meeting of the American Society of Retina Specialists (ASRS) have found that use of injectable agonists of glucagonlike peptide-1 (GLP1) appears to hasten the progression of diabetic retinopathy and diabetic macular edema (DME).

Clinicians should be aware of these effects of GLP-1 inhibitors to ensure appropriate monitoring of patients for the possibility that retinopathy may accelerate, according to Ehsan Rahimy, MD, an adjunct clinical professor at Stanford (Calif.) University, and colleagues.

Dr. Rahimy presented results of a retrospective study of retinopathy progression in patients taking either GLP-1 agonists or sodium-glucose transporter-2 (SGLT-2) inhibitors, also known as gliflozins. “When we looked at the conversion to proliferative disease, you can see it was statistically higher in the GLP-1 group at all time points,” he said.

GLP-1 agonists can promote considerable weight loss in patients with and without diabetes. Moreover, the finding that gliflozins improve cardiovascular and renal function in patients with type 2 diabetes has accelerated the use of these agents for blood glucose control.

Using a repository of data from more than 13,500 people taking either of the two kinds of medication, the researchers looked for conversion of diabetic eye disease to proliferative diabetic retinopathy (PDR) or DME. Secondary outcomes were the need for intravitreal injections, panretinal photocoagulation (PRP), or pars plana vitrectomy (PPV).

Propensity score matching for age, sex, race, ethnicity, and baseline hemoglobin A1c resulted in the inclusion of 5,446 participants in each treatment group. After matching, the mean age of participants in either group was 64 years, and the mean A1c was 8.5%. Slightly more than half the participants were insulin-dependent.

Patients taking GLP-1 inhibitors had higher rates of conversion to PDR than those taking gliflozins at 3 years (6% vs. 4%; P < .01), the researchers found. Nearly 25% of those taking a GLP-1 agonist had progressed to DME after 3 years, compared with 18% of those taking a gliflozin.

People in the group taking GLP-1 inhibitors also had a greater need for interventions than those on a gliflozin; 8% vs. roughly 6%, respectively, required intravitreal injections, Dr. Rahimy reported. Similar trends were noted for need for PRP and PPV, he added, although the absolute numbers of patients were small.
 

Albiglutide the key culprit?

In other research reported at the meeting, a meta-analysis of data collected in 93 randomized clinical trials of the seven currently available GLP-1 agonists found only albiglutide was associated with diabetic retinopathy to a statistically significant degree. Compared with placebo, albiglutide more than doubled the risk for early-stage diabetic retinopathy (relative risk 2.18; 95% confidence interval, 1.01-4.67; P = .05).

Other GLP-1 agonists evaluated in the meta-analysis included semaglutide, tirzepatide, dulaglutide, exenatide, liraglutide, and lixisenatide. These findings were reported in a poster presented at the meeting by Ishani Kapoor, MD candidate, Drexel University, Philadelphia.

“The strength of these effects depends on the specific GLP-1 receptor agonist used, patient-specific clinical characteristics, and demographics,” Ms. Kapoor and coauthors reported. “Further studies are needed to clarify the patient populations that would benefit from GLP-1 receptor agonists and those at risk for [the] development of additional ocular damage.”
 

What causes progression?

Whether worsening of retinopathy stems from rapid weight loss and acute reductions in concentrations of blood glucose or is a direct effect of GLP-1 agonists on the eye is unclear.

“That rapid reduction is thought to play some role,” Dr. Rahimy said. “But if you actually look out there in the basic science literature, it’s suggested that there are direct effects of these medications on the retina too. That being said, it’s suggested that they may be protective to the retina. And I think that’s where we’ve gotten a lot of mixed signals in our community between what we’ve seen on the basic science side vs. what we’re seeing on the real-world side.”

The study was independently funded. Dr. Rahimy reports consultancies or speakerships with AbbVie, Allergan, Apellis, Carl Zeiss, Genentech, and Google, and research support from Regeneron. Ms. Kapoor reports no relevant financial relationships.

A version of this article appeared on Medscape.com.

SEATTLE – A family of blockbuster drugs for managing blood glucose – and now for promoting weight loss – has been linked to exacerbation of macular disease that frequently accompanies diabetes, new data show.

Two studies presented at the annual meeting of the American Society of Retina Specialists (ASRS) have found that use of injectable agonists of glucagonlike peptide-1 (GLP1) appears to hasten the progression of diabetic retinopathy and diabetic macular edema (DME).

Clinicians should be aware of these effects of GLP-1 inhibitors to ensure appropriate monitoring of patients for the possibility that retinopathy may accelerate, according to Ehsan Rahimy, MD, an adjunct clinical professor at Stanford (Calif.) University, and colleagues.

Dr. Rahimy presented results of a retrospective study of retinopathy progression in patients taking either GLP-1 agonists or sodium-glucose transporter-2 (SGLT-2) inhibitors, also known as gliflozins. “When we looked at the conversion to proliferative disease, you can see it was statistically higher in the GLP-1 group at all time points,” he said.

GLP-1 agonists can promote considerable weight loss in patients with and without diabetes. Moreover, the finding that gliflozins improve cardiovascular and renal function in patients with type 2 diabetes has accelerated the use of these agents for blood glucose control.

Using a repository of data from more than 13,500 people taking either of the two kinds of medication, the researchers looked for conversion of diabetic eye disease to proliferative diabetic retinopathy (PDR) or DME. Secondary outcomes were the need for intravitreal injections, panretinal photocoagulation (PRP), or pars plana vitrectomy (PPV).

Propensity score matching for age, sex, race, ethnicity, and baseline hemoglobin A1c resulted in the inclusion of 5,446 participants in each treatment group. After matching, the mean age of participants in either group was 64 years, and the mean A1c was 8.5%. Slightly more than half the participants were insulin-dependent.

Patients taking GLP-1 inhibitors had higher rates of conversion to PDR than those taking gliflozins at 3 years (6% vs. 4%; P < .01), the researchers found. Nearly 25% of those taking a GLP-1 agonist had progressed to DME after 3 years, compared with 18% of those taking a gliflozin.

People in the group taking GLP-1 inhibitors also had a greater need for interventions than those on a gliflozin; 8% vs. roughly 6%, respectively, required intravitreal injections, Dr. Rahimy reported. Similar trends were noted for need for PRP and PPV, he added, although the absolute numbers of patients were small.
 

Albiglutide the key culprit?

In other research reported at the meeting, a meta-analysis of data collected in 93 randomized clinical trials of the seven currently available GLP-1 agonists found only albiglutide was associated with diabetic retinopathy to a statistically significant degree. Compared with placebo, albiglutide more than doubled the risk for early-stage diabetic retinopathy (relative risk 2.18; 95% confidence interval, 1.01-4.67; P = .05).

Other GLP-1 agonists evaluated in the meta-analysis included semaglutide, tirzepatide, dulaglutide, exenatide, liraglutide, and lixisenatide. These findings were reported in a poster presented at the meeting by Ishani Kapoor, MD candidate, Drexel University, Philadelphia.

“The strength of these effects depends on the specific GLP-1 receptor agonist used, patient-specific clinical characteristics, and demographics,” Ms. Kapoor and coauthors reported. “Further studies are needed to clarify the patient populations that would benefit from GLP-1 receptor agonists and those at risk for [the] development of additional ocular damage.”
 

What causes progression?

Whether worsening of retinopathy stems from rapid weight loss and acute reductions in concentrations of blood glucose or is a direct effect of GLP-1 agonists on the eye is unclear.

“That rapid reduction is thought to play some role,” Dr. Rahimy said. “But if you actually look out there in the basic science literature, it’s suggested that there are direct effects of these medications on the retina too. That being said, it’s suggested that they may be protective to the retina. And I think that’s where we’ve gotten a lot of mixed signals in our community between what we’ve seen on the basic science side vs. what we’re seeing on the real-world side.”

The study was independently funded. Dr. Rahimy reports consultancies or speakerships with AbbVie, Allergan, Apellis, Carl Zeiss, Genentech, and Google, and research support from Regeneron. Ms. Kapoor reports no relevant financial relationships.

A version of this article appeared on Medscape.com.

Some clinicians say it’s “confusing” and “ridiculous” to change the name and diagnostic criteria of an established liver disease, while others bemoan the seemingly political reasons why it happened. Yet recently, 236 panelists from 56 countries decided that the terms nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) rely on “exclusionary confounder terms and the use of potentially stigmatizing language.”

In a report published in Hepatology, the panelists, members of the NAFLD Nomenclature Consensus Group, determined that steatotic liver disease (SLD) would be used as an “overarching term to encompass the various etiologies of steatosis.”

Metabolic dysfunction–associated steatotic liver disease (MASLD) was chosen to replace NAFLD, and the definition was changed to include at least one of five cardiometabolic risk factors.

Metabolic dysfunction–associated steatohepatitis (MASH) replaces NASH. 

Those with no metabolic parameters and no known cause will be diagnosed with cryptogenic SLD.

A new category, MetALD, now describes those with MASLD who drink more alcohol per week – 140-350 g for men and 210-420 g for women.

The changes did not sit well with this news organization’s readers from diverse specialties, including family practice, critical care, and gastroenterology.

In its report, the consensus group wrote that 74% of respondents to its rounds of surveys felt the current nomenclature “was sufficiently flawed to consider a name change.”

The terms “nonalcoholic” and “fatty” were felt to be stigmatizing by 61% and 66% of respondents, respectively, according to the group, a multi-stakeholder effort under the auspices of the American Association for Study of Liver Disease and the European Association for Study of the Liver, in collaboration with the Asociación Latinoamericana para el Estudio del Hígado.

Consensus was defined a priori as a supermajority (67%) vote. 

“The new nomenclature and diagnostic criteria are widely supported, nonstigmatizing, and can improve awareness and patient identification,” the group concluded.

“No way” sums up many of the almost 60 reader comments received on this news organization’s story covering the change. Readers must share medical credentials to publicly comment on stories.
 

‘Confusing’ and ‘ridiculous’

A number of readers questioned how the changes will help practice.

“Once again, the specialists and other experts are changing the nomenclature to make the subject even more confusing for us primary care practitioners,” an HIV/AIDS physician wrote. “They obviously have no idea what [primary care practitioners] have to put up with day in and day out. All such revisions do is increase the cynicism and anger so many [primary care practitioners] have.”

Similarly, an internist said, “These new terms are going to confuse both doctors and patients. When you give a patient a diagnosis like this, they will not understand it, and will not be able to act as they should to correct it.”

“ ‘Fatty liver’ is a jargon-free diagnosis, easy to understand and easy for patients to know what they need to do,” the internist continued. “You think patients are gonna be educated when you tell them they have a ‘metabolic disease’? 100% they will not know what you’re talking about.”

Yet another wondered, “If SLD is the ‘umbrella’ term, why (are) MetALD and ALD not MetASLD and ASLD, respectively? Furthermore, efforts to ‘destigmatize’ terminology will inadvertently condemn cryptogenic SLD (CSLD) as the new ‘closet alcoholic.’ “

“Perhaps a subclassification, CSLD-HDIRDD (CSLD–Honest, Doc, I Really Don’t Drink),” the reader added.

“Everything about this is ridiculous,” a family physician wrote. “How long will it be until the experts change obesity to ‘gravitationally challenged’ as a diagnosis!”

“I was thinking of ‘circumferentially challenged,’” a reader in Canada chimed in. “But that would be ‘body shaming’ would it not?”

This reader continued, asking, “What about returning to the old practice of using Latin names patients don’t understand so there is no ‘shame’ attached to them? Or what about this revolutionary idea: To just say it as it is – fat?”
 

Acceding to ‘wokeness’

A sizable number of readers felt the name changes were motivated by a “woke” awareness.

“The effect of this new ‘woke’ clarity is ridiculous and simply not worth it! Can we justify the cost of this? Patients will have to learn all over again how to discuss their condition,” said one reader.

The reader continued, saying, “The Internet and social media freely use the term ‘fat’ – and despite not wanting to offend – there seems to be universal agreement that FAT, in certain conditions or places, is unhealthy and undesirable.

“Why is the medical community so afraid to tell it like it is? I might hurt your feelings, but I could save your life,” concluded the reader.
 

Defending change

One commentator, a hepatologist in France, defended the changes and responded to some of complaints.

“Maybe people who comment here should read the article, reflect, and understand the reasons why the old nomenclature and definition were scientifically inaccurate and needed to be changed,” the commentator wrote.

“It was an exclusionary, negative definition not recognizing the root of the disease (adipose tissue dysfunction with insulin resistance – instead defining it by what it is not ...) and not allowing the recognition of a large segment of the population [that] accumulates metabolic risk factors and moderate alcohol consumption. These patients were left out of all studies. Those were the main reasons for change and not the stigma part – with the word ‘fatty’ only being an issue in English-speaking countries, not elsewhere,” the commentator continued.

“Calls for change have been voiced for 20 years and a first comprehensive attempt (called MAFLD) was introduced 3 years ago (J Hepatol. 2020;73:202-9). Please, a little bit of respect and restraint in the comments recognizing the research efforts and publications for those that contributed to the field over the past 25 years ...” the hepatologist wrote.

The reader added, “Clinicians and researchers were dissatisfied for a long time, but it took years to gather overwhelming evidence demonstrating what causes the disease and then to kickstart a process under the auspices of several multinational scientific societies and come up with something consensually agreed upon by a large number of clinician researchers.

“Now you can tell your patient that he has metabolic liver disease instead of telling him that the problem at the root of his disease is that he is not drinking alcohol (nonalcoholic steatohepatitis). So, again, it is not so much about changing a name but about redefining diagnostic criteria and a nosological framework,” the reader wrote.

Other readers responded to the defender:

“This nomenclature issue has been churned for 20+ years? Well, the mountain has labored heavily, and given birth to a mouse,” one said.

“Still, how is this going to help in the clinical management? The whole gamut of conditions are evaluated and treated as a whole, not in isolation,” a general practitioner in India said. “If someone has a risk factor or not, continuous follow-up is required as a whole, whether it’s nonalcoholic or alcoholic, or whatever term is coined up.”

Finally, a family physician said, “It just rolls off the tongue, doesn’t it? But I have to admit, it’s the one place where ‘persons’ from 56 countries can get together and agree on something. Not even politicians can do that! Me, I’m sticking with NAFLD.”

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

Some clinicians say it’s “confusing” and “ridiculous” to change the name and diagnostic criteria of an established liver disease, while others bemoan the seemingly political reasons why it happened. Yet recently, 236 panelists from 56 countries decided that the terms nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) rely on “exclusionary confounder terms and the use of potentially stigmatizing language.”

In a report published in Hepatology, the panelists, members of the NAFLD Nomenclature Consensus Group, determined that steatotic liver disease (SLD) would be used as an “overarching term to encompass the various etiologies of steatosis.”

Metabolic dysfunction–associated steatotic liver disease (MASLD) was chosen to replace NAFLD, and the definition was changed to include at least one of five cardiometabolic risk factors.

Metabolic dysfunction–associated steatohepatitis (MASH) replaces NASH. 

Those with no metabolic parameters and no known cause will be diagnosed with cryptogenic SLD.

A new category, MetALD, now describes those with MASLD who drink more alcohol per week – 140-350 g for men and 210-420 g for women.

The changes did not sit well with this news organization’s readers from diverse specialties, including family practice, critical care, and gastroenterology.

In its report, the consensus group wrote that 74% of respondents to its rounds of surveys felt the current nomenclature “was sufficiently flawed to consider a name change.”

The terms “nonalcoholic” and “fatty” were felt to be stigmatizing by 61% and 66% of respondents, respectively, according to the group, a multi-stakeholder effort under the auspices of the American Association for Study of Liver Disease and the European Association for Study of the Liver, in collaboration with the Asociación Latinoamericana para el Estudio del Hígado.

Consensus was defined a priori as a supermajority (67%) vote. 

“The new nomenclature and diagnostic criteria are widely supported, nonstigmatizing, and can improve awareness and patient identification,” the group concluded.

“No way” sums up many of the almost 60 reader comments received on this news organization’s story covering the change. Readers must share medical credentials to publicly comment on stories.
 

‘Confusing’ and ‘ridiculous’

A number of readers questioned how the changes will help practice.

“Once again, the specialists and other experts are changing the nomenclature to make the subject even more confusing for us primary care practitioners,” an HIV/AIDS physician wrote. “They obviously have no idea what [primary care practitioners] have to put up with day in and day out. All such revisions do is increase the cynicism and anger so many [primary care practitioners] have.”

Similarly, an internist said, “These new terms are going to confuse both doctors and patients. When you give a patient a diagnosis like this, they will not understand it, and will not be able to act as they should to correct it.”

“ ‘Fatty liver’ is a jargon-free diagnosis, easy to understand and easy for patients to know what they need to do,” the internist continued. “You think patients are gonna be educated when you tell them they have a ‘metabolic disease’? 100% they will not know what you’re talking about.”

Yet another wondered, “If SLD is the ‘umbrella’ term, why (are) MetALD and ALD not MetASLD and ASLD, respectively? Furthermore, efforts to ‘destigmatize’ terminology will inadvertently condemn cryptogenic SLD (CSLD) as the new ‘closet alcoholic.’ “

“Perhaps a subclassification, CSLD-HDIRDD (CSLD–Honest, Doc, I Really Don’t Drink),” the reader added.

“Everything about this is ridiculous,” a family physician wrote. “How long will it be until the experts change obesity to ‘gravitationally challenged’ as a diagnosis!”

“I was thinking of ‘circumferentially challenged,’” a reader in Canada chimed in. “But that would be ‘body shaming’ would it not?”

This reader continued, asking, “What about returning to the old practice of using Latin names patients don’t understand so there is no ‘shame’ attached to them? Or what about this revolutionary idea: To just say it as it is – fat?”
 

Acceding to ‘wokeness’

A sizable number of readers felt the name changes were motivated by a “woke” awareness.

“The effect of this new ‘woke’ clarity is ridiculous and simply not worth it! Can we justify the cost of this? Patients will have to learn all over again how to discuss their condition,” said one reader.

The reader continued, saying, “The Internet and social media freely use the term ‘fat’ – and despite not wanting to offend – there seems to be universal agreement that FAT, in certain conditions or places, is unhealthy and undesirable.

“Why is the medical community so afraid to tell it like it is? I might hurt your feelings, but I could save your life,” concluded the reader.
 

Defending change

One commentator, a hepatologist in France, defended the changes and responded to some of complaints.

“Maybe people who comment here should read the article, reflect, and understand the reasons why the old nomenclature and definition were scientifically inaccurate and needed to be changed,” the commentator wrote.

“It was an exclusionary, negative definition not recognizing the root of the disease (adipose tissue dysfunction with insulin resistance – instead defining it by what it is not ...) and not allowing the recognition of a large segment of the population [that] accumulates metabolic risk factors and moderate alcohol consumption. These patients were left out of all studies. Those were the main reasons for change and not the stigma part – with the word ‘fatty’ only being an issue in English-speaking countries, not elsewhere,” the commentator continued.

“Calls for change have been voiced for 20 years and a first comprehensive attempt (called MAFLD) was introduced 3 years ago (J Hepatol. 2020;73:202-9). Please, a little bit of respect and restraint in the comments recognizing the research efforts and publications for those that contributed to the field over the past 25 years ...” the hepatologist wrote.

The reader added, “Clinicians and researchers were dissatisfied for a long time, but it took years to gather overwhelming evidence demonstrating what causes the disease and then to kickstart a process under the auspices of several multinational scientific societies and come up with something consensually agreed upon by a large number of clinician researchers.

“Now you can tell your patient that he has metabolic liver disease instead of telling him that the problem at the root of his disease is that he is not drinking alcohol (nonalcoholic steatohepatitis). So, again, it is not so much about changing a name but about redefining diagnostic criteria and a nosological framework,” the reader wrote.

Other readers responded to the defender:

“This nomenclature issue has been churned for 20+ years? Well, the mountain has labored heavily, and given birth to a mouse,” one said.

“Still, how is this going to help in the clinical management? The whole gamut of conditions are evaluated and treated as a whole, not in isolation,” a general practitioner in India said. “If someone has a risk factor or not, continuous follow-up is required as a whole, whether it’s nonalcoholic or alcoholic, or whatever term is coined up.”

Finally, a family physician said, “It just rolls off the tongue, doesn’t it? But I have to admit, it’s the one place where ‘persons’ from 56 countries can get together and agree on something. Not even politicians can do that! Me, I’m sticking with NAFLD.”

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

Some clinicians say it’s “confusing” and “ridiculous” to change the name and diagnostic criteria of an established liver disease, while others bemoan the seemingly political reasons why it happened. Yet recently, 236 panelists from 56 countries decided that the terms nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) rely on “exclusionary confounder terms and the use of potentially stigmatizing language.”

In a report published in Hepatology, the panelists, members of the NAFLD Nomenclature Consensus Group, determined that steatotic liver disease (SLD) would be used as an “overarching term to encompass the various etiologies of steatosis.”

Metabolic dysfunction–associated steatotic liver disease (MASLD) was chosen to replace NAFLD, and the definition was changed to include at least one of five cardiometabolic risk factors.

Metabolic dysfunction–associated steatohepatitis (MASH) replaces NASH. 

Those with no metabolic parameters and no known cause will be diagnosed with cryptogenic SLD.

A new category, MetALD, now describes those with MASLD who drink more alcohol per week – 140-350 g for men and 210-420 g for women.

The changes did not sit well with this news organization’s readers from diverse specialties, including family practice, critical care, and gastroenterology.

In its report, the consensus group wrote that 74% of respondents to its rounds of surveys felt the current nomenclature “was sufficiently flawed to consider a name change.”

The terms “nonalcoholic” and “fatty” were felt to be stigmatizing by 61% and 66% of respondents, respectively, according to the group, a multi-stakeholder effort under the auspices of the American Association for Study of Liver Disease and the European Association for Study of the Liver, in collaboration with the Asociación Latinoamericana para el Estudio del Hígado.

Consensus was defined a priori as a supermajority (67%) vote. 

“The new nomenclature and diagnostic criteria are widely supported, nonstigmatizing, and can improve awareness and patient identification,” the group concluded.

“No way” sums up many of the almost 60 reader comments received on this news organization’s story covering the change. Readers must share medical credentials to publicly comment on stories.
 

‘Confusing’ and ‘ridiculous’

A number of readers questioned how the changes will help practice.

“Once again, the specialists and other experts are changing the nomenclature to make the subject even more confusing for us primary care practitioners,” an HIV/AIDS physician wrote. “They obviously have no idea what [primary care practitioners] have to put up with day in and day out. All such revisions do is increase the cynicism and anger so many [primary care practitioners] have.”

Similarly, an internist said, “These new terms are going to confuse both doctors and patients. When you give a patient a diagnosis like this, they will not understand it, and will not be able to act as they should to correct it.”

“ ‘Fatty liver’ is a jargon-free diagnosis, easy to understand and easy for patients to know what they need to do,” the internist continued. “You think patients are gonna be educated when you tell them they have a ‘metabolic disease’? 100% they will not know what you’re talking about.”

Yet another wondered, “If SLD is the ‘umbrella’ term, why (are) MetALD and ALD not MetASLD and ASLD, respectively? Furthermore, efforts to ‘destigmatize’ terminology will inadvertently condemn cryptogenic SLD (CSLD) as the new ‘closet alcoholic.’ “

“Perhaps a subclassification, CSLD-HDIRDD (CSLD–Honest, Doc, I Really Don’t Drink),” the reader added.

“Everything about this is ridiculous,” a family physician wrote. “How long will it be until the experts change obesity to ‘gravitationally challenged’ as a diagnosis!”

“I was thinking of ‘circumferentially challenged,’” a reader in Canada chimed in. “But that would be ‘body shaming’ would it not?”

This reader continued, asking, “What about returning to the old practice of using Latin names patients don’t understand so there is no ‘shame’ attached to them? Or what about this revolutionary idea: To just say it as it is – fat?”
 

Acceding to ‘wokeness’

A sizable number of readers felt the name changes were motivated by a “woke” awareness.

“The effect of this new ‘woke’ clarity is ridiculous and simply not worth it! Can we justify the cost of this? Patients will have to learn all over again how to discuss their condition,” said one reader.

The reader continued, saying, “The Internet and social media freely use the term ‘fat’ – and despite not wanting to offend – there seems to be universal agreement that FAT, in certain conditions or places, is unhealthy and undesirable.

“Why is the medical community so afraid to tell it like it is? I might hurt your feelings, but I could save your life,” concluded the reader.
 

Defending change

One commentator, a hepatologist in France, defended the changes and responded to some of complaints.

“Maybe people who comment here should read the article, reflect, and understand the reasons why the old nomenclature and definition were scientifically inaccurate and needed to be changed,” the commentator wrote.

“It was an exclusionary, negative definition not recognizing the root of the disease (adipose tissue dysfunction with insulin resistance – instead defining it by what it is not ...) and not allowing the recognition of a large segment of the population [that] accumulates metabolic risk factors and moderate alcohol consumption. These patients were left out of all studies. Those were the main reasons for change and not the stigma part – with the word ‘fatty’ only being an issue in English-speaking countries, not elsewhere,” the commentator continued.

“Calls for change have been voiced for 20 years and a first comprehensive attempt (called MAFLD) was introduced 3 years ago (J Hepatol. 2020;73:202-9). Please, a little bit of respect and restraint in the comments recognizing the research efforts and publications for those that contributed to the field over the past 25 years ...” the hepatologist wrote.

The reader added, “Clinicians and researchers were dissatisfied for a long time, but it took years to gather overwhelming evidence demonstrating what causes the disease and then to kickstart a process under the auspices of several multinational scientific societies and come up with something consensually agreed upon by a large number of clinician researchers.

“Now you can tell your patient that he has metabolic liver disease instead of telling him that the problem at the root of his disease is that he is not drinking alcohol (nonalcoholic steatohepatitis). So, again, it is not so much about changing a name but about redefining diagnostic criteria and a nosological framework,” the reader wrote.

Other readers responded to the defender:

“This nomenclature issue has been churned for 20+ years? Well, the mountain has labored heavily, and given birth to a mouse,” one said.

“Still, how is this going to help in the clinical management? The whole gamut of conditions are evaluated and treated as a whole, not in isolation,” a general practitioner in India said. “If someone has a risk factor or not, continuous follow-up is required as a whole, whether it’s nonalcoholic or alcoholic, or whatever term is coined up.”

Finally, a family physician said, “It just rolls off the tongue, doesn’t it? But I have to admit, it’s the one place where ‘persons’ from 56 countries can get together and agree on something. Not even politicians can do that! Me, I’m sticking with NAFLD.”

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

Time-restricted eating (TRE) can be a practical, easy-to-follow way for some people to control their daily food intake and lose weight. It precludes a person’s need to pay close attention to how much they eat as long as they confine consumption to a limited time window. Plus, results from several recent studies show TRE can further benefit people with type 2 diabetes as well as obesity via mechanisms beyond weight loss.

The most tested and recommended eating window is 8 hours long, although periods up to roughly 10 hours may provide some benefits. Results from multiple studies document that TRE produces modest but consistent weight loss of less than 5% in many people. A recent meta-analysis of 17 randomized controlled studies involving 899 people showed an overall incremental weight loss, compared with controls of 1.60 kg on a TRE regimen.

The more limited data collected so far in people with type 2 diabetes show additional metabolic benefits from TRE, including improved beta-cell responsiveness, increased insulin sensitivity, nonoxidative glucose disposal, increased time in glycemic range, and virtually no hypoglycemic events, Courtney Peterson, PhD, said at the annual scientific sessions of the American Diabetes Association.

‘Eating earlier is better’

An advantage of TRE is that it is “agnostic to food preferences and quality,” said Lisa S. Chow, MD, during a separate session at the meeting. TRE “may have benefits beyond calorie restriction” that appear related to “the timing of eating and the extent of the eating window restriction. Eating earlier [in the day] is better” for markers of metabolic health regardless of how much weight a person may lose on a TRE regimen, noted Dr. Chow, an endocrinologist and professor at the University of Minnesota Medical School, Minneapolis.

But the TRE paradigm seems amenable to some flexibility on the timing for the eating window while still having benefit.

“Self-selected eating windows are usually late,” Dr. Chow observed, and because compliance with a constrained eating window matters, it may be worth allowing people to choose whichever time window for eating works best for them.

“If you let people pick their eating window, they typically include dinner,” said Dr. Chow, who has run a small TRE study that showed this.

“To maximize the effects [of TRE] people should use the eating window that best fits their life,” agreed Kelsey Gabel, PhD, who also gave a TRE talk during the meeting. “Eating most of your [daily] calories first thing in the morning would have the best cardiometabolic benefit, but reduced adherence would mitigate the benefit,” said Dr. Gabel, a nutrition researcher at the University of Illinois.
 

‘Meeting people where they’re at’

“We can have a larger public health impact by meeting people where they’re at. People should position their eating window where it best fits so they can achieve calorie restriction without even knowing it,” Dr. Gabel advised.

She cited a report as evidence that most people prefer a later eating window. The report reviewed observational data from nearly 800,000 people who used either of two different TRE phone apps. The data showed that most people opted to start their daily eating during 11:00 AM-1:00 PM, and then stop during 6:00 PM-8:00 PM.

“TRE will not solve all of our obesity problems, but it’s a good place to start,” Dr. Gabel declared.

For people who include dinner at a typical evening time in their TRE window, a key message is that “dinner is your last food of the day. There’s no snacking later,” said Dr. Chow.

“The biggest challenge is adherence,” said Dr. Peterson. “Fewer people want to do TRE than you think. We know that calorie restriction works. We just need a way for people to do it,” and for at least some people, TRE is that way. While no evidence clearly shows that 8 hours is the best eating-window duration, “we think 8 hours is a good sweet-spot for motivated people,” she said.
 

Sparser data on TRE in people with T2D

Fewer studies have examined the impact of TRE on glycemic control, insulin sensitivity, and related effects in people with type 2 diabetes. According to Dr. Peterson, published reports currently include two randomized controlled studies and three single-arm studies in people with type 2 diabetes and an additional two studies in people with prediabetes.

The largest of these reports randomized 120 adults in China with type 2 diabetes and overweight to TRE using a 10-hour eating window (8:00 AM-6:00 PM) or unrestricted eating for 12 weeks. By the end of the study, those on the TRE regimen had an average reduction in their hemoglobin A1c from baseline that was 0.88 percentage points greater than among the controls, and the TRE arm had also lost an average of nearly 2.15 kg more from baseline than the controls.

Dr. Peterson highlighted the importance of expanding research using TRE in people with type 2 diabetes.

Dr. Peterson and Dr. Gabel report no relevant financial relationships. Dr. Chow has received research support from Dexcom.

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

Time-restricted eating (TRE) can be a practical, easy-to-follow way for some people to control their daily food intake and lose weight. It precludes a person’s need to pay close attention to how much they eat as long as they confine consumption to a limited time window. Plus, results from several recent studies show TRE can further benefit people with type 2 diabetes as well as obesity via mechanisms beyond weight loss.

The most tested and recommended eating window is 8 hours long, although periods up to roughly 10 hours may provide some benefits. Results from multiple studies document that TRE produces modest but consistent weight loss of less than 5% in many people. A recent meta-analysis of 17 randomized controlled studies involving 899 people showed an overall incremental weight loss, compared with controls of 1.60 kg on a TRE regimen.

The more limited data collected so far in people with type 2 diabetes show additional metabolic benefits from TRE, including improved beta-cell responsiveness, increased insulin sensitivity, nonoxidative glucose disposal, increased time in glycemic range, and virtually no hypoglycemic events, Courtney Peterson, PhD, said at the annual scientific sessions of the American Diabetes Association.

‘Eating earlier is better’

An advantage of TRE is that it is “agnostic to food preferences and quality,” said Lisa S. Chow, MD, during a separate session at the meeting. TRE “may have benefits beyond calorie restriction” that appear related to “the timing of eating and the extent of the eating window restriction. Eating earlier [in the day] is better” for markers of metabolic health regardless of how much weight a person may lose on a TRE regimen, noted Dr. Chow, an endocrinologist and professor at the University of Minnesota Medical School, Minneapolis.

But the TRE paradigm seems amenable to some flexibility on the timing for the eating window while still having benefit.

“Self-selected eating windows are usually late,” Dr. Chow observed, and because compliance with a constrained eating window matters, it may be worth allowing people to choose whichever time window for eating works best for them.

“If you let people pick their eating window, they typically include dinner,” said Dr. Chow, who has run a small TRE study that showed this.

“To maximize the effects [of TRE] people should use the eating window that best fits their life,” agreed Kelsey Gabel, PhD, who also gave a TRE talk during the meeting. “Eating most of your [daily] calories first thing in the morning would have the best cardiometabolic benefit, but reduced adherence would mitigate the benefit,” said Dr. Gabel, a nutrition researcher at the University of Illinois.
 

‘Meeting people where they’re at’

“We can have a larger public health impact by meeting people where they’re at. People should position their eating window where it best fits so they can achieve calorie restriction without even knowing it,” Dr. Gabel advised.

She cited a report as evidence that most people prefer a later eating window. The report reviewed observational data from nearly 800,000 people who used either of two different TRE phone apps. The data showed that most people opted to start their daily eating during 11:00 AM-1:00 PM, and then stop during 6:00 PM-8:00 PM.

“TRE will not solve all of our obesity problems, but it’s a good place to start,” Dr. Gabel declared.

For people who include dinner at a typical evening time in their TRE window, a key message is that “dinner is your last food of the day. There’s no snacking later,” said Dr. Chow.

“The biggest challenge is adherence,” said Dr. Peterson. “Fewer people want to do TRE than you think. We know that calorie restriction works. We just need a way for people to do it,” and for at least some people, TRE is that way. While no evidence clearly shows that 8 hours is the best eating-window duration, “we think 8 hours is a good sweet-spot for motivated people,” she said.
 

Sparser data on TRE in people with T2D

Fewer studies have examined the impact of TRE on glycemic control, insulin sensitivity, and related effects in people with type 2 diabetes. According to Dr. Peterson, published reports currently include two randomized controlled studies and three single-arm studies in people with type 2 diabetes and an additional two studies in people with prediabetes.

The largest of these reports randomized 120 adults in China with type 2 diabetes and overweight to TRE using a 10-hour eating window (8:00 AM-6:00 PM) or unrestricted eating for 12 weeks. By the end of the study, those on the TRE regimen had an average reduction in their hemoglobin A1c from baseline that was 0.88 percentage points greater than among the controls, and the TRE arm had also lost an average of nearly 2.15 kg more from baseline than the controls.

Dr. Peterson highlighted the importance of expanding research using TRE in people with type 2 diabetes.

Dr. Peterson and Dr. Gabel report no relevant financial relationships. Dr. Chow has received research support from Dexcom.

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

Time-restricted eating (TRE) can be a practical, easy-to-follow way for some people to control their daily food intake and lose weight. It precludes a person’s need to pay close attention to how much they eat as long as they confine consumption to a limited time window. Plus, results from several recent studies show TRE can further benefit people with type 2 diabetes as well as obesity via mechanisms beyond weight loss.

The most tested and recommended eating window is 8 hours long, although periods up to roughly 10 hours may provide some benefits. Results from multiple studies document that TRE produces modest but consistent weight loss of less than 5% in many people. A recent meta-analysis of 17 randomized controlled studies involving 899 people showed an overall incremental weight loss, compared with controls of 1.60 kg on a TRE regimen.

The more limited data collected so far in people with type 2 diabetes show additional metabolic benefits from TRE, including improved beta-cell responsiveness, increased insulin sensitivity, nonoxidative glucose disposal, increased time in glycemic range, and virtually no hypoglycemic events, Courtney Peterson, PhD, said at the annual scientific sessions of the American Diabetes Association.

‘Eating earlier is better’

An advantage of TRE is that it is “agnostic to food preferences and quality,” said Lisa S. Chow, MD, during a separate session at the meeting. TRE “may have benefits beyond calorie restriction” that appear related to “the timing of eating and the extent of the eating window restriction. Eating earlier [in the day] is better” for markers of metabolic health regardless of how much weight a person may lose on a TRE regimen, noted Dr. Chow, an endocrinologist and professor at the University of Minnesota Medical School, Minneapolis.

But the TRE paradigm seems amenable to some flexibility on the timing for the eating window while still having benefit.

“Self-selected eating windows are usually late,” Dr. Chow observed, and because compliance with a constrained eating window matters, it may be worth allowing people to choose whichever time window for eating works best for them.

“If you let people pick their eating window, they typically include dinner,” said Dr. Chow, who has run a small TRE study that showed this.

“To maximize the effects [of TRE] people should use the eating window that best fits their life,” agreed Kelsey Gabel, PhD, who also gave a TRE talk during the meeting. “Eating most of your [daily] calories first thing in the morning would have the best cardiometabolic benefit, but reduced adherence would mitigate the benefit,” said Dr. Gabel, a nutrition researcher at the University of Illinois.
 

‘Meeting people where they’re at’

“We can have a larger public health impact by meeting people where they’re at. People should position their eating window where it best fits so they can achieve calorie restriction without even knowing it,” Dr. Gabel advised.

She cited a report as evidence that most people prefer a later eating window. The report reviewed observational data from nearly 800,000 people who used either of two different TRE phone apps. The data showed that most people opted to start their daily eating during 11:00 AM-1:00 PM, and then stop during 6:00 PM-8:00 PM.

“TRE will not solve all of our obesity problems, but it’s a good place to start,” Dr. Gabel declared.

For people who include dinner at a typical evening time in their TRE window, a key message is that “dinner is your last food of the day. There’s no snacking later,” said Dr. Chow.

“The biggest challenge is adherence,” said Dr. Peterson. “Fewer people want to do TRE than you think. We know that calorie restriction works. We just need a way for people to do it,” and for at least some people, TRE is that way. While no evidence clearly shows that 8 hours is the best eating-window duration, “we think 8 hours is a good sweet-spot for motivated people,” she said.
 

Sparser data on TRE in people with T2D

Fewer studies have examined the impact of TRE on glycemic control, insulin sensitivity, and related effects in people with type 2 diabetes. According to Dr. Peterson, published reports currently include two randomized controlled studies and three single-arm studies in people with type 2 diabetes and an additional two studies in people with prediabetes.

The largest of these reports randomized 120 adults in China with type 2 diabetes and overweight to TRE using a 10-hour eating window (8:00 AM-6:00 PM) or unrestricted eating for 12 weeks. By the end of the study, those on the TRE regimen had an average reduction in their hemoglobin A1c from baseline that was 0.88 percentage points greater than among the controls, and the TRE arm had also lost an average of nearly 2.15 kg more from baseline than the controls.

Dr. Peterson highlighted the importance of expanding research using TRE in people with type 2 diabetes.

Dr. Peterson and Dr. Gabel report no relevant financial relationships. Dr. Chow has received research support from Dexcom.

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

A new lawsuit from a woman with type 2 diabetes alleges that the makers of the drugs Ozempic and Mounjaro did not provide adequate warnings for the severity of stomach problems caused by the popular medicines.

The two drugs, which are Food and Drug Administration approved to treat type 2 diabetes, have become well known for their weight loss properties. Ozempic is made by Danish drug maker Novo Nordisk, and Mounjaro is made by Indiana-based Eli Lilly and Co.

In the lawsuit, Jaclyn Bjorklund, 44, of Louisiana, asserts that she was “severely injured” after using Ozempic and Mounjaro and that the pharmaceutical companies failed to disclose the drugs’ risk of causing vomiting and diarrhea due to inflammation of the stomach lining, as well as the risk of gastroparesis.

The prescribing labels for Mounjaro and Ozempic state that each “delays gastric emptying” and warn of the risk of severe gastrointestinal adverse reactions. The prescribing labels for both drugs state that the most common side effects include vomiting, diarrhea, and stomach pain. The Ozempic label does not mention gastroparesis, and the Mounjaro label states that the drug has not been studied in people with the condition and is therefore not recommended for people who have it. 

Ms. Bjorklund has not been diagnosed with gastroparesis, but her symptoms are “indicative of” the condition, her lawyer, Paul Pennock, told NBC News.

Ms. Bjorklund used Ozempic for more than 1 year, and in July 2023 switched to Mounjaro, the lawsuit states. The document, posted on her law firm’s website, details that using the drugs resulted in “severe vomiting, stomach pain, gastrointestinal burning, being hospitalized for stomach issues on several occasions including visits to the emergency room, [and] teeth falling out due to excessive vomiting, requiring additional medications to alleviate her excessive vomiting, and throwing up whole food hours after eating.”

Novo Nordisk spokesperson Natalia Salomao told NBC News that patient safety is “of utmost importance to Novo Nordisk,” and she also noted that gastroparesis is a known risk for people with diabetes. The Food and Drug Administration declined to comment on the case, and Eli Lilly did not immediately respond to a request for comment, NBC News reported.
 

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

A new lawsuit from a woman with type 2 diabetes alleges that the makers of the drugs Ozempic and Mounjaro did not provide adequate warnings for the severity of stomach problems caused by the popular medicines.

The two drugs, which are Food and Drug Administration approved to treat type 2 diabetes, have become well known for their weight loss properties. Ozempic is made by Danish drug maker Novo Nordisk, and Mounjaro is made by Indiana-based Eli Lilly and Co.

In the lawsuit, Jaclyn Bjorklund, 44, of Louisiana, asserts that she was “severely injured” after using Ozempic and Mounjaro and that the pharmaceutical companies failed to disclose the drugs’ risk of causing vomiting and diarrhea due to inflammation of the stomach lining, as well as the risk of gastroparesis.

The prescribing labels for Mounjaro and Ozempic state that each “delays gastric emptying” and warn of the risk of severe gastrointestinal adverse reactions. The prescribing labels for both drugs state that the most common side effects include vomiting, diarrhea, and stomach pain. The Ozempic label does not mention gastroparesis, and the Mounjaro label states that the drug has not been studied in people with the condition and is therefore not recommended for people who have it. 

Ms. Bjorklund has not been diagnosed with gastroparesis, but her symptoms are “indicative of” the condition, her lawyer, Paul Pennock, told NBC News.

Ms. Bjorklund used Ozempic for more than 1 year, and in July 2023 switched to Mounjaro, the lawsuit states. The document, posted on her law firm’s website, details that using the drugs resulted in “severe vomiting, stomach pain, gastrointestinal burning, being hospitalized for stomach issues on several occasions including visits to the emergency room, [and] teeth falling out due to excessive vomiting, requiring additional medications to alleviate her excessive vomiting, and throwing up whole food hours after eating.”

Novo Nordisk spokesperson Natalia Salomao told NBC News that patient safety is “of utmost importance to Novo Nordisk,” and she also noted that gastroparesis is a known risk for people with diabetes. The Food and Drug Administration declined to comment on the case, and Eli Lilly did not immediately respond to a request for comment, NBC News reported.
 

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

A new lawsuit from a woman with type 2 diabetes alleges that the makers of the drugs Ozempic and Mounjaro did not provide adequate warnings for the severity of stomach problems caused by the popular medicines.

The two drugs, which are Food and Drug Administration approved to treat type 2 diabetes, have become well known for their weight loss properties. Ozempic is made by Danish drug maker Novo Nordisk, and Mounjaro is made by Indiana-based Eli Lilly and Co.

In the lawsuit, Jaclyn Bjorklund, 44, of Louisiana, asserts that she was “severely injured” after using Ozempic and Mounjaro and that the pharmaceutical companies failed to disclose the drugs’ risk of causing vomiting and diarrhea due to inflammation of the stomach lining, as well as the risk of gastroparesis.

The prescribing labels for Mounjaro and Ozempic state that each “delays gastric emptying” and warn of the risk of severe gastrointestinal adverse reactions. The prescribing labels for both drugs state that the most common side effects include vomiting, diarrhea, and stomach pain. The Ozempic label does not mention gastroparesis, and the Mounjaro label states that the drug has not been studied in people with the condition and is therefore not recommended for people who have it. 

Ms. Bjorklund has not been diagnosed with gastroparesis, but her symptoms are “indicative of” the condition, her lawyer, Paul Pennock, told NBC News.

Ms. Bjorklund used Ozempic for more than 1 year, and in July 2023 switched to Mounjaro, the lawsuit states. The document, posted on her law firm’s website, details that using the drugs resulted in “severe vomiting, stomach pain, gastrointestinal burning, being hospitalized for stomach issues on several occasions including visits to the emergency room, [and] teeth falling out due to excessive vomiting, requiring additional medications to alleviate her excessive vomiting, and throwing up whole food hours after eating.”

Novo Nordisk spokesperson Natalia Salomao told NBC News that patient safety is “of utmost importance to Novo Nordisk,” and she also noted that gastroparesis is a known risk for people with diabetes. The Food and Drug Administration declined to comment on the case, and Eli Lilly did not immediately respond to a request for comment, NBC News reported.
 

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

Consuming a higher percentage of calories from added sugars is linked with a higher prevalence of kidney stones, new research suggests.

Though added sugars have been linked with multiple poor health outcomes, their link with kidney stones has been unclear.

Added sugars are sugars or caloric sweeteners added to foods or drinks during processing or preparation to add flavor or shelf life. They do not include natural sugars such as lactose in milk and fructose in fruits.

Researchers, led by Shan Yin, a urologist at Affiliated Hospital of North Sichuan Medical College, in Nanchong, China, compared the added-sugar intake by quartiles in the U.S. National Health and Nutrition Examination Survey 2007-2018.

A total of 28,303 adults were included in this study, with an average age of 48. Women who consumed less than 600 or more than 3,500 kcal or men who consumed less than 800 or more than 4,200 kcal were excluded.

Researchers adjusted for factors including age, race, education, income, physical activity, and marital, employment, and smoking status.

Compared with the first quartile of percentage added-sugar calorie intake, the population in the fourth quartile, with the highest added sugar intake, had a higher prevalence of kidney stones (odds ratio, 1.39; 95% confidence interval, 1.17-1.65).

Compared with the group with fewer than 5% of calories from added sugar, the group that consumed at least 25% of calories from added sugar had nearly twice the prevalence of kidney stones (OR, 1.88; 95% CI, 1.52-2.32).

Findings were published online in Frontiers in Nutrition.

“By identifying this association, policymakers and health professionals can emphasize the need for public health initiatives to reduce added sugar consumption and promote healthy dietary habits,” the authors write.
 

Added sugar in the U.S. diet

Sugar-sweetened beverages such as soft drinks and energy and sports drinks account for 34.4% of added sugars in the American diet. Previous studies have shown the relationship between consuming sugar-sweetened beverages and a higher risk of obesity, diabetes, and cardiovascular disease, diseases that often co-occur with kidney stones.

Researchers note that even though most added sugars in the United States come from sugar-sweetened beverages, it’s unclear whether the association between added sugars and kidney stones is caused by the beverages or other sources. For instance, fructose intake has been found to be independently associated with kidney stones.

How much is too much?

The recommended upper limit on added sugar is controversial and varies widely by health organization. The American Heart Association says daily average intake from added sugars should be no more than 150 kcal for adult males (about 9 teaspoons) and no more than 100 kcal for women (about 6 teaspoons). The Institute of Medicine allows up to 25% of calories to be consumed from added sugars. The 2020 Dietary Guidelines for Americans and World Health Organization set 10% of calories as the recommended upper limit.

Further investigating what causes kidney stones is critical as kidney stones are common worldwide, affecting about 1 in 10 people in the United States alone, and occurrence is increasing. Kidney stones have a high recurrence rate – about half of people who get them have a second episode within 10 years, the authors note.

The researchers acknowledge that because participants self-reported food intake, there is the potential for recall bias. Additionally, because of the cross-sectional design, the researchers were not able to determine whether sugar intake or kidney stone occurrence came first.

This work was supported by the Doctoral Fund Project of North Sichuan Medical College. The authors declare no relevant financial relationships.

Consuming a higher percentage of calories from added sugars is linked with a higher prevalence of kidney stones, new research suggests.

Though added sugars have been linked with multiple poor health outcomes, their link with kidney stones has been unclear.

Added sugars are sugars or caloric sweeteners added to foods or drinks during processing or preparation to add flavor or shelf life. They do not include natural sugars such as lactose in milk and fructose in fruits.

Researchers, led by Shan Yin, a urologist at Affiliated Hospital of North Sichuan Medical College, in Nanchong, China, compared the added-sugar intake by quartiles in the U.S. National Health and Nutrition Examination Survey 2007-2018.

A total of 28,303 adults were included in this study, with an average age of 48. Women who consumed less than 600 or more than 3,500 kcal or men who consumed less than 800 or more than 4,200 kcal were excluded.

Researchers adjusted for factors including age, race, education, income, physical activity, and marital, employment, and smoking status.

Compared with the first quartile of percentage added-sugar calorie intake, the population in the fourth quartile, with the highest added sugar intake, had a higher prevalence of kidney stones (odds ratio, 1.39; 95% confidence interval, 1.17-1.65).

Compared with the group with fewer than 5% of calories from added sugar, the group that consumed at least 25% of calories from added sugar had nearly twice the prevalence of kidney stones (OR, 1.88; 95% CI, 1.52-2.32).

Findings were published online in Frontiers in Nutrition.

“By identifying this association, policymakers and health professionals can emphasize the need for public health initiatives to reduce added sugar consumption and promote healthy dietary habits,” the authors write.
 

Added sugar in the U.S. diet

Sugar-sweetened beverages such as soft drinks and energy and sports drinks account for 34.4% of added sugars in the American diet. Previous studies have shown the relationship between consuming sugar-sweetened beverages and a higher risk of obesity, diabetes, and cardiovascular disease, diseases that often co-occur with kidney stones.

Researchers note that even though most added sugars in the United States come from sugar-sweetened beverages, it’s unclear whether the association between added sugars and kidney stones is caused by the beverages or other sources. For instance, fructose intake has been found to be independently associated with kidney stones.

How much is too much?

The recommended upper limit on added sugar is controversial and varies widely by health organization. The American Heart Association says daily average intake from added sugars should be no more than 150 kcal for adult males (about 9 teaspoons) and no more than 100 kcal for women (about 6 teaspoons). The Institute of Medicine allows up to 25% of calories to be consumed from added sugars. The 2020 Dietary Guidelines for Americans and World Health Organization set 10% of calories as the recommended upper limit.

Further investigating what causes kidney stones is critical as kidney stones are common worldwide, affecting about 1 in 10 people in the United States alone, and occurrence is increasing. Kidney stones have a high recurrence rate – about half of people who get them have a second episode within 10 years, the authors note.

The researchers acknowledge that because participants self-reported food intake, there is the potential for recall bias. Additionally, because of the cross-sectional design, the researchers were not able to determine whether sugar intake or kidney stone occurrence came first.

This work was supported by the Doctoral Fund Project of North Sichuan Medical College. The authors declare no relevant financial relationships.

Consuming a higher percentage of calories from added sugars is linked with a higher prevalence of kidney stones, new research suggests.

Though added sugars have been linked with multiple poor health outcomes, their link with kidney stones has been unclear.

Added sugars are sugars or caloric sweeteners added to foods or drinks during processing or preparation to add flavor or shelf life. They do not include natural sugars such as lactose in milk and fructose in fruits.

Researchers, led by Shan Yin, a urologist at Affiliated Hospital of North Sichuan Medical College, in Nanchong, China, compared the added-sugar intake by quartiles in the U.S. National Health and Nutrition Examination Survey 2007-2018.

A total of 28,303 adults were included in this study, with an average age of 48. Women who consumed less than 600 or more than 3,500 kcal or men who consumed less than 800 or more than 4,200 kcal were excluded.

Researchers adjusted for factors including age, race, education, income, physical activity, and marital, employment, and smoking status.

Compared with the first quartile of percentage added-sugar calorie intake, the population in the fourth quartile, with the highest added sugar intake, had a higher prevalence of kidney stones (odds ratio, 1.39; 95% confidence interval, 1.17-1.65).

Compared with the group with fewer than 5% of calories from added sugar, the group that consumed at least 25% of calories from added sugar had nearly twice the prevalence of kidney stones (OR, 1.88; 95% CI, 1.52-2.32).

Findings were published online in Frontiers in Nutrition.

“By identifying this association, policymakers and health professionals can emphasize the need for public health initiatives to reduce added sugar consumption and promote healthy dietary habits,” the authors write.
 

Added sugar in the U.S. diet

Sugar-sweetened beverages such as soft drinks and energy and sports drinks account for 34.4% of added sugars in the American diet. Previous studies have shown the relationship between consuming sugar-sweetened beverages and a higher risk of obesity, diabetes, and cardiovascular disease, diseases that often co-occur with kidney stones.

Researchers note that even though most added sugars in the United States come from sugar-sweetened beverages, it’s unclear whether the association between added sugars and kidney stones is caused by the beverages or other sources. For instance, fructose intake has been found to be independently associated with kidney stones.

How much is too much?

The recommended upper limit on added sugar is controversial and varies widely by health organization. The American Heart Association says daily average intake from added sugars should be no more than 150 kcal for adult males (about 9 teaspoons) and no more than 100 kcal for women (about 6 teaspoons). The Institute of Medicine allows up to 25% of calories to be consumed from added sugars. The 2020 Dietary Guidelines for Americans and World Health Organization set 10% of calories as the recommended upper limit.

Further investigating what causes kidney stones is critical as kidney stones are common worldwide, affecting about 1 in 10 people in the United States alone, and occurrence is increasing. Kidney stones have a high recurrence rate – about half of people who get them have a second episode within 10 years, the authors note.

The researchers acknowledge that because participants self-reported food intake, there is the potential for recall bias. Additionally, because of the cross-sectional design, the researchers were not able to determine whether sugar intake or kidney stone occurrence came first.

This work was supported by the Doctoral Fund Project of North Sichuan Medical College. The authors declare no relevant financial relationships.

Ashley Raibick is familiar with the weight loss yo-yo. She’s bounced through the big names: Weight Watchers, Jenny Craig, and so on. She drops 10 pounds and then slides off the plan only to see her weight pop back up.

But a day at her local med spa – where she gets facials, Botox, and fillers – changed all that for the 28-year-old hairstylist who just wanted to lose 18 pounds.

During one of her visits, she noticed that the spa’s owner was thinner. When Ms. Raibick asked her how she did it, the owner explained that she was on semaglutide and talked Ms. Raibick through the process. Ms. Raibick was convinced. That same day, she got a prescription from a doctor at the spa and got her first shot.

“Are people going to think I’m crazy for doing this?” she recalls thinking.

At 5 foot 4, her starting weight before the drug was 158, which would put her in the overweight, but not obese, category based on body mass index (BMI). And she really just wanted to get down to 140 and stop there.

Ozempic is part of an ever-growing group of GLP-1 receptor agonists that contain a peptide called semaglutide as its main ingredient. Although first meant to treat type 2 diabetes, the reputation of Ozempic and its siblings picked up when already-thin celebrities were suspected of using the injectable drugs to become even slimmer.

The FDA approved Ozempic’s cousin, Wegovy, for “weight management” in patients with obesity a few years ago, whereas Ozempic is currently approved only for diabetes treatment. Curious patients who don’t fit the criteria can – and do – get off-label prescriptions if they can afford to pay out of pocket, often to the tune of more than $1,400 a month. But is Ozempic worth it, especially if one has a relatively minor amount of weight to lose?

For many – mainly those who have been on the drug for a couple of months and have lost weight as a result – taking Ozempic has not only helped them shed stubborn weight, but has also freed them from the constant internal chatter around eating, commonly called “food noise.” But experts do not all agree that semaglutide is the right path for those who aren’t technically obese – especially in the long term.

After her first 9 weeks on semaglutide, Ms. Raibick had already lost 18 pounds. That’s when she decided to post about it on TikTok, and her videos on GLP-1s were viewed hundreds of thousands of times.

For the time being, there is no data on how many semaglutide takers are using the drug for diabetes and/or obesity, and how many are using it off-label for weight loss alone. But the company that makes Ozempic, Novo Nordisk, has reported sharp increases in sales and projects more profits down the road.

Ms. Raibick knows of others like her, who sought out the drug for more minor weight loss but aren’t as candid about their journeys. Some feel a stigma about having to resort to a weight-loss drug intended to treat obesity, rather than achieving their goals with diet and lifestyle change alone.

Another reason for the secrecy is the guilt some who take Ozempic feel about using their financial privilege to get a drug that had serious shortages, which made it harder for some patients who need the drug for diabetes or obesity treatment to get their doses.

That’s what Diana Thiara, MD, the medical director of the University of California, San Francisco’s weight management program, has been seeing on the ground.

“It’s one of the most depressing things I’ve experienced as a physician,” she said. In her practice, she has seen patients who have finally been able to access GLP-1s and have started to lose weight, only for them to regain the weight in the time it takes to find another prescription under their insurance coverage.

“It’s just horrible, there are patients spending all day calling dozens of pharmacies. I’ve never had a situation like this in my career,” said Dr. Thiara.

Ann, 48, a mom who works from home full-time, has been taking Ozempic since the end of January. (Ann is not her real name; she asked that we use a pseudonym in order to feel comfortable speaking publicly about her use of Ozempic). Like Ms. Raibick, she has been paying out of pocket for her shots. At first, she was going to have to pay $1,400 a month, but she found a pharmacy in Canada that offers the medication for $350. It’s sourced globally, she said, so sometimes her Ozempic boxes will be in Czech or another foreign language.

Unlike a lot of women, Ann never had any qualms with her weight or the way her body looked. She was never big on exercise, but it wasn’t until the pandemic that she started to gain weight. She noticed the changes in her body once places started opening back up, and her clothes didn’t fit anymore.

She tried moving more and eating healthier. She tried former Real Housewives of Beverly Hills cast member Teddi Mellencamp’s controversial weight-loss program, infamous for its incredibly restrictive dietary plan and excessive cardio recommendations. Nothing worked until another mom at her daughter’s school mentioned that she was on Ozempic.

Ann also started to get hot flashes and missed periods. The doctor who prescribed her Ozempic confirmed that she was perimenopausal and that, for women in this stage of life, losing weight can be harder than ever.

Ann, who is 5 foot 7, started out at 176 pounds (considered overweight) and now weighs in at 151, which is considered a normal weight by BMI measurements. She’s still on Ozempic but continues to struggle with the shame around the idea she’s potentially taking the drug away from someone else who might desperately need it. And she doesn’t know how long she’ll have to stay on Ozempic to maintain her weight loss.

Ann has reason for concern. A 2022 study found that most people regain the weight they lost within a year of stopping Ozempic.

Once Ms. Raibick hit her initial goal weight, she felt that she could keep going and lose a little more. It wasn’t until she got into the 120-pound range that she decided it was time to wean off the dose of semaglutide she had been taking.

“I got to the point where my mom was like, ‘All right, you’re a little too thin.’ But I’m just so happy where I’m at. I’m not mentally stressed out about fitting into clothes or getting into a bathing suit,” said Ms. Raibick, who has now lost around 30 pounds in total since she started the shots.

At one point, she stopped taking the drug altogether, and all of the hunger cravings and food noise semaglutide had suppressed came back to the surface. She didn’t gain any weight that month, she said, but the internal chatter around food was enough to make her start back on a lower dose, geared toward weight maintenance.

There’s also the issue of side effects. Ms. Raibick says she never had the overwhelming nausea and digestive problems that so many on the drug – including Ann – have reported. But Dr. Thiara said that even beyond these more common side effects, there are a number of other concerns – like the long-lasting effects on thyroid and reproductive health, especially for women – that we still don’t know enough about. And just recently, CNN reported that some Ozempic users have developed stomach paralysis due to the drug’s ability to slow down the passage of food through the digestive tract.

For Ms. Raibick, the out-of-pocket cost for the drug is around $600 a month. It’s an expense she’s willing to keep paying for, even just for the peace of mind the drug provides. She doesn’t have any plans to stop her semaglutide shots soon.

“There is nothing stopping me from – a year from now, when I’ve put a little weight back on – looking back at photos from this time and thinking I was way too skinny.”

Dan Azagury, MD, a bariatric surgeon and associate professor of surgery at Stanford (Calif.) University, tries GLP-1s for patients with obesity before considering bariatric surgery. For his patient population, it’s possible that drugs like Ozempic will be part of their lifelong treatment plans.

“We’re not doing it for the cosmetic part of it, we’re doing it for health,” he said. “What I tell my patients is, if you’re planning to start on this medication, you should be OK with the idea of staying on it forever.”

For doctors like Dr. Thiara who specialize in weight management, using Ozempic long-term for patients in a healthy weight range is the wrong approach.

“It’s not about the way people look, it’s about health. If you’re a normal weight or even in an overweight category, but not showing signs of risk of having elevated cardiometabolic disease ... You don’t need to be taking medications for weight loss,” she said. “This idea of using medications for aesthetic reasons is really more related to societal ills around how we value fitness above anything else. That’s not the goal, and it’s not safe.”

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

Ashley Raibick is familiar with the weight loss yo-yo. She’s bounced through the big names: Weight Watchers, Jenny Craig, and so on. She drops 10 pounds and then slides off the plan only to see her weight pop back up.

But a day at her local med spa – where she gets facials, Botox, and fillers – changed all that for the 28-year-old hairstylist who just wanted to lose 18 pounds.

During one of her visits, she noticed that the spa’s owner was thinner. When Ms. Raibick asked her how she did it, the owner explained that she was on semaglutide and talked Ms. Raibick through the process. Ms. Raibick was convinced. That same day, she got a prescription from a doctor at the spa and got her first shot.

“Are people going to think I’m crazy for doing this?” she recalls thinking.

At 5 foot 4, her starting weight before the drug was 158, which would put her in the overweight, but not obese, category based on body mass index (BMI). And she really just wanted to get down to 140 and stop there.

Ozempic is part of an ever-growing group of GLP-1 receptor agonists that contain a peptide called semaglutide as its main ingredient. Although first meant to treat type 2 diabetes, the reputation of Ozempic and its siblings picked up when already-thin celebrities were suspected of using the injectable drugs to become even slimmer.

The FDA approved Ozempic’s cousin, Wegovy, for “weight management” in patients with obesity a few years ago, whereas Ozempic is currently approved only for diabetes treatment. Curious patients who don’t fit the criteria can – and do – get off-label prescriptions if they can afford to pay out of pocket, often to the tune of more than $1,400 a month. But is Ozempic worth it, especially if one has a relatively minor amount of weight to lose?

For many – mainly those who have been on the drug for a couple of months and have lost weight as a result – taking Ozempic has not only helped them shed stubborn weight, but has also freed them from the constant internal chatter around eating, commonly called “food noise.” But experts do not all agree that semaglutide is the right path for those who aren’t technically obese – especially in the long term.

After her first 9 weeks on semaglutide, Ms. Raibick had already lost 18 pounds. That’s when she decided to post about it on TikTok, and her videos on GLP-1s were viewed hundreds of thousands of times.

For the time being, there is no data on how many semaglutide takers are using the drug for diabetes and/or obesity, and how many are using it off-label for weight loss alone. But the company that makes Ozempic, Novo Nordisk, has reported sharp increases in sales and projects more profits down the road.

Ms. Raibick knows of others like her, who sought out the drug for more minor weight loss but aren’t as candid about their journeys. Some feel a stigma about having to resort to a weight-loss drug intended to treat obesity, rather than achieving their goals with diet and lifestyle change alone.

Another reason for the secrecy is the guilt some who take Ozempic feel about using their financial privilege to get a drug that had serious shortages, which made it harder for some patients who need the drug for diabetes or obesity treatment to get their doses.

That’s what Diana Thiara, MD, the medical director of the University of California, San Francisco’s weight management program, has been seeing on the ground.

“It’s one of the most depressing things I’ve experienced as a physician,” she said. In her practice, she has seen patients who have finally been able to access GLP-1s and have started to lose weight, only for them to regain the weight in the time it takes to find another prescription under their insurance coverage.

“It’s just horrible, there are patients spending all day calling dozens of pharmacies. I’ve never had a situation like this in my career,” said Dr. Thiara.

Ann, 48, a mom who works from home full-time, has been taking Ozempic since the end of January. (Ann is not her real name; she asked that we use a pseudonym in order to feel comfortable speaking publicly about her use of Ozempic). Like Ms. Raibick, she has been paying out of pocket for her shots. At first, she was going to have to pay $1,400 a month, but she found a pharmacy in Canada that offers the medication for $350. It’s sourced globally, she said, so sometimes her Ozempic boxes will be in Czech or another foreign language.

Unlike a lot of women, Ann never had any qualms with her weight or the way her body looked. She was never big on exercise, but it wasn’t until the pandemic that she started to gain weight. She noticed the changes in her body once places started opening back up, and her clothes didn’t fit anymore.

She tried moving more and eating healthier. She tried former Real Housewives of Beverly Hills cast member Teddi Mellencamp’s controversial weight-loss program, infamous for its incredibly restrictive dietary plan and excessive cardio recommendations. Nothing worked until another mom at her daughter’s school mentioned that she was on Ozempic.

Ann also started to get hot flashes and missed periods. The doctor who prescribed her Ozempic confirmed that she was perimenopausal and that, for women in this stage of life, losing weight can be harder than ever.

Ann, who is 5 foot 7, started out at 176 pounds (considered overweight) and now weighs in at 151, which is considered a normal weight by BMI measurements. She’s still on Ozempic but continues to struggle with the shame around the idea she’s potentially taking the drug away from someone else who might desperately need it. And she doesn’t know how long she’ll have to stay on Ozempic to maintain her weight loss.

Ann has reason for concern. A 2022 study found that most people regain the weight they lost within a year of stopping Ozempic.

Once Ms. Raibick hit her initial goal weight, she felt that she could keep going and lose a little more. It wasn’t until she got into the 120-pound range that she decided it was time to wean off the dose of semaglutide she had been taking.

“I got to the point where my mom was like, ‘All right, you’re a little too thin.’ But I’m just so happy where I’m at. I’m not mentally stressed out about fitting into clothes or getting into a bathing suit,” said Ms. Raibick, who has now lost around 30 pounds in total since she started the shots.

At one point, she stopped taking the drug altogether, and all of the hunger cravings and food noise semaglutide had suppressed came back to the surface. She didn’t gain any weight that month, she said, but the internal chatter around food was enough to make her start back on a lower dose, geared toward weight maintenance.

There’s also the issue of side effects. Ms. Raibick says she never had the overwhelming nausea and digestive problems that so many on the drug – including Ann – have reported. But Dr. Thiara said that even beyond these more common side effects, there are a number of other concerns – like the long-lasting effects on thyroid and reproductive health, especially for women – that we still don’t know enough about. And just recently, CNN reported that some Ozempic users have developed stomach paralysis due to the drug’s ability to slow down the passage of food through the digestive tract.

For Ms. Raibick, the out-of-pocket cost for the drug is around $600 a month. It’s an expense she’s willing to keep paying for, even just for the peace of mind the drug provides. She doesn’t have any plans to stop her semaglutide shots soon.

“There is nothing stopping me from – a year from now, when I’ve put a little weight back on – looking back at photos from this time and thinking I was way too skinny.”

Dan Azagury, MD, a bariatric surgeon and associate professor of surgery at Stanford (Calif.) University, tries GLP-1s for patients with obesity before considering bariatric surgery. For his patient population, it’s possible that drugs like Ozempic will be part of their lifelong treatment plans.

“We’re not doing it for the cosmetic part of it, we’re doing it for health,” he said. “What I tell my patients is, if you’re planning to start on this medication, you should be OK with the idea of staying on it forever.”

For doctors like Dr. Thiara who specialize in weight management, using Ozempic long-term for patients in a healthy weight range is the wrong approach.

“It’s not about the way people look, it’s about health. If you’re a normal weight or even in an overweight category, but not showing signs of risk of having elevated cardiometabolic disease ... You don’t need to be taking medications for weight loss,” she said. “This idea of using medications for aesthetic reasons is really more related to societal ills around how we value fitness above anything else. That’s not the goal, and it’s not safe.”

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

Ashley Raibick is familiar with the weight loss yo-yo. She’s bounced through the big names: Weight Watchers, Jenny Craig, and so on. She drops 10 pounds and then slides off the plan only to see her weight pop back up.

But a day at her local med spa – where she gets facials, Botox, and fillers – changed all that for the 28-year-old hairstylist who just wanted to lose 18 pounds.

During one of her visits, she noticed that the spa’s owner was thinner. When Ms. Raibick asked her how she did it, the owner explained that she was on semaglutide and talked Ms. Raibick through the process. Ms. Raibick was convinced. That same day, she got a prescription from a doctor at the spa and got her first shot.

“Are people going to think I’m crazy for doing this?” she recalls thinking.

At 5 foot 4, her starting weight before the drug was 158, which would put her in the overweight, but not obese, category based on body mass index (BMI). And she really just wanted to get down to 140 and stop there.

Ozempic is part of an ever-growing group of GLP-1 receptor agonists that contain a peptide called semaglutide as its main ingredient. Although first meant to treat type 2 diabetes, the reputation of Ozempic and its siblings picked up when already-thin celebrities were suspected of using the injectable drugs to become even slimmer.

The FDA approved Ozempic’s cousin, Wegovy, for “weight management” in patients with obesity a few years ago, whereas Ozempic is currently approved only for diabetes treatment. Curious patients who don’t fit the criteria can – and do – get off-label prescriptions if they can afford to pay out of pocket, often to the tune of more than $1,400 a month. But is Ozempic worth it, especially if one has a relatively minor amount of weight to lose?

For many – mainly those who have been on the drug for a couple of months and have lost weight as a result – taking Ozempic has not only helped them shed stubborn weight, but has also freed them from the constant internal chatter around eating, commonly called “food noise.” But experts do not all agree that semaglutide is the right path for those who aren’t technically obese – especially in the long term.

After her first 9 weeks on semaglutide, Ms. Raibick had already lost 18 pounds. That’s when she decided to post about it on TikTok, and her videos on GLP-1s were viewed hundreds of thousands of times.

For the time being, there is no data on how many semaglutide takers are using the drug for diabetes and/or obesity, and how many are using it off-label for weight loss alone. But the company that makes Ozempic, Novo Nordisk, has reported sharp increases in sales and projects more profits down the road.

Ms. Raibick knows of others like her, who sought out the drug for more minor weight loss but aren’t as candid about their journeys. Some feel a stigma about having to resort to a weight-loss drug intended to treat obesity, rather than achieving their goals with diet and lifestyle change alone.

Another reason for the secrecy is the guilt some who take Ozempic feel about using their financial privilege to get a drug that had serious shortages, which made it harder for some patients who need the drug for diabetes or obesity treatment to get their doses.

That’s what Diana Thiara, MD, the medical director of the University of California, San Francisco’s weight management program, has been seeing on the ground.

“It’s one of the most depressing things I’ve experienced as a physician,” she said. In her practice, she has seen patients who have finally been able to access GLP-1s and have started to lose weight, only for them to regain the weight in the time it takes to find another prescription under their insurance coverage.

“It’s just horrible, there are patients spending all day calling dozens of pharmacies. I’ve never had a situation like this in my career,” said Dr. Thiara.

Ann, 48, a mom who works from home full-time, has been taking Ozempic since the end of January. (Ann is not her real name; she asked that we use a pseudonym in order to feel comfortable speaking publicly about her use of Ozempic). Like Ms. Raibick, she has been paying out of pocket for her shots. At first, she was going to have to pay $1,400 a month, but she found a pharmacy in Canada that offers the medication for $350. It’s sourced globally, she said, so sometimes her Ozempic boxes will be in Czech or another foreign language.

Unlike a lot of women, Ann never had any qualms with her weight or the way her body looked. She was never big on exercise, but it wasn’t until the pandemic that she started to gain weight. She noticed the changes in her body once places started opening back up, and her clothes didn’t fit anymore.

She tried moving more and eating healthier. She tried former Real Housewives of Beverly Hills cast member Teddi Mellencamp’s controversial weight-loss program, infamous for its incredibly restrictive dietary plan and excessive cardio recommendations. Nothing worked until another mom at her daughter’s school mentioned that she was on Ozempic.

Ann also started to get hot flashes and missed periods. The doctor who prescribed her Ozempic confirmed that she was perimenopausal and that, for women in this stage of life, losing weight can be harder than ever.

Ann, who is 5 foot 7, started out at 176 pounds (considered overweight) and now weighs in at 151, which is considered a normal weight by BMI measurements. She’s still on Ozempic but continues to struggle with the shame around the idea she’s potentially taking the drug away from someone else who might desperately need it. And she doesn’t know how long she’ll have to stay on Ozempic to maintain her weight loss.

Ann has reason for concern. A 2022 study found that most people regain the weight they lost within a year of stopping Ozempic.

Once Ms. Raibick hit her initial goal weight, she felt that she could keep going and lose a little more. It wasn’t until she got into the 120-pound range that she decided it was time to wean off the dose of semaglutide she had been taking.

“I got to the point where my mom was like, ‘All right, you’re a little too thin.’ But I’m just so happy where I’m at. I’m not mentally stressed out about fitting into clothes or getting into a bathing suit,” said Ms. Raibick, who has now lost around 30 pounds in total since she started the shots.

At one point, she stopped taking the drug altogether, and all of the hunger cravings and food noise semaglutide had suppressed came back to the surface. She didn’t gain any weight that month, she said, but the internal chatter around food was enough to make her start back on a lower dose, geared toward weight maintenance.

There’s also the issue of side effects. Ms. Raibick says she never had the overwhelming nausea and digestive problems that so many on the drug – including Ann – have reported. But Dr. Thiara said that even beyond these more common side effects, there are a number of other concerns – like the long-lasting effects on thyroid and reproductive health, especially for women – that we still don’t know enough about. And just recently, CNN reported that some Ozempic users have developed stomach paralysis due to the drug’s ability to slow down the passage of food through the digestive tract.

For Ms. Raibick, the out-of-pocket cost for the drug is around $600 a month. It’s an expense she’s willing to keep paying for, even just for the peace of mind the drug provides. She doesn’t have any plans to stop her semaglutide shots soon.

“There is nothing stopping me from – a year from now, when I’ve put a little weight back on – looking back at photos from this time and thinking I was way too skinny.”

Dan Azagury, MD, a bariatric surgeon and associate professor of surgery at Stanford (Calif.) University, tries GLP-1s for patients with obesity before considering bariatric surgery. For his patient population, it’s possible that drugs like Ozempic will be part of their lifelong treatment plans.

“We’re not doing it for the cosmetic part of it, we’re doing it for health,” he said. “What I tell my patients is, if you’re planning to start on this medication, you should be OK with the idea of staying on it forever.”

For doctors like Dr. Thiara who specialize in weight management, using Ozempic long-term for patients in a healthy weight range is the wrong approach.

“It’s not about the way people look, it’s about health. If you’re a normal weight or even in an overweight category, but not showing signs of risk of having elevated cardiometabolic disease ... You don’t need to be taking medications for weight loss,” she said. “This idea of using medications for aesthetic reasons is really more related to societal ills around how we value fitness above anything else. That’s not the goal, and it’s not safe.”

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

A popular ingredient in the American diet has been linked to ulcerative colitis. The ingredient is soybean oil, which is very common in processed foods. In fact, U.S. per capita consumption of soybean oil increased more than 1,000-fold during the 20th century.

In a study from the University of California, Riverside, and UC Davis, published in Gut Microbes, mice fed a diet high in soybean oil were more at risk of developing colitis. 

The likely culprit? Linoleic acid, an omega-6 fatty acid that composes up to 60% of soybean oil.

Small amounts of linoleic acid help maintain the body’s water balance. But Americans derive as much as 10% of their daily energy from linoleic acid, when they need only 1%-2%, the researchers say.

The findings build on earlier research linking a high-linoleic acid diet with inflammatory bowel disease, or IBD, in humans. (Previous research in mice has also linked high consumption of the oil with obesity and diabetes in the rodents.)

For the new study, the researchers wanted to drill down into how linoleic acid affects the gut.
 

How linoleic acid may promote inflammation

In mice, the soybean oil diet upset the ratio of omega-3 to omega-6 fatty acids in the gut. This led to a decrease in endocannabinoids, lipid-based molecules that help block inflammation.

Enzymes that metabolize fatty acids are “shared between two pathways,” said study coauthor Frances Sladek, PhD, professor of cell biology at UC Riverside. “If you swamp the system with linoleic acid, you’ll have less enzymes available to metabolize omega-3s into good endocannabinoids.”

The endocannabinoid system has been linked to “visceral pain” in the gut,  said Punyanganie de Silva, MD, MPH, an assistant professor at Brigham & Women’s Hospital, Boston, who was not involved in the study. But the relationship between the endocannabinoid system and inflammation has yet to be fully explored.

“This is one of the first papers that has looked at the association between linoleic acid and the endocannabinoid system,” Dr. de Silva said. “[The researchers] propose a potential new mechanism of how linoleic acid may increase inflammation” – that is, through its impact on the endocannabinoid system. 
 

Changes in the gut microbiome

The gut microbiome of the mice also showed increased amounts of adherent invasive E. coli, a type of bacteria that grows by using linoleic acid as a carbon source. A “very close relative” of this bacteria has been linked to IBD in humans, Dr. Sladek said.

Using a method known as metabolomics, the researchers studied 3,000 metabolites in the intestinal cells of both the mice and the bacteria. Endocannabinoids decreased in both.

“We were actually quite surprised. I didn’t realize that bacteria made endocannabinoids,” Dr. Sladek said.

Helpful bacteria, such as the probiotic lactobacillus species, died off. The mice also had increased levels of oxylipins, which are correlated with obesity in mice and colitis in humans.
 

A high–linoleic acid diet could mean a leaky gut

Linoleic acid binds to a protein known as HNF-4 alpha. Disrupting the expression of this protein can weaken the intestinal barrier, letting toxins flow into the body – more commonly known as leaky gut. Mice on the soybean oil diet had decreased levels of the protein and more porous intestinal barriers, raising the risk for inflammation and colitis. “The HNF-4 alpha protein is conserved from mouse to human, so whatever’s happening to it in the context of the mouse gut, there’s a very high chance that a similar effect could be seen in humans as well,” said study coauthor Poonamjot Deol, PhD, an assistant professional researcher at UC Riverside.

Still, Dr. de Silva urges “some caution when interpreting these results,” given that “this is still experimental and needs to be reproduced in clinical studies as humans have a far more varied microbiome and more variable environmental exposures than these very controlled mouse model studies.”

Dr. de Silva says cooking with olive oil can “help increase omega-3 to omega-6 ratios” and advises eating a varied diet that includes omega-3 fats, such as flaxseed and walnuts, and minimal amounts of processed foods and saturated fats.

Looking ahead, endocannabinoids are being explored as “a potential therapy for treating IBD symptoms,” said Dr. Deol. She hopes to delve further into how linoleic acid affects the endocannabinoid system.

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

A popular ingredient in the American diet has been linked to ulcerative colitis. The ingredient is soybean oil, which is very common in processed foods. In fact, U.S. per capita consumption of soybean oil increased more than 1,000-fold during the 20th century.

In a study from the University of California, Riverside, and UC Davis, published in Gut Microbes, mice fed a diet high in soybean oil were more at risk of developing colitis. 

The likely culprit? Linoleic acid, an omega-6 fatty acid that composes up to 60% of soybean oil.

Small amounts of linoleic acid help maintain the body’s water balance. But Americans derive as much as 10% of their daily energy from linoleic acid, when they need only 1%-2%, the researchers say.

The findings build on earlier research linking a high-linoleic acid diet with inflammatory bowel disease, or IBD, in humans. (Previous research in mice has also linked high consumption of the oil with obesity and diabetes in the rodents.)

For the new study, the researchers wanted to drill down into how linoleic acid affects the gut.
 

How linoleic acid may promote inflammation

In mice, the soybean oil diet upset the ratio of omega-3 to omega-6 fatty acids in the gut. This led to a decrease in endocannabinoids, lipid-based molecules that help block inflammation.

Enzymes that metabolize fatty acids are “shared between two pathways,” said study coauthor Frances Sladek, PhD, professor of cell biology at UC Riverside. “If you swamp the system with linoleic acid, you’ll have less enzymes available to metabolize omega-3s into good endocannabinoids.”

The endocannabinoid system has been linked to “visceral pain” in the gut,  said Punyanganie de Silva, MD, MPH, an assistant professor at Brigham & Women’s Hospital, Boston, who was not involved in the study. But the relationship between the endocannabinoid system and inflammation has yet to be fully explored.

“This is one of the first papers that has looked at the association between linoleic acid and the endocannabinoid system,” Dr. de Silva said. “[The researchers] propose a potential new mechanism of how linoleic acid may increase inflammation” – that is, through its impact on the endocannabinoid system. 
 

Changes in the gut microbiome

The gut microbiome of the mice also showed increased amounts of adherent invasive E. coli, a type of bacteria that grows by using linoleic acid as a carbon source. A “very close relative” of this bacteria has been linked to IBD in humans, Dr. Sladek said.

Using a method known as metabolomics, the researchers studied 3,000 metabolites in the intestinal cells of both the mice and the bacteria. Endocannabinoids decreased in both.

“We were actually quite surprised. I didn’t realize that bacteria made endocannabinoids,” Dr. Sladek said.

Helpful bacteria, such as the probiotic lactobacillus species, died off. The mice also had increased levels of oxylipins, which are correlated with obesity in mice and colitis in humans.
 

A high–linoleic acid diet could mean a leaky gut

Linoleic acid binds to a protein known as HNF-4 alpha. Disrupting the expression of this protein can weaken the intestinal barrier, letting toxins flow into the body – more commonly known as leaky gut. Mice on the soybean oil diet had decreased levels of the protein and more porous intestinal barriers, raising the risk for inflammation and colitis. “The HNF-4 alpha protein is conserved from mouse to human, so whatever’s happening to it in the context of the mouse gut, there’s a very high chance that a similar effect could be seen in humans as well,” said study coauthor Poonamjot Deol, PhD, an assistant professional researcher at UC Riverside.

Still, Dr. de Silva urges “some caution when interpreting these results,” given that “this is still experimental and needs to be reproduced in clinical studies as humans have a far more varied microbiome and more variable environmental exposures than these very controlled mouse model studies.”

Dr. de Silva says cooking with olive oil can “help increase omega-3 to omega-6 ratios” and advises eating a varied diet that includes omega-3 fats, such as flaxseed and walnuts, and minimal amounts of processed foods and saturated fats.

Looking ahead, endocannabinoids are being explored as “a potential therapy for treating IBD symptoms,” said Dr. Deol. She hopes to delve further into how linoleic acid affects the endocannabinoid system.

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

A popular ingredient in the American diet has been linked to ulcerative colitis. The ingredient is soybean oil, which is very common in processed foods. In fact, U.S. per capita consumption of soybean oil increased more than 1,000-fold during the 20th century.

In a study from the University of California, Riverside, and UC Davis, published in Gut Microbes, mice fed a diet high in soybean oil were more at risk of developing colitis. 

The likely culprit? Linoleic acid, an omega-6 fatty acid that composes up to 60% of soybean oil.

Small amounts of linoleic acid help maintain the body’s water balance. But Americans derive as much as 10% of their daily energy from linoleic acid, when they need only 1%-2%, the researchers say.

The findings build on earlier research linking a high-linoleic acid diet with inflammatory bowel disease, or IBD, in humans. (Previous research in mice has also linked high consumption of the oil with obesity and diabetes in the rodents.)

For the new study, the researchers wanted to drill down into how linoleic acid affects the gut.
 

How linoleic acid may promote inflammation

In mice, the soybean oil diet upset the ratio of omega-3 to omega-6 fatty acids in the gut. This led to a decrease in endocannabinoids, lipid-based molecules that help block inflammation.

Enzymes that metabolize fatty acids are “shared between two pathways,” said study coauthor Frances Sladek, PhD, professor of cell biology at UC Riverside. “If you swamp the system with linoleic acid, you’ll have less enzymes available to metabolize omega-3s into good endocannabinoids.”

The endocannabinoid system has been linked to “visceral pain” in the gut,  said Punyanganie de Silva, MD, MPH, an assistant professor at Brigham & Women’s Hospital, Boston, who was not involved in the study. But the relationship between the endocannabinoid system and inflammation has yet to be fully explored.

“This is one of the first papers that has looked at the association between linoleic acid and the endocannabinoid system,” Dr. de Silva said. “[The researchers] propose a potential new mechanism of how linoleic acid may increase inflammation” – that is, through its impact on the endocannabinoid system. 
 

Changes in the gut microbiome

The gut microbiome of the mice also showed increased amounts of adherent invasive E. coli, a type of bacteria that grows by using linoleic acid as a carbon source. A “very close relative” of this bacteria has been linked to IBD in humans, Dr. Sladek said.

Using a method known as metabolomics, the researchers studied 3,000 metabolites in the intestinal cells of both the mice and the bacteria. Endocannabinoids decreased in both.

“We were actually quite surprised. I didn’t realize that bacteria made endocannabinoids,” Dr. Sladek said.

Helpful bacteria, such as the probiotic lactobacillus species, died off. The mice also had increased levels of oxylipins, which are correlated with obesity in mice and colitis in humans.
 

A high–linoleic acid diet could mean a leaky gut

Linoleic acid binds to a protein known as HNF-4 alpha. Disrupting the expression of this protein can weaken the intestinal barrier, letting toxins flow into the body – more commonly known as leaky gut. Mice on the soybean oil diet had decreased levels of the protein and more porous intestinal barriers, raising the risk for inflammation and colitis. “The HNF-4 alpha protein is conserved from mouse to human, so whatever’s happening to it in the context of the mouse gut, there’s a very high chance that a similar effect could be seen in humans as well,” said study coauthor Poonamjot Deol, PhD, an assistant professional researcher at UC Riverside.

Still, Dr. de Silva urges “some caution when interpreting these results,” given that “this is still experimental and needs to be reproduced in clinical studies as humans have a far more varied microbiome and more variable environmental exposures than these very controlled mouse model studies.”

Dr. de Silva says cooking with olive oil can “help increase omega-3 to omega-6 ratios” and advises eating a varied diet that includes omega-3 fats, such as flaxseed and walnuts, and minimal amounts of processed foods and saturated fats.

Looking ahead, endocannabinoids are being explored as “a potential therapy for treating IBD symptoms,” said Dr. Deol. She hopes to delve further into how linoleic acid affects the endocannabinoid system.

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

Although it’s easy to jump to the conclusion that facial erythema is rosacea, there are multiple other conditions that can lead to reddening of the face. In this case, excessive sun exposure had resulted in a diffuse actinic change of the malar and lateral aspects of this patient’s face. The palpably rough lesions were actinic keratoses.

Actinic keratoses are caused by exposure to ultraviolet radiation. These lesions are premalignant and common. Areas of the body at greatest risk include those not typically covered by clothing (eg, face, hands, arms, ears, forehead, and top of the scalp—especially in individuals with hair loss). There is a range of estimates regarding the percentage of actinic keratoses that will progress to squamous cell carcinoma in situ, and then invasive squamous cell carcinoma. One study determined that 10% of actinic keratoses progress to squamous cell carcinoma over the course of 2 years.¹

In patients with broad areas of multiple clinically palpable lesions with rough sandpapery texture or visible white scale, there are likely preclinical lesions in the same areas. With so many lesions, field therapy of the entire region is often performed instead of treating the lesions 1 at a time.

There are multiple topical agents for field therapy, including 5-fluorouracil, diclofenac gel, and imiquimod gel.² Since significant erythema and inflammation usually follow application of the topical agent, clinicians may want to have patients treat in segments to make the process more tolerable.

5-fluorouracil has a complete clearance rate (CCR) of 75% to 90% and is usually applied twice daily for 2 weeks, although there are multiple different protocols. Diclofenac has a CCR of 58% over a 60- to 90-day course, and imiquimod has a CCR of 54% after a 120-day course. Photodynamic therapy (PDT) has the advantage of a single treatment but a CCR of 38%. PDT may be advantageous for a patient who has difficulty applying topical medication over a period of weeks.

Niacinamide has been shown to help with skin repair and reduce the risk of additional nonmelanoma skin cancers (NMSC) by 23% and additional actinic keratoses by about 15% in individuals with a history of actinic keratoses or NMSC.³ In contrast to niacin, niacinamide does not cause flushing. Niacinamide is used long term; if discontinued, it no longer confers benefit in helping the skin repair itself.

The patient in this case was prescribed topical 5% fluorouracil cream to be applied twice daily to the malar regions bilaterally for 2 weeks and, if not inflamed by 2 weeks, to extend the treatment until there is robust inflammation (but not to exceed 3 weeks). He was scheduled to follow up in 3 months for reexamination. He was also advised to start taking niacinamide 500 mg twice daily to reduce his risk of additional precancerous and cancerous skin lesions and counseled on the importance of sunscreen, hats, and sun-protective clothing.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

Although it’s easy to jump to the conclusion that facial erythema is rosacea, there are multiple other conditions that can lead to reddening of the face. In this case, excessive sun exposure had resulted in a diffuse actinic change of the malar and lateral aspects of this patient’s face. The palpably rough lesions were actinic keratoses.

Actinic keratoses are caused by exposure to ultraviolet radiation. These lesions are premalignant and common. Areas of the body at greatest risk include those not typically covered by clothing (eg, face, hands, arms, ears, forehead, and top of the scalp—especially in individuals with hair loss). There is a range of estimates regarding the percentage of actinic keratoses that will progress to squamous cell carcinoma in situ, and then invasive squamous cell carcinoma. One study determined that 10% of actinic keratoses progress to squamous cell carcinoma over the course of 2 years.¹

In patients with broad areas of multiple clinically palpable lesions with rough sandpapery texture or visible white scale, there are likely preclinical lesions in the same areas. With so many lesions, field therapy of the entire region is often performed instead of treating the lesions 1 at a time.

There are multiple topical agents for field therapy, including 5-fluorouracil, diclofenac gel, and imiquimod gel.² Since significant erythema and inflammation usually follow application of the topical agent, clinicians may want to have patients treat in segments to make the process more tolerable.

5-fluorouracil has a complete clearance rate (CCR) of 75% to 90% and is usually applied twice daily for 2 weeks, although there are multiple different protocols. Diclofenac has a CCR of 58% over a 60- to 90-day course, and imiquimod has a CCR of 54% after a 120-day course. Photodynamic therapy (PDT) has the advantage of a single treatment but a CCR of 38%. PDT may be advantageous for a patient who has difficulty applying topical medication over a period of weeks.

Niacinamide has been shown to help with skin repair and reduce the risk of additional nonmelanoma skin cancers (NMSC) by 23% and additional actinic keratoses by about 15% in individuals with a history of actinic keratoses or NMSC.³ In contrast to niacin, niacinamide does not cause flushing. Niacinamide is used long term; if discontinued, it no longer confers benefit in helping the skin repair itself.

The patient in this case was prescribed topical 5% fluorouracil cream to be applied twice daily to the malar regions bilaterally for 2 weeks and, if not inflamed by 2 weeks, to extend the treatment until there is robust inflammation (but not to exceed 3 weeks). He was scheduled to follow up in 3 months for reexamination. He was also advised to start taking niacinamide 500 mg twice daily to reduce his risk of additional precancerous and cancerous skin lesions and counseled on the importance of sunscreen, hats, and sun-protective clothing.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

Although it’s easy to jump to the conclusion that facial erythema is rosacea, there are multiple other conditions that can lead to reddening of the face. In this case, excessive sun exposure had resulted in a diffuse actinic change of the malar and lateral aspects of this patient’s face. The palpably rough lesions were actinic keratoses.

Actinic keratoses are caused by exposure to ultraviolet radiation. These lesions are premalignant and common. Areas of the body at greatest risk include those not typically covered by clothing (eg, face, hands, arms, ears, forehead, and top of the scalp—especially in individuals with hair loss). There is a range of estimates regarding the percentage of actinic keratoses that will progress to squamous cell carcinoma in situ, and then invasive squamous cell carcinoma. One study determined that 10% of actinic keratoses progress to squamous cell carcinoma over the course of 2 years.¹

In patients with broad areas of multiple clinically palpable lesions with rough sandpapery texture or visible white scale, there are likely preclinical lesions in the same areas. With so many lesions, field therapy of the entire region is often performed instead of treating the lesions 1 at a time.

There are multiple topical agents for field therapy, including 5-fluorouracil, diclofenac gel, and imiquimod gel.² Since significant erythema and inflammation usually follow application of the topical agent, clinicians may want to have patients treat in segments to make the process more tolerable.

5-fluorouracil has a complete clearance rate (CCR) of 75% to 90% and is usually applied twice daily for 2 weeks, although there are multiple different protocols. Diclofenac has a CCR of 58% over a 60- to 90-day course, and imiquimod has a CCR of 54% after a 120-day course. Photodynamic therapy (PDT) has the advantage of a single treatment but a CCR of 38%. PDT may be advantageous for a patient who has difficulty applying topical medication over a period of weeks.

Niacinamide has been shown to help with skin repair and reduce the risk of additional nonmelanoma skin cancers (NMSC) by 23% and additional actinic keratoses by about 15% in individuals with a history of actinic keratoses or NMSC.³ In contrast to niacin, niacinamide does not cause flushing. Niacinamide is used long term; if discontinued, it no longer confers benefit in helping the skin repair itself.

The patient in this case was prescribed topical 5% fluorouracil cream to be applied twice daily to the malar regions bilaterally for 2 weeks and, if not inflamed by 2 weeks, to extend the treatment until there is robust inflammation (but not to exceed 3 weeks). He was scheduled to follow up in 3 months for reexamination. He was also advised to start taking niacinamide 500 mg twice daily to reduce his risk of additional precancerous and cancerous skin lesions and counseled on the importance of sunscreen, hats, and sun-protective clothing.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.