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A daily prednisolone dose of 5 mg or higher is associated with increased risk for major adverse cardiovascular events (MACE) among patients with rheumatoid arthritis (RA), data suggest. Patients taking daily doses below this threshold did not appear to have an increased risk of MACE, compared with those not taking glucocorticoids (GCs).

Chinese University of Hong Kong

Is there a ‘safe’ dose for glucocorticoids?

To analyze this relationship, Dr. Lam and colleagues used the Hospital Authority Data Collaboration Laboratory, a citywide health care database. The investigators recruited patients with RA who had no history of MACE from 2006 to 2015 and followed them until the end of 2018. The primary outcome was the first occurrence of a MACE, defined as a composite of myocardial infarction (MI), unstable angina, ischemic or hemorrhagic cerebrovascular accident, transient ischemic attack, and CV death.

The study was published in Annals of the Rheumatic Diseases.

The analysis included 12,233 patients with RA and had over 105,826 person-years of follow-up. The average follow-up time was 8.7 years. During the study period, 860 patients had their first MACE. After controlling for confounding factors, a daily prednisolone dose of 5 mg or higher doubled the risk for MACE, compared with GC nonusers. MACE risk increased by 7% per month.

University of Wisconsin School of Medicine and Public Health

Long-term glucocorticoid use discouraged

Daily doses of less than 5 mg were not associated with higher MACE risk, but more research is necessary to understand whether these low doses are clinically efficacious, Dr. Tam said. “The study results suggest that a very-low-dose GC (less than 5 mg prednisolone daily) may be cardiovascular risk–neutral. However, further evaluation is needed to determine whether this dose is therapeutic. Other potential side effects, such as bone loss, increased infection risk, dyslipidemia, and hyperglycemia, should also be considered.”

Both the American College of Rheumatology and the European Alliance of Associations for Rheumatology acknowledge that short-term GCs may be necessary for some RA patients, but they emphasize using the smallest necessary dose for the shortest period possible because of the known toxicity of GCs.

“We recommend stopping GCs as soon as it is clinically feasible, in line with previous recommendations, until these issues are investigated further,” Dr. Tam added.

Dr. Bartels agreed that long-term use of GCs should be avoided if possible, even at lower doses, because although CV risk may be less of an issue, studies have shown an increased risk for infection even at GC doses of less than 5 mg a day.
 

How might risk increase with dose?

While the study showed a distinct difference in risk with doses of prednisolone higher and lower than 5 mg, more information on how risk increases with dose could be useful, said Beth Wallace, MD, an assistant professor in internal medicine at the University of Michigan, Ann Arbor, and a staff rheumatologist at the VA Ann Arbor Healthcare Center. She was also unaffiliated with the research. “If someone is on 5-10 mg ... how much better is that than being on 10-20 mg or being on 20-30 mg?” she asked. While these study findings are “very important,” she said, it would be useful to know the risk associated with 7.5 mg vs. a higher dose.

University of Michigan

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

A daily prednisolone dose of 5 mg or higher is associated with increased risk for major adverse cardiovascular events (MACE) among patients with rheumatoid arthritis (RA), data suggest. Patients taking daily doses below this threshold did not appear to have an increased risk of MACE, compared with those not taking glucocorticoids (GCs).

Chinese University of Hong Kong

Is there a ‘safe’ dose for glucocorticoids?

To analyze this relationship, Dr. Lam and colleagues used the Hospital Authority Data Collaboration Laboratory, a citywide health care database. The investigators recruited patients with RA who had no history of MACE from 2006 to 2015 and followed them until the end of 2018. The primary outcome was the first occurrence of a MACE, defined as a composite of myocardial infarction (MI), unstable angina, ischemic or hemorrhagic cerebrovascular accident, transient ischemic attack, and CV death.

The study was published in Annals of the Rheumatic Diseases.

The analysis included 12,233 patients with RA and had over 105,826 person-years of follow-up. The average follow-up time was 8.7 years. During the study period, 860 patients had their first MACE. After controlling for confounding factors, a daily prednisolone dose of 5 mg or higher doubled the risk for MACE, compared with GC nonusers. MACE risk increased by 7% per month.

University of Wisconsin School of Medicine and Public Health

Long-term glucocorticoid use discouraged

Daily doses of less than 5 mg were not associated with higher MACE risk, but more research is necessary to understand whether these low doses are clinically efficacious, Dr. Tam said. “The study results suggest that a very-low-dose GC (less than 5 mg prednisolone daily) may be cardiovascular risk–neutral. However, further evaluation is needed to determine whether this dose is therapeutic. Other potential side effects, such as bone loss, increased infection risk, dyslipidemia, and hyperglycemia, should also be considered.”

Both the American College of Rheumatology and the European Alliance of Associations for Rheumatology acknowledge that short-term GCs may be necessary for some RA patients, but they emphasize using the smallest necessary dose for the shortest period possible because of the known toxicity of GCs.

“We recommend stopping GCs as soon as it is clinically feasible, in line with previous recommendations, until these issues are investigated further,” Dr. Tam added.

Dr. Bartels agreed that long-term use of GCs should be avoided if possible, even at lower doses, because although CV risk may be less of an issue, studies have shown an increased risk for infection even at GC doses of less than 5 mg a day.
 

How might risk increase with dose?

While the study showed a distinct difference in risk with doses of prednisolone higher and lower than 5 mg, more information on how risk increases with dose could be useful, said Beth Wallace, MD, an assistant professor in internal medicine at the University of Michigan, Ann Arbor, and a staff rheumatologist at the VA Ann Arbor Healthcare Center. She was also unaffiliated with the research. “If someone is on 5-10 mg ... how much better is that than being on 10-20 mg or being on 20-30 mg?” she asked. While these study findings are “very important,” she said, it would be useful to know the risk associated with 7.5 mg vs. a higher dose.

University of Michigan

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

A daily prednisolone dose of 5 mg or higher is associated with increased risk for major adverse cardiovascular events (MACE) among patients with rheumatoid arthritis (RA), data suggest. Patients taking daily doses below this threshold did not appear to have an increased risk of MACE, compared with those not taking glucocorticoids (GCs).

Chinese University of Hong Kong

Is there a ‘safe’ dose for glucocorticoids?

To analyze this relationship, Dr. Lam and colleagues used the Hospital Authority Data Collaboration Laboratory, a citywide health care database. The investigators recruited patients with RA who had no history of MACE from 2006 to 2015 and followed them until the end of 2018. The primary outcome was the first occurrence of a MACE, defined as a composite of myocardial infarction (MI), unstable angina, ischemic or hemorrhagic cerebrovascular accident, transient ischemic attack, and CV death.

The study was published in Annals of the Rheumatic Diseases.

The analysis included 12,233 patients with RA and had over 105,826 person-years of follow-up. The average follow-up time was 8.7 years. During the study period, 860 patients had their first MACE. After controlling for confounding factors, a daily prednisolone dose of 5 mg or higher doubled the risk for MACE, compared with GC nonusers. MACE risk increased by 7% per month.

University of Wisconsin School of Medicine and Public Health

Long-term glucocorticoid use discouraged

Daily doses of less than 5 mg were not associated with higher MACE risk, but more research is necessary to understand whether these low doses are clinically efficacious, Dr. Tam said. “The study results suggest that a very-low-dose GC (less than 5 mg prednisolone daily) may be cardiovascular risk–neutral. However, further evaluation is needed to determine whether this dose is therapeutic. Other potential side effects, such as bone loss, increased infection risk, dyslipidemia, and hyperglycemia, should also be considered.”

Both the American College of Rheumatology and the European Alliance of Associations for Rheumatology acknowledge that short-term GCs may be necessary for some RA patients, but they emphasize using the smallest necessary dose for the shortest period possible because of the known toxicity of GCs.

“We recommend stopping GCs as soon as it is clinically feasible, in line with previous recommendations, until these issues are investigated further,” Dr. Tam added.

Dr. Bartels agreed that long-term use of GCs should be avoided if possible, even at lower doses, because although CV risk may be less of an issue, studies have shown an increased risk for infection even at GC doses of less than 5 mg a day.
 

How might risk increase with dose?

While the study showed a distinct difference in risk with doses of prednisolone higher and lower than 5 mg, more information on how risk increases with dose could be useful, said Beth Wallace, MD, an assistant professor in internal medicine at the University of Michigan, Ann Arbor, and a staff rheumatologist at the VA Ann Arbor Healthcare Center. She was also unaffiliated with the research. “If someone is on 5-10 mg ... how much better is that than being on 10-20 mg or being on 20-30 mg?” she asked. While these study findings are “very important,” she said, it would be useful to know the risk associated with 7.5 mg vs. a higher dose.

University of Michigan

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

Public perception of disease is everything. “Diabetics” are now referred to as “people living with diabetes,” and an “obese person” is now an “individual living with obesity.”

But what is the definition of obesity? Does it refer to a disease or a risk factor? And is the term so tainted in negativity, blame, and bias that the only solution is to scrap it and completely rename it? Society (and medicine) have changed significantly since the Latin word obesitas was adopted back in the 1600s.

Despite so much hinging on the word “obesity,” it’s remarkable that the label persists while the concepts underpinning it have evolved significantly. So perhaps it is more about finding the least-worst option rather than pursuing the impossibility of a solution that suits all?

This is precisely the challenge faced by a Lancet Diabetes & Endocrinology Commission on the Definition and Diagnosis of Clinical Obesity, which is due to publish its initial findings this coming fall. The global task force has 60 leaders in the clinical management of obesity, including representatives with lived experiences of obesity. Leading the project is Francesco Rubino, MD, chair of metabolic and bariatric surgery at King’s College London.

“Renaming ‘obesity’ is very important,” states Dr. Rubino. “The word is so stigmatized, with so much misunderstanding and misperception, some might say the only solution is to change the name.”

One possibility for a new name, introduced by the American Association of Clinical Endocrinologists (now –Endocrinology) and the American College of Endocrinology back in 2016, was based on framing the disease on the central characteristic of adiposity and was termed ABCD, for adiposity-based chronic disease.

Dr. Rubino welcomes “ABCD” but has some reservations. “It is good from a physiological point of view, but the problem is it speaks to scientists and medical professionals. I don’t know how much it would appeal to the general public. ‘ABCD’ still falls short of telling us what the illness is.”

He adds that the Lancet Commission’s approach is rather to call it “clinical obesity.” “ ‘Obesity’ itself doesn’t necessarily convey the message that you have a disease or an illness,” he observes. “It is similar to the difference in meaning between depression and clinical depression, which communicate two different things.”

But underpinning any renaming is greater clarification of the definition and diagnosis of obesity. In 1997, the World Health Organization recognized obesity as a chronic disease; in 2013, the American Medical Association did likewise, adding that it warranted medical attention; while it took until 2021 for the European Commission to define obesity as a “chronic relapsing disease, which in turn acts as a gateway to a range of other non-communicable diseases.”

Yet, 25 years after the initial recognition of obesity as a disease, the concept is still riddled with negativity, whether openly or unconsciously. Such stigma denigrates overweight people and those with obesity as “lazy, sloppy, unintelligent, and unattractive.”

Dr. Rubino explains that first, it’s important to establish and define the essential components and characteristics of the disease of obesity. This is key to improving access to clinical care, reducing personal blame, and nurturing a more supportive research environment to help inform both clinical and policy decision-making.

“This is the question that is at the core of our commission. We have a problem with the current definition of obesity, and the way we measure it does not allow us to accurately define a state of illness with obesity,” he explains.
 

Labels shape public perceptions of disease; ‘obesity’ epitomizes this

Another expert championing the need for a name that better reflects the definition – whatever that turns out to be – is Margaret Steele, PhD, School of Public Health, University College Cork (Ireland), who, according to her university webpage, has a special interest in “ ‘fatness’ as a cultural, social and political phenomenon.”

She believes that labels, including “obesity,” have a pivotal role in shaping public perceptions. In our digital, information-rich age, the boundaries of medicine and society overlap, with public perception shaping decisions of a medical nature as never before. But with this comes controversy and division – obesity management being a case in point.

Specifically, the word “obesity” is too widely associated with negative connotations, she says, and therefore she welcomes the dialogue around redefining and renaming it. Despite wide general support for a name and definition that reflects adiposity, due to its central physiologic role in the complications of obesity, Dr. Steele believes that the “effects on adipose tissue are downstream of brain issues and the food environment,” and she wants to see more attention brought to this.

Referring to most Westernized societies, she describes how people who grew up in times of food scarcity, before processed foods became widely available, have a different taste profile from those who grew up afterwards. “Growing up in 1940s and ‘50s Ireland, people recall how they remember getting an orange as a treat at Christmas, because the idea that you could have food all year-round – any fruit and veg that you want, when you want it – just wasn’t there.”

By comparison, societal changes leading to more financial and time pressure in later decades meant that fast, high-fat, high-sugar, and processed foods became more desirable, she points out. “Most young children now recognize the company name, and even the specific fast-food brand [they like], before they know their alphabet.”

The current environment has cultivated “a very different physical reaction to foods, maybe a different kind of emotional response,” she believes, highlighting the tightly woven relationship between obesity, society, mental health, and food options.

Dr. Steele wants to stimulate a conversation about the term used to describe individuals, conventionally described as ‘”obese” or using the word “obesity.” “We’re thinking in terms of maybe chronic appetite, chronic food intake, or dietary intake dysregulation.”

Changing medical terminology when it has become useless or harmful is not new, she argues, with co-author, Francis Finucane, MD, consultant endocrinologist at Galway University Hospitals, Ireland, in a recent paper on the subject.

“In the 20th century, the terms ‘feeble-minded’ and ‘moron’ had become used in a pejorative way in the wider culture and were dropped from medical usage,” Dr. Steele points out. She adds that changing the term “obesity” can facilitate pursuit of the strategic goals of clinical medicine “without causing needless controversy with those who, given their own goals and contexts, understand body mass index or body weight in a radically different way.”
 

Obesity: Disease, risk factor, or both?

Dr. Rubino stresses that prior to any renaming, there is a need to establish and define the essential components and characteristics of the disease of obesity. “This question is at the core of our Commission, and it is not an easy conversation to have.” He further explains that the struggle with the current definition of obesity, and the way it is conceived, is largely centered on it still being considered a risk factor for something else.

Disease is characterized by three things, says Dr. Rubino. These comprise the phenomenon of having a pathogenic cause, leading to pathophysiologic alterations (of the organs), causing clinical manifestations.

He adds that obesity is currently described by what it can cause – for example, type 2 diabetes, cancer, or hypertension. “Each of these things have their own clinical manifestations but obesity doesn’t. [As a disease], we don’t have a definition of the clinical manifestations of obesity other than excess adiposity.”

“If we use BMI, this does not predict excess adiposity, nor does it determine a disease here and now. There is no disease without an illness, which is the clinical manifestation, and the perception by the patient of it being an illness,” explains Dr. Rubino, pointing out that the Lancet Commission is filling this gap in knowledge by asking, “If obesity is an illness, then what does it look like?”

He adds that waist circumference probably provides a better measure than BMI in directly indicating the abnormal distribution of adiposity, known to be associated with poor cardiometabolic outcomes, “but it doesn’t tell you if you have an illness here and now – only that someone is at risk of developing cardiovascular disease in the future. Most people with some excess fat around the waist are perfectly functional and don’t feel ill.”

He also explains that confusion persists around whether obesity – or excess adiposity – is a risk factor for or a symptom of another disease. “The picture is blurred, and we do not know how to discriminate between these. We only have one name, and it applies to all those things, and we have one criterion – BMI – to diagnose it!”

Dr. Rubino adds, “So, what defines it? Is it diabetes? No, because that is another disease. You don’t define a disease by another. It has to stand on its own.”

Recently, the American Medical Association advised that BMI now be used in conjunction with other valid measures of risk such as, but not limited to, measurements of visceral fat, body adiposity index, body composition, relative fat mass, waist circumference, and genetic/metabolic factors.

Aayush Visaria, MD, an internal medicine resident at Rutgers University, New Brunswick, New Jersey, agrees that a new name might help change public perception of obesity for the better. A study he presented at the 2023 Endocrine Society Meeting found that BMI “vastly underestimates” obesity.

He agrees with Dr. Rubino that the challenge lies in the lack of precise understanding of the mechanisms driving obesity: “It’s multifactorial, so not just appetite or food intake. Putting this into one phrase is difficult.”

However, if a new term can incorporate the many facets of the disease, “overall, it’ll reduce stigma because we’ll start to think about obesity as a disease process, not a personal thing with blame attached,” says Dr. Visaria.

But simultaneously, he expresses caution around possible negative connotations associated with the classification of obesity as a disease. Dr. Steele also reflects on this risk, highlighting that medicalizing body size can be counterproductive in feeding into weight stigma and fatphobia.

“Medicalizing obesity can be discouraging rather than empowering, but by specifying more clearly that we’re talking about a specific set of interrelated metabolic conditions, it would make it much clearer, and that ... this isn’t about making people skinny, it isn’t about an aesthetic thing,” Dr. Steele observes.
 

The word ‘obesity’ hinders disease explanations

Dr. Steele explains that her goal is to overcome the ambiguity around the word “obesity” that hinders explanations of the disease of obesity to the wider public.

“Much confusion and controversy might be avoided if we were to clarify that when doctors say that obesity is a disease, they do not mean that being ‘fat’ is a disease.”

Nevertheless, adipose tissue is an active endocrine organ, producing hormones that function less well in people with obesity, she notes. “This new knowledge has led to better treatments, including drugs like semaglutide and tirzepatide. These drugs, like bariatric surgery, typically lead to significant weight loss and to improvements in overall metabolic health.”

Dr. Rubino also expresses concerns around medicalization, as determined by definition and diagnosis and the availability of drug treatment that could potentially lead to overtreatment. “Currently, when everyone with a BMI of greater than 30 gets access to every obesity treatment out there, we see drugs are running out of stock. We should prioritize that treatment.”

Ultimately, the diagnosis of obesity as a disease needs an anthropometric biomarker that provides, on an individual level, the confidence that a person has a disease today, or at least close to a 100% likelihood of developing this disease and illness, asserts Dr. Rubino.

“If we use BMI, or even waist circumference, these might diagnose the disease; but if the person lives to 90 years, what’s the point of labeling somebody as having an illness?” he points out.

“As doctors, we have to be cautious. We say this is a disease, but you must think about the implications for the person on the receiving end of that diagnosis of a chronic disease that is substantially incurable. When we say it, we need to be certain.”

Dr. Steele and Dr. Visaria have disclosed no relevant financial relationships. Dr. Rubino disclosed that he has received research grants from Novo Nordisk, Medtronic, and Johnson & Johnson. He has undertaken paid consultancy work for GI Dynamics and received honoraria for lectures from Medtronic, Novo Nordisk, and Johnson & Johnson. He is a member of the data safety monitoring board for GT Metabolic Solutions and has provided scientific advice to Keyron, Metadeq, GHP Scientific, and ViBo Health for no remuneration.

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

Public perception of disease is everything. “Diabetics” are now referred to as “people living with diabetes,” and an “obese person” is now an “individual living with obesity.”

But what is the definition of obesity? Does it refer to a disease or a risk factor? And is the term so tainted in negativity, blame, and bias that the only solution is to scrap it and completely rename it? Society (and medicine) have changed significantly since the Latin word obesitas was adopted back in the 1600s.

Despite so much hinging on the word “obesity,” it’s remarkable that the label persists while the concepts underpinning it have evolved significantly. So perhaps it is more about finding the least-worst option rather than pursuing the impossibility of a solution that suits all?

This is precisely the challenge faced by a Lancet Diabetes & Endocrinology Commission on the Definition and Diagnosis of Clinical Obesity, which is due to publish its initial findings this coming fall. The global task force has 60 leaders in the clinical management of obesity, including representatives with lived experiences of obesity. Leading the project is Francesco Rubino, MD, chair of metabolic and bariatric surgery at King’s College London.

“Renaming ‘obesity’ is very important,” states Dr. Rubino. “The word is so stigmatized, with so much misunderstanding and misperception, some might say the only solution is to change the name.”

One possibility for a new name, introduced by the American Association of Clinical Endocrinologists (now –Endocrinology) and the American College of Endocrinology back in 2016, was based on framing the disease on the central characteristic of adiposity and was termed ABCD, for adiposity-based chronic disease.

Dr. Rubino welcomes “ABCD” but has some reservations. “It is good from a physiological point of view, but the problem is it speaks to scientists and medical professionals. I don’t know how much it would appeal to the general public. ‘ABCD’ still falls short of telling us what the illness is.”

He adds that the Lancet Commission’s approach is rather to call it “clinical obesity.” “ ‘Obesity’ itself doesn’t necessarily convey the message that you have a disease or an illness,” he observes. “It is similar to the difference in meaning between depression and clinical depression, which communicate two different things.”

But underpinning any renaming is greater clarification of the definition and diagnosis of obesity. In 1997, the World Health Organization recognized obesity as a chronic disease; in 2013, the American Medical Association did likewise, adding that it warranted medical attention; while it took until 2021 for the European Commission to define obesity as a “chronic relapsing disease, which in turn acts as a gateway to a range of other non-communicable diseases.”

Yet, 25 years after the initial recognition of obesity as a disease, the concept is still riddled with negativity, whether openly or unconsciously. Such stigma denigrates overweight people and those with obesity as “lazy, sloppy, unintelligent, and unattractive.”

Dr. Rubino explains that first, it’s important to establish and define the essential components and characteristics of the disease of obesity. This is key to improving access to clinical care, reducing personal blame, and nurturing a more supportive research environment to help inform both clinical and policy decision-making.

“This is the question that is at the core of our commission. We have a problem with the current definition of obesity, and the way we measure it does not allow us to accurately define a state of illness with obesity,” he explains.
 

Labels shape public perceptions of disease; ‘obesity’ epitomizes this

Another expert championing the need for a name that better reflects the definition – whatever that turns out to be – is Margaret Steele, PhD, School of Public Health, University College Cork (Ireland), who, according to her university webpage, has a special interest in “ ‘fatness’ as a cultural, social and political phenomenon.”

She believes that labels, including “obesity,” have a pivotal role in shaping public perceptions. In our digital, information-rich age, the boundaries of medicine and society overlap, with public perception shaping decisions of a medical nature as never before. But with this comes controversy and division – obesity management being a case in point.

Specifically, the word “obesity” is too widely associated with negative connotations, she says, and therefore she welcomes the dialogue around redefining and renaming it. Despite wide general support for a name and definition that reflects adiposity, due to its central physiologic role in the complications of obesity, Dr. Steele believes that the “effects on adipose tissue are downstream of brain issues and the food environment,” and she wants to see more attention brought to this.

Referring to most Westernized societies, she describes how people who grew up in times of food scarcity, before processed foods became widely available, have a different taste profile from those who grew up afterwards. “Growing up in 1940s and ‘50s Ireland, people recall how they remember getting an orange as a treat at Christmas, because the idea that you could have food all year-round – any fruit and veg that you want, when you want it – just wasn’t there.”

By comparison, societal changes leading to more financial and time pressure in later decades meant that fast, high-fat, high-sugar, and processed foods became more desirable, she points out. “Most young children now recognize the company name, and even the specific fast-food brand [they like], before they know their alphabet.”

The current environment has cultivated “a very different physical reaction to foods, maybe a different kind of emotional response,” she believes, highlighting the tightly woven relationship between obesity, society, mental health, and food options.

Dr. Steele wants to stimulate a conversation about the term used to describe individuals, conventionally described as ‘”obese” or using the word “obesity.” “We’re thinking in terms of maybe chronic appetite, chronic food intake, or dietary intake dysregulation.”

Changing medical terminology when it has become useless or harmful is not new, she argues, with co-author, Francis Finucane, MD, consultant endocrinologist at Galway University Hospitals, Ireland, in a recent paper on the subject.

“In the 20th century, the terms ‘feeble-minded’ and ‘moron’ had become used in a pejorative way in the wider culture and were dropped from medical usage,” Dr. Steele points out. She adds that changing the term “obesity” can facilitate pursuit of the strategic goals of clinical medicine “without causing needless controversy with those who, given their own goals and contexts, understand body mass index or body weight in a radically different way.”
 

Obesity: Disease, risk factor, or both?

Dr. Rubino stresses that prior to any renaming, there is a need to establish and define the essential components and characteristics of the disease of obesity. “This question is at the core of our Commission, and it is not an easy conversation to have.” He further explains that the struggle with the current definition of obesity, and the way it is conceived, is largely centered on it still being considered a risk factor for something else.

Disease is characterized by three things, says Dr. Rubino. These comprise the phenomenon of having a pathogenic cause, leading to pathophysiologic alterations (of the organs), causing clinical manifestations.

He adds that obesity is currently described by what it can cause – for example, type 2 diabetes, cancer, or hypertension. “Each of these things have their own clinical manifestations but obesity doesn’t. [As a disease], we don’t have a definition of the clinical manifestations of obesity other than excess adiposity.”

“If we use BMI, this does not predict excess adiposity, nor does it determine a disease here and now. There is no disease without an illness, which is the clinical manifestation, and the perception by the patient of it being an illness,” explains Dr. Rubino, pointing out that the Lancet Commission is filling this gap in knowledge by asking, “If obesity is an illness, then what does it look like?”

He adds that waist circumference probably provides a better measure than BMI in directly indicating the abnormal distribution of adiposity, known to be associated with poor cardiometabolic outcomes, “but it doesn’t tell you if you have an illness here and now – only that someone is at risk of developing cardiovascular disease in the future. Most people with some excess fat around the waist are perfectly functional and don’t feel ill.”

He also explains that confusion persists around whether obesity – or excess adiposity – is a risk factor for or a symptom of another disease. “The picture is blurred, and we do not know how to discriminate between these. We only have one name, and it applies to all those things, and we have one criterion – BMI – to diagnose it!”

Dr. Rubino adds, “So, what defines it? Is it diabetes? No, because that is another disease. You don’t define a disease by another. It has to stand on its own.”

Recently, the American Medical Association advised that BMI now be used in conjunction with other valid measures of risk such as, but not limited to, measurements of visceral fat, body adiposity index, body composition, relative fat mass, waist circumference, and genetic/metabolic factors.

Aayush Visaria, MD, an internal medicine resident at Rutgers University, New Brunswick, New Jersey, agrees that a new name might help change public perception of obesity for the better. A study he presented at the 2023 Endocrine Society Meeting found that BMI “vastly underestimates” obesity.

He agrees with Dr. Rubino that the challenge lies in the lack of precise understanding of the mechanisms driving obesity: “It’s multifactorial, so not just appetite or food intake. Putting this into one phrase is difficult.”

However, if a new term can incorporate the many facets of the disease, “overall, it’ll reduce stigma because we’ll start to think about obesity as a disease process, not a personal thing with blame attached,” says Dr. Visaria.

But simultaneously, he expresses caution around possible negative connotations associated with the classification of obesity as a disease. Dr. Steele also reflects on this risk, highlighting that medicalizing body size can be counterproductive in feeding into weight stigma and fatphobia.

“Medicalizing obesity can be discouraging rather than empowering, but by specifying more clearly that we’re talking about a specific set of interrelated metabolic conditions, it would make it much clearer, and that ... this isn’t about making people skinny, it isn’t about an aesthetic thing,” Dr. Steele observes.
 

The word ‘obesity’ hinders disease explanations

Dr. Steele explains that her goal is to overcome the ambiguity around the word “obesity” that hinders explanations of the disease of obesity to the wider public.

“Much confusion and controversy might be avoided if we were to clarify that when doctors say that obesity is a disease, they do not mean that being ‘fat’ is a disease.”

Nevertheless, adipose tissue is an active endocrine organ, producing hormones that function less well in people with obesity, she notes. “This new knowledge has led to better treatments, including drugs like semaglutide and tirzepatide. These drugs, like bariatric surgery, typically lead to significant weight loss and to improvements in overall metabolic health.”

Dr. Rubino also expresses concerns around medicalization, as determined by definition and diagnosis and the availability of drug treatment that could potentially lead to overtreatment. “Currently, when everyone with a BMI of greater than 30 gets access to every obesity treatment out there, we see drugs are running out of stock. We should prioritize that treatment.”

Ultimately, the diagnosis of obesity as a disease needs an anthropometric biomarker that provides, on an individual level, the confidence that a person has a disease today, or at least close to a 100% likelihood of developing this disease and illness, asserts Dr. Rubino.

“If we use BMI, or even waist circumference, these might diagnose the disease; but if the person lives to 90 years, what’s the point of labeling somebody as having an illness?” he points out.

“As doctors, we have to be cautious. We say this is a disease, but you must think about the implications for the person on the receiving end of that diagnosis of a chronic disease that is substantially incurable. When we say it, we need to be certain.”

Dr. Steele and Dr. Visaria have disclosed no relevant financial relationships. Dr. Rubino disclosed that he has received research grants from Novo Nordisk, Medtronic, and Johnson & Johnson. He has undertaken paid consultancy work for GI Dynamics and received honoraria for lectures from Medtronic, Novo Nordisk, and Johnson & Johnson. He is a member of the data safety monitoring board for GT Metabolic Solutions and has provided scientific advice to Keyron, Metadeq, GHP Scientific, and ViBo Health for no remuneration.

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

Public perception of disease is everything. “Diabetics” are now referred to as “people living with diabetes,” and an “obese person” is now an “individual living with obesity.”

But what is the definition of obesity? Does it refer to a disease or a risk factor? And is the term so tainted in negativity, blame, and bias that the only solution is to scrap it and completely rename it? Society (and medicine) have changed significantly since the Latin word obesitas was adopted back in the 1600s.

Despite so much hinging on the word “obesity,” it’s remarkable that the label persists while the concepts underpinning it have evolved significantly. So perhaps it is more about finding the least-worst option rather than pursuing the impossibility of a solution that suits all?

This is precisely the challenge faced by a Lancet Diabetes & Endocrinology Commission on the Definition and Diagnosis of Clinical Obesity, which is due to publish its initial findings this coming fall. The global task force has 60 leaders in the clinical management of obesity, including representatives with lived experiences of obesity. Leading the project is Francesco Rubino, MD, chair of metabolic and bariatric surgery at King’s College London.

“Renaming ‘obesity’ is very important,” states Dr. Rubino. “The word is so stigmatized, with so much misunderstanding and misperception, some might say the only solution is to change the name.”

One possibility for a new name, introduced by the American Association of Clinical Endocrinologists (now –Endocrinology) and the American College of Endocrinology back in 2016, was based on framing the disease on the central characteristic of adiposity and was termed ABCD, for adiposity-based chronic disease.

Dr. Rubino welcomes “ABCD” but has some reservations. “It is good from a physiological point of view, but the problem is it speaks to scientists and medical professionals. I don’t know how much it would appeal to the general public. ‘ABCD’ still falls short of telling us what the illness is.”

He adds that the Lancet Commission’s approach is rather to call it “clinical obesity.” “ ‘Obesity’ itself doesn’t necessarily convey the message that you have a disease or an illness,” he observes. “It is similar to the difference in meaning between depression and clinical depression, which communicate two different things.”

But underpinning any renaming is greater clarification of the definition and diagnosis of obesity. In 1997, the World Health Organization recognized obesity as a chronic disease; in 2013, the American Medical Association did likewise, adding that it warranted medical attention; while it took until 2021 for the European Commission to define obesity as a “chronic relapsing disease, which in turn acts as a gateway to a range of other non-communicable diseases.”

Yet, 25 years after the initial recognition of obesity as a disease, the concept is still riddled with negativity, whether openly or unconsciously. Such stigma denigrates overweight people and those with obesity as “lazy, sloppy, unintelligent, and unattractive.”

Dr. Rubino explains that first, it’s important to establish and define the essential components and characteristics of the disease of obesity. This is key to improving access to clinical care, reducing personal blame, and nurturing a more supportive research environment to help inform both clinical and policy decision-making.

“This is the question that is at the core of our commission. We have a problem with the current definition of obesity, and the way we measure it does not allow us to accurately define a state of illness with obesity,” he explains.
 

Labels shape public perceptions of disease; ‘obesity’ epitomizes this

Another expert championing the need for a name that better reflects the definition – whatever that turns out to be – is Margaret Steele, PhD, School of Public Health, University College Cork (Ireland), who, according to her university webpage, has a special interest in “ ‘fatness’ as a cultural, social and political phenomenon.”

She believes that labels, including “obesity,” have a pivotal role in shaping public perceptions. In our digital, information-rich age, the boundaries of medicine and society overlap, with public perception shaping decisions of a medical nature as never before. But with this comes controversy and division – obesity management being a case in point.

Specifically, the word “obesity” is too widely associated with negative connotations, she says, and therefore she welcomes the dialogue around redefining and renaming it. Despite wide general support for a name and definition that reflects adiposity, due to its central physiologic role in the complications of obesity, Dr. Steele believes that the “effects on adipose tissue are downstream of brain issues and the food environment,” and she wants to see more attention brought to this.

Referring to most Westernized societies, she describes how people who grew up in times of food scarcity, before processed foods became widely available, have a different taste profile from those who grew up afterwards. “Growing up in 1940s and ‘50s Ireland, people recall how they remember getting an orange as a treat at Christmas, because the idea that you could have food all year-round – any fruit and veg that you want, when you want it – just wasn’t there.”

By comparison, societal changes leading to more financial and time pressure in later decades meant that fast, high-fat, high-sugar, and processed foods became more desirable, she points out. “Most young children now recognize the company name, and even the specific fast-food brand [they like], before they know their alphabet.”

The current environment has cultivated “a very different physical reaction to foods, maybe a different kind of emotional response,” she believes, highlighting the tightly woven relationship between obesity, society, mental health, and food options.

Dr. Steele wants to stimulate a conversation about the term used to describe individuals, conventionally described as ‘”obese” or using the word “obesity.” “We’re thinking in terms of maybe chronic appetite, chronic food intake, or dietary intake dysregulation.”

Changing medical terminology when it has become useless or harmful is not new, she argues, with co-author, Francis Finucane, MD, consultant endocrinologist at Galway University Hospitals, Ireland, in a recent paper on the subject.

“In the 20th century, the terms ‘feeble-minded’ and ‘moron’ had become used in a pejorative way in the wider culture and were dropped from medical usage,” Dr. Steele points out. She adds that changing the term “obesity” can facilitate pursuit of the strategic goals of clinical medicine “without causing needless controversy with those who, given their own goals and contexts, understand body mass index or body weight in a radically different way.”
 

Obesity: Disease, risk factor, or both?

Dr. Rubino stresses that prior to any renaming, there is a need to establish and define the essential components and characteristics of the disease of obesity. “This question is at the core of our Commission, and it is not an easy conversation to have.” He further explains that the struggle with the current definition of obesity, and the way it is conceived, is largely centered on it still being considered a risk factor for something else.

Disease is characterized by three things, says Dr. Rubino. These comprise the phenomenon of having a pathogenic cause, leading to pathophysiologic alterations (of the organs), causing clinical manifestations.

He adds that obesity is currently described by what it can cause – for example, type 2 diabetes, cancer, or hypertension. “Each of these things have their own clinical manifestations but obesity doesn’t. [As a disease], we don’t have a definition of the clinical manifestations of obesity other than excess adiposity.”

“If we use BMI, this does not predict excess adiposity, nor does it determine a disease here and now. There is no disease without an illness, which is the clinical manifestation, and the perception by the patient of it being an illness,” explains Dr. Rubino, pointing out that the Lancet Commission is filling this gap in knowledge by asking, “If obesity is an illness, then what does it look like?”

He adds that waist circumference probably provides a better measure than BMI in directly indicating the abnormal distribution of adiposity, known to be associated with poor cardiometabolic outcomes, “but it doesn’t tell you if you have an illness here and now – only that someone is at risk of developing cardiovascular disease in the future. Most people with some excess fat around the waist are perfectly functional and don’t feel ill.”

He also explains that confusion persists around whether obesity – or excess adiposity – is a risk factor for or a symptom of another disease. “The picture is blurred, and we do not know how to discriminate between these. We only have one name, and it applies to all those things, and we have one criterion – BMI – to diagnose it!”

Dr. Rubino adds, “So, what defines it? Is it diabetes? No, because that is another disease. You don’t define a disease by another. It has to stand on its own.”

Recently, the American Medical Association advised that BMI now be used in conjunction with other valid measures of risk such as, but not limited to, measurements of visceral fat, body adiposity index, body composition, relative fat mass, waist circumference, and genetic/metabolic factors.

Aayush Visaria, MD, an internal medicine resident at Rutgers University, New Brunswick, New Jersey, agrees that a new name might help change public perception of obesity for the better. A study he presented at the 2023 Endocrine Society Meeting found that BMI “vastly underestimates” obesity.

He agrees with Dr. Rubino that the challenge lies in the lack of precise understanding of the mechanisms driving obesity: “It’s multifactorial, so not just appetite or food intake. Putting this into one phrase is difficult.”

However, if a new term can incorporate the many facets of the disease, “overall, it’ll reduce stigma because we’ll start to think about obesity as a disease process, not a personal thing with blame attached,” says Dr. Visaria.

But simultaneously, he expresses caution around possible negative connotations associated with the classification of obesity as a disease. Dr. Steele also reflects on this risk, highlighting that medicalizing body size can be counterproductive in feeding into weight stigma and fatphobia.

“Medicalizing obesity can be discouraging rather than empowering, but by specifying more clearly that we’re talking about a specific set of interrelated metabolic conditions, it would make it much clearer, and that ... this isn’t about making people skinny, it isn’t about an aesthetic thing,” Dr. Steele observes.
 

The word ‘obesity’ hinders disease explanations

Dr. Steele explains that her goal is to overcome the ambiguity around the word “obesity” that hinders explanations of the disease of obesity to the wider public.

“Much confusion and controversy might be avoided if we were to clarify that when doctors say that obesity is a disease, they do not mean that being ‘fat’ is a disease.”

Nevertheless, adipose tissue is an active endocrine organ, producing hormones that function less well in people with obesity, she notes. “This new knowledge has led to better treatments, including drugs like semaglutide and tirzepatide. These drugs, like bariatric surgery, typically lead to significant weight loss and to improvements in overall metabolic health.”

Dr. Rubino also expresses concerns around medicalization, as determined by definition and diagnosis and the availability of drug treatment that could potentially lead to overtreatment. “Currently, when everyone with a BMI of greater than 30 gets access to every obesity treatment out there, we see drugs are running out of stock. We should prioritize that treatment.”

Ultimately, the diagnosis of obesity as a disease needs an anthropometric biomarker that provides, on an individual level, the confidence that a person has a disease today, or at least close to a 100% likelihood of developing this disease and illness, asserts Dr. Rubino.

“If we use BMI, or even waist circumference, these might diagnose the disease; but if the person lives to 90 years, what’s the point of labeling somebody as having an illness?” he points out.

“As doctors, we have to be cautious. We say this is a disease, but you must think about the implications for the person on the receiving end of that diagnosis of a chronic disease that is substantially incurable. When we say it, we need to be certain.”

Dr. Steele and Dr. Visaria have disclosed no relevant financial relationships. Dr. Rubino disclosed that he has received research grants from Novo Nordisk, Medtronic, and Johnson & Johnson. He has undertaken paid consultancy work for GI Dynamics and received honoraria for lectures from Medtronic, Novo Nordisk, and Johnson & Johnson. He is a member of the data safety monitoring board for GT Metabolic Solutions and has provided scientific advice to Keyron, Metadeq, GHP Scientific, and ViBo Health for no remuneration.

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

Use of dural-puncture epidural (DPE) shortened the onset time to surgical anesthesia by approximately 3 minutes, compared with standard epidural in patients undergoing cesarean delivery, based on data from 140 individuals.

DPE, while not new, has become more popular as an option for initiating labor analgesia, but data comparing DPE with standard epidural in conversion to surgical anesthesia for cesarean deliveries are limited, Nadir Sharawi, MD, of the University of Arkansas for Medical Sciences, Little Rock, and colleagues wrote.

courtesy University of Arkansas for Medical Sciences

DPE involves no injection of intrathecal drugs, and the potential advantages include easier translocation of epidural medications into the intrathecal space for improved analgesia, but the effects of DPE on the onset and reliability of surgical anesthesia remain unknown, they said.

In a study published in JAMA Network Open, the researchers randomized 70 women scheduled for cesarean delivery of singleton pregnancies to DPE and 70 to a standard epidural. The participants were aged 18 years and older, with a mean age of the 30.1 years; the study was conducted between April 2019 and October 2022 at a single center.

The primary outcome was the time to the loss of sharp sensation at T6, defined as “the start of epidural extension anesthesia (time zero on the stopwatch) to when the patient could no longer feel sharp sensation at T6 (assessed bilaterally at the midclavicular line),” the researchers wrote.

The onset time to surgical anesthesia was faster in the DPE group, compared with the standard group, with a median of 422 seconds versus 655 seconds.

A key secondary outcome was a composite measure of the quality of epidural anesthesia that included failure to achieve a T10 bilateral block preoperatively in the delivery room, failure to achieve a surgical block at T6 within 15 minutes of chloroprocaine administration, requirement for intraoperative analgesia, repeat neuraxial procedure, and conversion to general anesthesia. The composite rates of lower quality anesthesia were significantly less in the DPE group, compared with the standard group (15.7% vs. 36.3%; P = .007).

Additional secondary outcomes included maternal satisfaction and pain score during surgery, adverse events, opioid use in the first 24 hours, maternal vasopressor requirements, epidural block assessments, and neonatal outcomes. No significant differences in these outcomes were noted between the groups, and no instances of local anesthetic systemic toxicity or neurological complications were reported.

The findings were limited by several factors including the study population of women scheduled for cesarean delivery and not in labor, and the inability to detect less frequent complications such as post–dural-puncture headache and accidental dural puncture, the researchers noted.

In addition, the results may vary with the use of other combinations of local anesthetics and opioids. “Chloroprocaine was chosen in this study because of its ease of administration without the need for opioids and other additives along with the low risk of systemic toxic effects, which favors rapid administration for emergent cesarean delivery,” they wrote.

However, the results show an association between DPE within an hour of epidural extension for elective cesarean delivery and a faster onset of anesthesia, improved block quality, and a more favorable ratio of risks versus benefits, compared with the use of standard epidural, the researchers concluded.
 

No need for general anesthesia?

“There is controversy over whether the dural puncture epidural technique improves labor analgesia when compared to a standard epidural,” Dr. Shawari said in an interview. “However, there are limited data on whether the dural puncture epidural technique decreases the onset time to surgical anesthesia when compared to a standard epidural for cesarean delivery. This is important as a pre-existing epidural is commonly used to convert labor analgesia to surgical anesthesia in the setting of urgent cesarean delivery. A faster onset of epidural anesthesia could potentially avoid the need for general anesthesia in an emergency.”

The researchers were not surprised by the findings given their experience with performing dural puncture epidurals for labor analgesia, Dr. Shawari said. In those cases, DPE provided a faster onset when converting cesarean anesthesia, compared with a standard epidural.

The takeaway from the current study is that DPE also provided “a faster onset and improved quality of anesthesia when compared to standard epidural for elective cesarean delivery,” Dr. Shawari said. However, additional research is needed to confirm the findings for intrapartum cesarean delivery.
 

Progress in improving pain control

“Adequate pain control during cesarean delivery is incredibly important,” Catherine Albright, MD, a maternal-fetal medicine specialist at the University of Washington, Seattle, said in an interview. “Inadequate pain control leads to the need to provide additional intravenous medications or the need to be put under general anesthesia, which changes the birth experience and is more dangerous for the birthing person and the neonate.

courtesy University of Washington

“In my clinical experience, there are many times when patients do not have adequate pain control during a cesarean delivery,” said Dr. Albright, who was not involved in the current study. “I am pleased to see that there is research underway about how to best manage pain on labor and delivery, especially in the setting of conversion from labor anesthesia to cesarean anesthesia.”

The findings may have implications for clinical practice, said Dr. Albright. If the dural puncture epidural can improve cesarean anesthesia following an epidural during labor, rather than anesthesia provided for an elective cesarean), “then I believe it would reduce the number of patients who require additional pain medication, have a poor cesarean experience, and/or need to be put under general anesthesia.”

However, “as noted by the authors, additional research is needed to further determine possible risks and side effects from this technique, and also to ensure that it also works in the setting of labor, rather than for an elective cesarean,” Dr. Albright added.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. Albright had no financial conflicts to disclose.

Use of dural-puncture epidural (DPE) shortened the onset time to surgical anesthesia by approximately 3 minutes, compared with standard epidural in patients undergoing cesarean delivery, based on data from 140 individuals.

DPE, while not new, has become more popular as an option for initiating labor analgesia, but data comparing DPE with standard epidural in conversion to surgical anesthesia for cesarean deliveries are limited, Nadir Sharawi, MD, of the University of Arkansas for Medical Sciences, Little Rock, and colleagues wrote.

courtesy University of Arkansas for Medical Sciences

DPE involves no injection of intrathecal drugs, and the potential advantages include easier translocation of epidural medications into the intrathecal space for improved analgesia, but the effects of DPE on the onset and reliability of surgical anesthesia remain unknown, they said.

In a study published in JAMA Network Open, the researchers randomized 70 women scheduled for cesarean delivery of singleton pregnancies to DPE and 70 to a standard epidural. The participants were aged 18 years and older, with a mean age of the 30.1 years; the study was conducted between April 2019 and October 2022 at a single center.

The primary outcome was the time to the loss of sharp sensation at T6, defined as “the start of epidural extension anesthesia (time zero on the stopwatch) to when the patient could no longer feel sharp sensation at T6 (assessed bilaterally at the midclavicular line),” the researchers wrote.

The onset time to surgical anesthesia was faster in the DPE group, compared with the standard group, with a median of 422 seconds versus 655 seconds.

A key secondary outcome was a composite measure of the quality of epidural anesthesia that included failure to achieve a T10 bilateral block preoperatively in the delivery room, failure to achieve a surgical block at T6 within 15 minutes of chloroprocaine administration, requirement for intraoperative analgesia, repeat neuraxial procedure, and conversion to general anesthesia. The composite rates of lower quality anesthesia were significantly less in the DPE group, compared with the standard group (15.7% vs. 36.3%; P = .007).

Additional secondary outcomes included maternal satisfaction and pain score during surgery, adverse events, opioid use in the first 24 hours, maternal vasopressor requirements, epidural block assessments, and neonatal outcomes. No significant differences in these outcomes were noted between the groups, and no instances of local anesthetic systemic toxicity or neurological complications were reported.

The findings were limited by several factors including the study population of women scheduled for cesarean delivery and not in labor, and the inability to detect less frequent complications such as post–dural-puncture headache and accidental dural puncture, the researchers noted.

In addition, the results may vary with the use of other combinations of local anesthetics and opioids. “Chloroprocaine was chosen in this study because of its ease of administration without the need for opioids and other additives along with the low risk of systemic toxic effects, which favors rapid administration for emergent cesarean delivery,” they wrote.

However, the results show an association between DPE within an hour of epidural extension for elective cesarean delivery and a faster onset of anesthesia, improved block quality, and a more favorable ratio of risks versus benefits, compared with the use of standard epidural, the researchers concluded.
 

No need for general anesthesia?

“There is controversy over whether the dural puncture epidural technique improves labor analgesia when compared to a standard epidural,” Dr. Shawari said in an interview. “However, there are limited data on whether the dural puncture epidural technique decreases the onset time to surgical anesthesia when compared to a standard epidural for cesarean delivery. This is important as a pre-existing epidural is commonly used to convert labor analgesia to surgical anesthesia in the setting of urgent cesarean delivery. A faster onset of epidural anesthesia could potentially avoid the need for general anesthesia in an emergency.”

The researchers were not surprised by the findings given their experience with performing dural puncture epidurals for labor analgesia, Dr. Shawari said. In those cases, DPE provided a faster onset when converting cesarean anesthesia, compared with a standard epidural.

The takeaway from the current study is that DPE also provided “a faster onset and improved quality of anesthesia when compared to standard epidural for elective cesarean delivery,” Dr. Shawari said. However, additional research is needed to confirm the findings for intrapartum cesarean delivery.
 

Progress in improving pain control

“Adequate pain control during cesarean delivery is incredibly important,” Catherine Albright, MD, a maternal-fetal medicine specialist at the University of Washington, Seattle, said in an interview. “Inadequate pain control leads to the need to provide additional intravenous medications or the need to be put under general anesthesia, which changes the birth experience and is more dangerous for the birthing person and the neonate.

courtesy University of Washington

“In my clinical experience, there are many times when patients do not have adequate pain control during a cesarean delivery,” said Dr. Albright, who was not involved in the current study. “I am pleased to see that there is research underway about how to best manage pain on labor and delivery, especially in the setting of conversion from labor anesthesia to cesarean anesthesia.”

The findings may have implications for clinical practice, said Dr. Albright. If the dural puncture epidural can improve cesarean anesthesia following an epidural during labor, rather than anesthesia provided for an elective cesarean), “then I believe it would reduce the number of patients who require additional pain medication, have a poor cesarean experience, and/or need to be put under general anesthesia.”

However, “as noted by the authors, additional research is needed to further determine possible risks and side effects from this technique, and also to ensure that it also works in the setting of labor, rather than for an elective cesarean,” Dr. Albright added.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. Albright had no financial conflicts to disclose.

Use of dural-puncture epidural (DPE) shortened the onset time to surgical anesthesia by approximately 3 minutes, compared with standard epidural in patients undergoing cesarean delivery, based on data from 140 individuals.

DPE, while not new, has become more popular as an option for initiating labor analgesia, but data comparing DPE with standard epidural in conversion to surgical anesthesia for cesarean deliveries are limited, Nadir Sharawi, MD, of the University of Arkansas for Medical Sciences, Little Rock, and colleagues wrote.

courtesy University of Arkansas for Medical Sciences

DPE involves no injection of intrathecal drugs, and the potential advantages include easier translocation of epidural medications into the intrathecal space for improved analgesia, but the effects of DPE on the onset and reliability of surgical anesthesia remain unknown, they said.

In a study published in JAMA Network Open, the researchers randomized 70 women scheduled for cesarean delivery of singleton pregnancies to DPE and 70 to a standard epidural. The participants were aged 18 years and older, with a mean age of the 30.1 years; the study was conducted between April 2019 and October 2022 at a single center.

The primary outcome was the time to the loss of sharp sensation at T6, defined as “the start of epidural extension anesthesia (time zero on the stopwatch) to when the patient could no longer feel sharp sensation at T6 (assessed bilaterally at the midclavicular line),” the researchers wrote.

The onset time to surgical anesthesia was faster in the DPE group, compared with the standard group, with a median of 422 seconds versus 655 seconds.

A key secondary outcome was a composite measure of the quality of epidural anesthesia that included failure to achieve a T10 bilateral block preoperatively in the delivery room, failure to achieve a surgical block at T6 within 15 minutes of chloroprocaine administration, requirement for intraoperative analgesia, repeat neuraxial procedure, and conversion to general anesthesia. The composite rates of lower quality anesthesia were significantly less in the DPE group, compared with the standard group (15.7% vs. 36.3%; P = .007).

Additional secondary outcomes included maternal satisfaction and pain score during surgery, adverse events, opioid use in the first 24 hours, maternal vasopressor requirements, epidural block assessments, and neonatal outcomes. No significant differences in these outcomes were noted between the groups, and no instances of local anesthetic systemic toxicity or neurological complications were reported.

The findings were limited by several factors including the study population of women scheduled for cesarean delivery and not in labor, and the inability to detect less frequent complications such as post–dural-puncture headache and accidental dural puncture, the researchers noted.

In addition, the results may vary with the use of other combinations of local anesthetics and opioids. “Chloroprocaine was chosen in this study because of its ease of administration without the need for opioids and other additives along with the low risk of systemic toxic effects, which favors rapid administration for emergent cesarean delivery,” they wrote.

However, the results show an association between DPE within an hour of epidural extension for elective cesarean delivery and a faster onset of anesthesia, improved block quality, and a more favorable ratio of risks versus benefits, compared with the use of standard epidural, the researchers concluded.
 

No need for general anesthesia?

“There is controversy over whether the dural puncture epidural technique improves labor analgesia when compared to a standard epidural,” Dr. Shawari said in an interview. “However, there are limited data on whether the dural puncture epidural technique decreases the onset time to surgical anesthesia when compared to a standard epidural for cesarean delivery. This is important as a pre-existing epidural is commonly used to convert labor analgesia to surgical anesthesia in the setting of urgent cesarean delivery. A faster onset of epidural anesthesia could potentially avoid the need for general anesthesia in an emergency.”

The researchers were not surprised by the findings given their experience with performing dural puncture epidurals for labor analgesia, Dr. Shawari said. In those cases, DPE provided a faster onset when converting cesarean anesthesia, compared with a standard epidural.

The takeaway from the current study is that DPE also provided “a faster onset and improved quality of anesthesia when compared to standard epidural for elective cesarean delivery,” Dr. Shawari said. However, additional research is needed to confirm the findings for intrapartum cesarean delivery.
 

Progress in improving pain control

“Adequate pain control during cesarean delivery is incredibly important,” Catherine Albright, MD, a maternal-fetal medicine specialist at the University of Washington, Seattle, said in an interview. “Inadequate pain control leads to the need to provide additional intravenous medications or the need to be put under general anesthesia, which changes the birth experience and is more dangerous for the birthing person and the neonate.

courtesy University of Washington

“In my clinical experience, there are many times when patients do not have adequate pain control during a cesarean delivery,” said Dr. Albright, who was not involved in the current study. “I am pleased to see that there is research underway about how to best manage pain on labor and delivery, especially in the setting of conversion from labor anesthesia to cesarean anesthesia.”

The findings may have implications for clinical practice, said Dr. Albright. If the dural puncture epidural can improve cesarean anesthesia following an epidural during labor, rather than anesthesia provided for an elective cesarean), “then I believe it would reduce the number of patients who require additional pain medication, have a poor cesarean experience, and/or need to be put under general anesthesia.”

However, “as noted by the authors, additional research is needed to further determine possible risks and side effects from this technique, and also to ensure that it also works in the setting of labor, rather than for an elective cesarean,” Dr. Albright added.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. Albright had no financial conflicts to disclose.

Deanna Denham Hughes was stunned when she was diagnosed with ovarian cancer in 2022. She was only 32. She had no family history of cancer, and tests found no genetic link. Ms. Hughes wondered why she, an otherwise healthy Black mother of two, would develop a malignancy known as a “silent killer.”

After emergency surgery to remove the mass, along with her ovaries, uterus, fallopian tubes, and appendix, Ms. Hughes said, she saw an Instagram post in which a woman with uterine cancer linked her condition to chemical hair straighteners.

“I almost fell over,” she said from her home in Smyrna, Ga.

When Ms. Hughes was about 4, her mother began applying a chemical straightener, or relaxer, to her hair every 6-8 weeks. “It burned, and it smelled awful,” Ms. Hughes recalled. “But it was just part of our routine to ‘deal with my hair.’ ”

The routine continued until she went to college and met other Black women who wore their hair naturally. Soon, Ms. Hughes quit relaxers.

Social and economic pressures have long compelled Black girls and women to straighten their hair to conform to Eurocentric beauty standards. But chemical straighteners are stinky and costly and sometimes cause painful scalp burns. Mounting evidence now shows they could be a health hazard.

Relaxers can contain carcinogens, such as formaldehyde-releasing agents, phthalates, and other endocrine-disrupting compounds, according to National Institutes of Health studies. The compounds can mimic the body’s hormones and have been linked to breast, uterine, and ovarian cancers, studies show.

African American women’s often frequent and lifelong application of chemical relaxers to their hair and scalp might explain why hormone-related cancers kill disproportionately more Black than White women, say researchers and cancer doctors.

“What’s in these products is harmful,” said Tamarra James-Todd, PhD, an epidemiology professor at Harvard T.H. Chan School of Public Health, Boston, who has studied straightening products for the past 20 years.

She believes manufacturers, policymakers, and physicians should warn consumers that relaxers might cause cancer and other health problems.

But regulators have been slow to act, physicians have been reluctant to take up the cause, and racism continues to dictate fashion standards that make it tough for women to quit relaxers, products so addictive they’re known as “creamy crack.”

Michelle Obama straightened her hair when Barack Obama served as president because she believed Americans were “not ready” to see her in braids, the former first lady said after leaving the White House. The U.S. military still prohibited popular Black hairstyles such as dreadlocks and twists while the nation’s first Black president was in office.

California in 2019 became the first of nearly two dozen states to ban race-based hair discrimination. Last year, the U.S. House of Representatives passed similar legislation, known as the CROWN Act, for Creating a Respectful and Open World for Natural Hair. But the bill failed in the Senate.

The need for legislation underscores the challenges Black girls and women face at school and in the workplace.

“You have to pick your struggles,” said Atlanta-based surgical oncologist Ryland J. Gore, MD. She informs her breast cancer patients about the increased cancer risk from relaxers. Despite her knowledge, however, Dr. Gore continues to use chemical straighteners on her own hair, as she has since she was about 7 years old.

“Your hair tells a story,” she said.

In conversations with patients, Dr. Gore sometimes talks about how African American women once wove messages into their braids about the route to take on the Underground Railroad as they sought freedom from slavery.

“It’s just a deep discussion,” one that touches on culture, history, and research into current hairstyling practices, she said. “The data is out there. So patients should be warned, and then they can make a decision.”

The first hint of a connection between hair products and health issues surfaced in the 1990s. Doctors began seeing signs of sexual maturation in Black babies and young girls who developed breasts and pubic hair after using shampoo containing estrogen or placental extract. When the girls stopped using the shampoo, the hair and breast development receded, according to a study published in the journal Clinical Pediatrics in 1998.

Since then, Dr. James-Todd and other researchers have linked chemicals in hair products to a variety of health issues more prevalent among Black women – from early puberty to preterm birth, obesity, and diabetes.

In recent years, researchers have focused on a possible connection between ingredients in chemical relaxers and hormone-related cancers, like the one Ms. Hughes developed, which tend to be more aggressive and deadly in Black women.

A 2017 study found White women who used chemical relaxers were nearly twice as likely to develop breast cancer as those who did not use them. Because the vast majority of the Black study participants used relaxers, researchers could not effectively test the association in Black women, said lead author Adana Llanos, PhD, associate professor of epidemiology at Columbia University’s Mailman School of Public Health, New York.

Researchers did test it in 2020.

The so-called Sister Study, a landmark National Institute of Environmental Health Sciences investigation into the causes of breast cancer and related diseases, followed 50,000 U.S. women whose sisters had been diagnosed with breast cancer and who were cancer-free when they enrolled. Regardless of race, women who reported using relaxers in the prior year were 18% more likely to be diagnosed with breast cancer. Those who used relaxers at least every 5-8 weeks had a 31% higher breast cancer risk.

Nearly 75% of the Black sisters used relaxers in the prior year, compared with 3% of the non-Hispanic White sisters. Three-quarters of Black women self-reported using the straighteners as adolescents, and frequent use of chemical straighteners during adolescence raised the risk of premenopausal breast cancer, a 2021 NIH-funded study in the International Journal of Cancer found.

Another 2021 analysis of the Sister Study data showed sisters who self-reported that they frequently used relaxers or pressing products doubled their ovarian cancer risk. In 2022, another study found frequent use more than doubled uterine cancer risk.

After researchers discovered the link with uterine cancer, some called for policy changes and other measures to reduce exposure to chemical relaxers.

“It is time to intervene,” Dr. Llanos and her colleagues wrote in a Journal of the National Cancer Institute editorial accompanying the uterine cancer analysis. While acknowledging the need for more research, they issued a “call for action.”

No one can say that using permanent hair straighteners will give you cancer, Dr. Llanos said in an interview. “That’s not how cancer works,” she said, noting that some smokers never develop lung cancer, despite tobacco use being a known risk factor.

The body of research linking hair straighteners and cancer is more limited, said Dr. Llanos, who quit using chemical relaxers 15 years ago. But, she asked rhetorically, “Do we need to do the research for 50 more years to know that chemical relaxers are harmful?”

Charlotte R. Gamble, MD, a gynecological oncologist whose Washington, D.C., practice includes Black women with uterine and ovarian cancer, said she and her colleagues see the uterine cancer study findings as worthy of further exploration – but not yet worthy of discussion with patients.

“The jury’s out for me personally,” she said. “There’s so much more data that’s needed.”

Meanwhile, Dr. James-Todd and other researchers believe they have built a solid body of evidence.

“There are enough things we do know to begin taking action, developing interventions, providing useful information to clinicians and patients and the general public,” said Traci N. Bethea, PhD, assistant professor in the Office of Minority Health and Health Disparities Research at Georgetown University.

Responsibility for regulating personal-care products, including chemical hair straighteners and hair dyes – which also have been linked to hormone-related cancers – lies with the Food and Drug Administration. But the FDA does not subject personal-care products to the same approval process it uses for food and drugs. The FDA restricts only 11 categories of chemicals used in cosmetics, while concerns about health effects have prompted the European Union to restrict the use of at least 2,400 substances.

In March, Reps. Ayanna Pressley (D-Mass.) and Shontel Brown (D-Ohio) asked the FDA to investigate the potential health threat posed by chemical relaxers. An FDA representative said the agency would look into it.

Natural hairstyles are enjoying a resurgence among Black girls and women, but many continue to rely on the creamy crack, said Dede Teteh, DrPH, assistant professor of public health at Chapman University, Irvine, Calif.

She had her first straightening perm at 8 and has struggled to withdraw from relaxers as an adult, said Dr. Teteh, who now wears locs. Not long ago, she considered chemically straightening her hair for an academic job interview because she didn’t want her hair to “be a hindrance” when she appeared before White professors.

Dr. Teteh led “The Cost of Beauty,” a hair-health research project published in 2017. She and her team interviewed 91 Black women in Southern California. Some became “combative” at the idea of quitting relaxers and claimed “everything can cause cancer.”

Their reactions speak to the challenges Black women face in America, Dr. Teteh said.

“It’s not that people do not want to hear the information related to their health,” she said. “But they want people to share the information in a way that it’s really empathetic to the plight of being Black here in the United States.”
 

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF – the independent source for health policy research, polling, and journalism.

Deanna Denham Hughes was stunned when she was diagnosed with ovarian cancer in 2022. She was only 32. She had no family history of cancer, and tests found no genetic link. Ms. Hughes wondered why she, an otherwise healthy Black mother of two, would develop a malignancy known as a “silent killer.”

After emergency surgery to remove the mass, along with her ovaries, uterus, fallopian tubes, and appendix, Ms. Hughes said, she saw an Instagram post in which a woman with uterine cancer linked her condition to chemical hair straighteners.

“I almost fell over,” she said from her home in Smyrna, Ga.

When Ms. Hughes was about 4, her mother began applying a chemical straightener, or relaxer, to her hair every 6-8 weeks. “It burned, and it smelled awful,” Ms. Hughes recalled. “But it was just part of our routine to ‘deal with my hair.’ ”

The routine continued until she went to college and met other Black women who wore their hair naturally. Soon, Ms. Hughes quit relaxers.

Social and economic pressures have long compelled Black girls and women to straighten their hair to conform to Eurocentric beauty standards. But chemical straighteners are stinky and costly and sometimes cause painful scalp burns. Mounting evidence now shows they could be a health hazard.

Relaxers can contain carcinogens, such as formaldehyde-releasing agents, phthalates, and other endocrine-disrupting compounds, according to National Institutes of Health studies. The compounds can mimic the body’s hormones and have been linked to breast, uterine, and ovarian cancers, studies show.

African American women’s often frequent and lifelong application of chemical relaxers to their hair and scalp might explain why hormone-related cancers kill disproportionately more Black than White women, say researchers and cancer doctors.

“What’s in these products is harmful,” said Tamarra James-Todd, PhD, an epidemiology professor at Harvard T.H. Chan School of Public Health, Boston, who has studied straightening products for the past 20 years.

She believes manufacturers, policymakers, and physicians should warn consumers that relaxers might cause cancer and other health problems.

But regulators have been slow to act, physicians have been reluctant to take up the cause, and racism continues to dictate fashion standards that make it tough for women to quit relaxers, products so addictive they’re known as “creamy crack.”

Michelle Obama straightened her hair when Barack Obama served as president because she believed Americans were “not ready” to see her in braids, the former first lady said after leaving the White House. The U.S. military still prohibited popular Black hairstyles such as dreadlocks and twists while the nation’s first Black president was in office.

California in 2019 became the first of nearly two dozen states to ban race-based hair discrimination. Last year, the U.S. House of Representatives passed similar legislation, known as the CROWN Act, for Creating a Respectful and Open World for Natural Hair. But the bill failed in the Senate.

The need for legislation underscores the challenges Black girls and women face at school and in the workplace.

“You have to pick your struggles,” said Atlanta-based surgical oncologist Ryland J. Gore, MD. She informs her breast cancer patients about the increased cancer risk from relaxers. Despite her knowledge, however, Dr. Gore continues to use chemical straighteners on her own hair, as she has since she was about 7 years old.

“Your hair tells a story,” she said.

In conversations with patients, Dr. Gore sometimes talks about how African American women once wove messages into their braids about the route to take on the Underground Railroad as they sought freedom from slavery.

“It’s just a deep discussion,” one that touches on culture, history, and research into current hairstyling practices, she said. “The data is out there. So patients should be warned, and then they can make a decision.”

The first hint of a connection between hair products and health issues surfaced in the 1990s. Doctors began seeing signs of sexual maturation in Black babies and young girls who developed breasts and pubic hair after using shampoo containing estrogen or placental extract. When the girls stopped using the shampoo, the hair and breast development receded, according to a study published in the journal Clinical Pediatrics in 1998.

Since then, Dr. James-Todd and other researchers have linked chemicals in hair products to a variety of health issues more prevalent among Black women – from early puberty to preterm birth, obesity, and diabetes.

In recent years, researchers have focused on a possible connection between ingredients in chemical relaxers and hormone-related cancers, like the one Ms. Hughes developed, which tend to be more aggressive and deadly in Black women.

A 2017 study found White women who used chemical relaxers were nearly twice as likely to develop breast cancer as those who did not use them. Because the vast majority of the Black study participants used relaxers, researchers could not effectively test the association in Black women, said lead author Adana Llanos, PhD, associate professor of epidemiology at Columbia University’s Mailman School of Public Health, New York.

Researchers did test it in 2020.

The so-called Sister Study, a landmark National Institute of Environmental Health Sciences investigation into the causes of breast cancer and related diseases, followed 50,000 U.S. women whose sisters had been diagnosed with breast cancer and who were cancer-free when they enrolled. Regardless of race, women who reported using relaxers in the prior year were 18% more likely to be diagnosed with breast cancer. Those who used relaxers at least every 5-8 weeks had a 31% higher breast cancer risk.

Nearly 75% of the Black sisters used relaxers in the prior year, compared with 3% of the non-Hispanic White sisters. Three-quarters of Black women self-reported using the straighteners as adolescents, and frequent use of chemical straighteners during adolescence raised the risk of premenopausal breast cancer, a 2021 NIH-funded study in the International Journal of Cancer found.

Another 2021 analysis of the Sister Study data showed sisters who self-reported that they frequently used relaxers or pressing products doubled their ovarian cancer risk. In 2022, another study found frequent use more than doubled uterine cancer risk.

After researchers discovered the link with uterine cancer, some called for policy changes and other measures to reduce exposure to chemical relaxers.

“It is time to intervene,” Dr. Llanos and her colleagues wrote in a Journal of the National Cancer Institute editorial accompanying the uterine cancer analysis. While acknowledging the need for more research, they issued a “call for action.”

No one can say that using permanent hair straighteners will give you cancer, Dr. Llanos said in an interview. “That’s not how cancer works,” she said, noting that some smokers never develop lung cancer, despite tobacco use being a known risk factor.

The body of research linking hair straighteners and cancer is more limited, said Dr. Llanos, who quit using chemical relaxers 15 years ago. But, she asked rhetorically, “Do we need to do the research for 50 more years to know that chemical relaxers are harmful?”

Charlotte R. Gamble, MD, a gynecological oncologist whose Washington, D.C., practice includes Black women with uterine and ovarian cancer, said she and her colleagues see the uterine cancer study findings as worthy of further exploration – but not yet worthy of discussion with patients.

“The jury’s out for me personally,” she said. “There’s so much more data that’s needed.”

Meanwhile, Dr. James-Todd and other researchers believe they have built a solid body of evidence.

“There are enough things we do know to begin taking action, developing interventions, providing useful information to clinicians and patients and the general public,” said Traci N. Bethea, PhD, assistant professor in the Office of Minority Health and Health Disparities Research at Georgetown University.

Responsibility for regulating personal-care products, including chemical hair straighteners and hair dyes – which also have been linked to hormone-related cancers – lies with the Food and Drug Administration. But the FDA does not subject personal-care products to the same approval process it uses for food and drugs. The FDA restricts only 11 categories of chemicals used in cosmetics, while concerns about health effects have prompted the European Union to restrict the use of at least 2,400 substances.

In March, Reps. Ayanna Pressley (D-Mass.) and Shontel Brown (D-Ohio) asked the FDA to investigate the potential health threat posed by chemical relaxers. An FDA representative said the agency would look into it.

Natural hairstyles are enjoying a resurgence among Black girls and women, but many continue to rely on the creamy crack, said Dede Teteh, DrPH, assistant professor of public health at Chapman University, Irvine, Calif.

She had her first straightening perm at 8 and has struggled to withdraw from relaxers as an adult, said Dr. Teteh, who now wears locs. Not long ago, she considered chemically straightening her hair for an academic job interview because she didn’t want her hair to “be a hindrance” when she appeared before White professors.

Dr. Teteh led “The Cost of Beauty,” a hair-health research project published in 2017. She and her team interviewed 91 Black women in Southern California. Some became “combative” at the idea of quitting relaxers and claimed “everything can cause cancer.”

Their reactions speak to the challenges Black women face in America, Dr. Teteh said.

“It’s not that people do not want to hear the information related to their health,” she said. “But they want people to share the information in a way that it’s really empathetic to the plight of being Black here in the United States.”
 

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF – the independent source for health policy research, polling, and journalism.

Deanna Denham Hughes was stunned when she was diagnosed with ovarian cancer in 2022. She was only 32. She had no family history of cancer, and tests found no genetic link. Ms. Hughes wondered why she, an otherwise healthy Black mother of two, would develop a malignancy known as a “silent killer.”

After emergency surgery to remove the mass, along with her ovaries, uterus, fallopian tubes, and appendix, Ms. Hughes said, she saw an Instagram post in which a woman with uterine cancer linked her condition to chemical hair straighteners.

“I almost fell over,” she said from her home in Smyrna, Ga.

When Ms. Hughes was about 4, her mother began applying a chemical straightener, or relaxer, to her hair every 6-8 weeks. “It burned, and it smelled awful,” Ms. Hughes recalled. “But it was just part of our routine to ‘deal with my hair.’ ”

The routine continued until she went to college and met other Black women who wore their hair naturally. Soon, Ms. Hughes quit relaxers.

Social and economic pressures have long compelled Black girls and women to straighten their hair to conform to Eurocentric beauty standards. But chemical straighteners are stinky and costly and sometimes cause painful scalp burns. Mounting evidence now shows they could be a health hazard.

Relaxers can contain carcinogens, such as formaldehyde-releasing agents, phthalates, and other endocrine-disrupting compounds, according to National Institutes of Health studies. The compounds can mimic the body’s hormones and have been linked to breast, uterine, and ovarian cancers, studies show.

African American women’s often frequent and lifelong application of chemical relaxers to their hair and scalp might explain why hormone-related cancers kill disproportionately more Black than White women, say researchers and cancer doctors.

“What’s in these products is harmful,” said Tamarra James-Todd, PhD, an epidemiology professor at Harvard T.H. Chan School of Public Health, Boston, who has studied straightening products for the past 20 years.

She believes manufacturers, policymakers, and physicians should warn consumers that relaxers might cause cancer and other health problems.

But regulators have been slow to act, physicians have been reluctant to take up the cause, and racism continues to dictate fashion standards that make it tough for women to quit relaxers, products so addictive they’re known as “creamy crack.”

Michelle Obama straightened her hair when Barack Obama served as president because she believed Americans were “not ready” to see her in braids, the former first lady said after leaving the White House. The U.S. military still prohibited popular Black hairstyles such as dreadlocks and twists while the nation’s first Black president was in office.

California in 2019 became the first of nearly two dozen states to ban race-based hair discrimination. Last year, the U.S. House of Representatives passed similar legislation, known as the CROWN Act, for Creating a Respectful and Open World for Natural Hair. But the bill failed in the Senate.

The need for legislation underscores the challenges Black girls and women face at school and in the workplace.

“You have to pick your struggles,” said Atlanta-based surgical oncologist Ryland J. Gore, MD. She informs her breast cancer patients about the increased cancer risk from relaxers. Despite her knowledge, however, Dr. Gore continues to use chemical straighteners on her own hair, as she has since she was about 7 years old.

“Your hair tells a story,” she said.

In conversations with patients, Dr. Gore sometimes talks about how African American women once wove messages into their braids about the route to take on the Underground Railroad as they sought freedom from slavery.

“It’s just a deep discussion,” one that touches on culture, history, and research into current hairstyling practices, she said. “The data is out there. So patients should be warned, and then they can make a decision.”

The first hint of a connection between hair products and health issues surfaced in the 1990s. Doctors began seeing signs of sexual maturation in Black babies and young girls who developed breasts and pubic hair after using shampoo containing estrogen or placental extract. When the girls stopped using the shampoo, the hair and breast development receded, according to a study published in the journal Clinical Pediatrics in 1998.

Since then, Dr. James-Todd and other researchers have linked chemicals in hair products to a variety of health issues more prevalent among Black women – from early puberty to preterm birth, obesity, and diabetes.

In recent years, researchers have focused on a possible connection between ingredients in chemical relaxers and hormone-related cancers, like the one Ms. Hughes developed, which tend to be more aggressive and deadly in Black women.

A 2017 study found White women who used chemical relaxers were nearly twice as likely to develop breast cancer as those who did not use them. Because the vast majority of the Black study participants used relaxers, researchers could not effectively test the association in Black women, said lead author Adana Llanos, PhD, associate professor of epidemiology at Columbia University’s Mailman School of Public Health, New York.

Researchers did test it in 2020.

The so-called Sister Study, a landmark National Institute of Environmental Health Sciences investigation into the causes of breast cancer and related diseases, followed 50,000 U.S. women whose sisters had been diagnosed with breast cancer and who were cancer-free when they enrolled. Regardless of race, women who reported using relaxers in the prior year were 18% more likely to be diagnosed with breast cancer. Those who used relaxers at least every 5-8 weeks had a 31% higher breast cancer risk.

Nearly 75% of the Black sisters used relaxers in the prior year, compared with 3% of the non-Hispanic White sisters. Three-quarters of Black women self-reported using the straighteners as adolescents, and frequent use of chemical straighteners during adolescence raised the risk of premenopausal breast cancer, a 2021 NIH-funded study in the International Journal of Cancer found.

Another 2021 analysis of the Sister Study data showed sisters who self-reported that they frequently used relaxers or pressing products doubled their ovarian cancer risk. In 2022, another study found frequent use more than doubled uterine cancer risk.

After researchers discovered the link with uterine cancer, some called for policy changes and other measures to reduce exposure to chemical relaxers.

“It is time to intervene,” Dr. Llanos and her colleagues wrote in a Journal of the National Cancer Institute editorial accompanying the uterine cancer analysis. While acknowledging the need for more research, they issued a “call for action.”

No one can say that using permanent hair straighteners will give you cancer, Dr. Llanos said in an interview. “That’s not how cancer works,” she said, noting that some smokers never develop lung cancer, despite tobacco use being a known risk factor.

The body of research linking hair straighteners and cancer is more limited, said Dr. Llanos, who quit using chemical relaxers 15 years ago. But, she asked rhetorically, “Do we need to do the research for 50 more years to know that chemical relaxers are harmful?”

Charlotte R. Gamble, MD, a gynecological oncologist whose Washington, D.C., practice includes Black women with uterine and ovarian cancer, said she and her colleagues see the uterine cancer study findings as worthy of further exploration – but not yet worthy of discussion with patients.

“The jury’s out for me personally,” she said. “There’s so much more data that’s needed.”

Meanwhile, Dr. James-Todd and other researchers believe they have built a solid body of evidence.

“There are enough things we do know to begin taking action, developing interventions, providing useful information to clinicians and patients and the general public,” said Traci N. Bethea, PhD, assistant professor in the Office of Minority Health and Health Disparities Research at Georgetown University.

Responsibility for regulating personal-care products, including chemical hair straighteners and hair dyes – which also have been linked to hormone-related cancers – lies with the Food and Drug Administration. But the FDA does not subject personal-care products to the same approval process it uses for food and drugs. The FDA restricts only 11 categories of chemicals used in cosmetics, while concerns about health effects have prompted the European Union to restrict the use of at least 2,400 substances.

In March, Reps. Ayanna Pressley (D-Mass.) and Shontel Brown (D-Ohio) asked the FDA to investigate the potential health threat posed by chemical relaxers. An FDA representative said the agency would look into it.

Natural hairstyles are enjoying a resurgence among Black girls and women, but many continue to rely on the creamy crack, said Dede Teteh, DrPH, assistant professor of public health at Chapman University, Irvine, Calif.

She had her first straightening perm at 8 and has struggled to withdraw from relaxers as an adult, said Dr. Teteh, who now wears locs. Not long ago, she considered chemically straightening her hair for an academic job interview because she didn’t want her hair to “be a hindrance” when she appeared before White professors.

Dr. Teteh led “The Cost of Beauty,” a hair-health research project published in 2017. She and her team interviewed 91 Black women in Southern California. Some became “combative” at the idea of quitting relaxers and claimed “everything can cause cancer.”

Their reactions speak to the challenges Black women face in America, Dr. Teteh said.

“It’s not that people do not want to hear the information related to their health,” she said. “But they want people to share the information in a way that it’s really empathetic to the plight of being Black here in the United States.”
 

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF – the independent source for health policy research, polling, and journalism.

The Food and Drug Administration has approved the first oral agent specifically for postpartum depression, a condition that affects an estimated one in seven mothers in the United States.

The pill, zuranolone (Zurzuvae), is a neuroactive steroid that acts on GABAA receptors in the brain responsible for regulating mood, arousal, behavior, and cognition, according to Biogen, which, along with Sage Therapeutics, developed the product. The recommended dose for Zurzuvae is 50 mg taken once daily for 14 days, in the evening with a fatty meal, according to the FDA.

Olivier Le Moal/Getty Images

Postpartum depression often goes undiagnosed and untreated. Many mothers are hesitant to reveal their symptoms to family and clinicians, fearing they’ll be judged on their parenting. A 2017 study found that suicide accounted for roughly 5% of perinatal deaths among women in Canada, with most of those deaths occurring in the first 3 months in the year after giving birth.

“Postpartum depression is a serious and potentially life-threatening condition in which women experience sadness, guilt, worthlessness – even, in severe cases, thoughts of harming themselves or their child. And, because postpartum depression can disrupt the maternal-infant bond, it can also have consequences for the child’s physical and emotional development,” Tiffany R. Farchione, MD, director of the division of psychiatry at the FDA’s Center for Drug Evaluation and Research, said in a statement about the approval. “Having access to an oral medication will be a beneficial option for many of these women coping with extreme, and sometimes life-threatening, feelings.”

The other approved therapy for postpartum depression is the intravenous agent brexanolone (Zulresso; Sage). But the product requires prolonged infusions in hospital settings and costs $34,000.

FDA approval of Zurzuvae was based in part on data reported in a 2023 study in the American Journal of Psychiatry, which showed that the drug led to significantly greater improvement in depressive symptoms at 15 days compared with the placebo group. Improvements were observed on day 3, the earliest assessment, and were sustained at all subsequent visits during the treatment and follow-up period (through day 42).

Patients with anxiety who received the active drug experienced improvement in related symptoms compared with the patients who received a placebo.

The most common adverse events reported in the trial were somnolence and headaches. Weight gain, sexual dysfunction, withdrawal symptoms, and increased suicidal ideation or behavior were not observed.

The packaging for Zurzuvae will include a boxed warning noting that the drug can affect a user’s ability to drive and perform other potentially hazardous activities, possibly without their knowledge of the impairment, the FDA said. As a result, people who use Zurzuvae should not drive or operate heavy machinery for at least 12 hours after taking the pill.

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

The Food and Drug Administration has approved the first oral agent specifically for postpartum depression, a condition that affects an estimated one in seven mothers in the United States.

The pill, zuranolone (Zurzuvae), is a neuroactive steroid that acts on GABAA receptors in the brain responsible for regulating mood, arousal, behavior, and cognition, according to Biogen, which, along with Sage Therapeutics, developed the product. The recommended dose for Zurzuvae is 50 mg taken once daily for 14 days, in the evening with a fatty meal, according to the FDA.

Olivier Le Moal/Getty Images

Postpartum depression often goes undiagnosed and untreated. Many mothers are hesitant to reveal their symptoms to family and clinicians, fearing they’ll be judged on their parenting. A 2017 study found that suicide accounted for roughly 5% of perinatal deaths among women in Canada, with most of those deaths occurring in the first 3 months in the year after giving birth.

“Postpartum depression is a serious and potentially life-threatening condition in which women experience sadness, guilt, worthlessness – even, in severe cases, thoughts of harming themselves or their child. And, because postpartum depression can disrupt the maternal-infant bond, it can also have consequences for the child’s physical and emotional development,” Tiffany R. Farchione, MD, director of the division of psychiatry at the FDA’s Center for Drug Evaluation and Research, said in a statement about the approval. “Having access to an oral medication will be a beneficial option for many of these women coping with extreme, and sometimes life-threatening, feelings.”

The other approved therapy for postpartum depression is the intravenous agent brexanolone (Zulresso; Sage). But the product requires prolonged infusions in hospital settings and costs $34,000.

FDA approval of Zurzuvae was based in part on data reported in a 2023 study in the American Journal of Psychiatry, which showed that the drug led to significantly greater improvement in depressive symptoms at 15 days compared with the placebo group. Improvements were observed on day 3, the earliest assessment, and were sustained at all subsequent visits during the treatment and follow-up period (through day 42).

Patients with anxiety who received the active drug experienced improvement in related symptoms compared with the patients who received a placebo.

The most common adverse events reported in the trial were somnolence and headaches. Weight gain, sexual dysfunction, withdrawal symptoms, and increased suicidal ideation or behavior were not observed.

The packaging for Zurzuvae will include a boxed warning noting that the drug can affect a user’s ability to drive and perform other potentially hazardous activities, possibly without their knowledge of the impairment, the FDA said. As a result, people who use Zurzuvae should not drive or operate heavy machinery for at least 12 hours after taking the pill.

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

The Food and Drug Administration has approved the first oral agent specifically for postpartum depression, a condition that affects an estimated one in seven mothers in the United States.

The pill, zuranolone (Zurzuvae), is a neuroactive steroid that acts on GABAA receptors in the brain responsible for regulating mood, arousal, behavior, and cognition, according to Biogen, which, along with Sage Therapeutics, developed the product. The recommended dose for Zurzuvae is 50 mg taken once daily for 14 days, in the evening with a fatty meal, according to the FDA.

Olivier Le Moal/Getty Images

Postpartum depression often goes undiagnosed and untreated. Many mothers are hesitant to reveal their symptoms to family and clinicians, fearing they’ll be judged on their parenting. A 2017 study found that suicide accounted for roughly 5% of perinatal deaths among women in Canada, with most of those deaths occurring in the first 3 months in the year after giving birth.

“Postpartum depression is a serious and potentially life-threatening condition in which women experience sadness, guilt, worthlessness – even, in severe cases, thoughts of harming themselves or their child. And, because postpartum depression can disrupt the maternal-infant bond, it can also have consequences for the child’s physical and emotional development,” Tiffany R. Farchione, MD, director of the division of psychiatry at the FDA’s Center for Drug Evaluation and Research, said in a statement about the approval. “Having access to an oral medication will be a beneficial option for many of these women coping with extreme, and sometimes life-threatening, feelings.”

The other approved therapy for postpartum depression is the intravenous agent brexanolone (Zulresso; Sage). But the product requires prolonged infusions in hospital settings and costs $34,000.

FDA approval of Zurzuvae was based in part on data reported in a 2023 study in the American Journal of Psychiatry, which showed that the drug led to significantly greater improvement in depressive symptoms at 15 days compared with the placebo group. Improvements were observed on day 3, the earliest assessment, and were sustained at all subsequent visits during the treatment and follow-up period (through day 42).

Patients with anxiety who received the active drug experienced improvement in related symptoms compared with the patients who received a placebo.

The most common adverse events reported in the trial were somnolence and headaches. Weight gain, sexual dysfunction, withdrawal symptoms, and increased suicidal ideation or behavior were not observed.

The packaging for Zurzuvae will include a boxed warning noting that the drug can affect a user’s ability to drive and perform other potentially hazardous activities, possibly without their knowledge of the impairment, the FDA said. As a result, people who use Zurzuvae should not drive or operate heavy machinery for at least 12 hours after taking the pill.

A version of this article first 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.

TOPLINE:

Five scleroderma immune responses have associations with cancer risk and could be used to stratify patients, researchers argue.

METHODOLOGY:

• Included patients from the Johns Hopkins Scleroderma Center Research Registry and the University of Pittsburgh Scleroderma Center, Pittsburgh.
• A total of 676 patients with scleroderma and a history of cancer were compared with 687 control patients with scleroderma but without a history of cancer.
• Serum tested via line blot and enzyme-linked immunosorbent assay for an array of scleroderma autoantibodies.
• Examined association between autoantibodies and overall cancer risk.

TAKEAWAYS:

• Anti-POLR3 and monospecific anti-Ro52 were associated with significantly increased overall cancer risk.
• Anti-centromere and anti-U1RNP were associated with a decreased cancer risk.
• These associations remained when looking specifically at cancer-associated scleroderma.
• Patients positive for anti-Ro52 in combination with either anti-U1RNP or anti-Th/To had a decreased risk of cancer, compared with those who had anti-Ro52 alone.

IN PRACTICE:

This study is too preliminary to have practice application.

SOURCE:

Ji Soo Kim, PhD, of John Hopkins University, Baltimore, was the first author of the study, published in Arthritis & Rheumatology on July 24, 2023. Fellow Johns Hopkins researchers Livia Casciola-Rosen, PhD, and Ami A. Shah, MD, were joint senior authors.

DISCLOSURES:

The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Donald B. and Dorothy L. Stabler Foundation, the Jerome L. Greene Foundation, the Chresanthe Staurulakis Memorial Discovery Fund, the Martha McCrory Professorship, and the Johns Hopkins inHealth initiative. The authors disclosed the following patents or patent applications: Autoimmune Antigens and Cancer, Materials and Methods for Assessing Cancer Risk and Treating Cancer.

A version of this article appeared on Medscape.com.

TOPLINE:

Five scleroderma immune responses have associations with cancer risk and could be used to stratify patients, researchers argue.

METHODOLOGY:

• Included patients from the Johns Hopkins Scleroderma Center Research Registry and the University of Pittsburgh Scleroderma Center, Pittsburgh.
• A total of 676 patients with scleroderma and a history of cancer were compared with 687 control patients with scleroderma but without a history of cancer.
• Serum tested via line blot and enzyme-linked immunosorbent assay for an array of scleroderma autoantibodies.
• Examined association between autoantibodies and overall cancer risk.

TAKEAWAYS:

• Anti-POLR3 and monospecific anti-Ro52 were associated with significantly increased overall cancer risk.
• Anti-centromere and anti-U1RNP were associated with a decreased cancer risk.
• These associations remained when looking specifically at cancer-associated scleroderma.
• Patients positive for anti-Ro52 in combination with either anti-U1RNP or anti-Th/To had a decreased risk of cancer, compared with those who had anti-Ro52 alone.

IN PRACTICE:

This study is too preliminary to have practice application.

SOURCE:

Ji Soo Kim, PhD, of John Hopkins University, Baltimore, was the first author of the study, published in Arthritis & Rheumatology on July 24, 2023. Fellow Johns Hopkins researchers Livia Casciola-Rosen, PhD, and Ami A. Shah, MD, were joint senior authors.

DISCLOSURES:

The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Donald B. and Dorothy L. Stabler Foundation, the Jerome L. Greene Foundation, the Chresanthe Staurulakis Memorial Discovery Fund, the Martha McCrory Professorship, and the Johns Hopkins inHealth initiative. The authors disclosed the following patents or patent applications: Autoimmune Antigens and Cancer, Materials and Methods for Assessing Cancer Risk and Treating Cancer.

A version of this article appeared on Medscape.com.

TOPLINE:

Five scleroderma immune responses have associations with cancer risk and could be used to stratify patients, researchers argue.

METHODOLOGY:

• Included patients from the Johns Hopkins Scleroderma Center Research Registry and the University of Pittsburgh Scleroderma Center, Pittsburgh.
• A total of 676 patients with scleroderma and a history of cancer were compared with 687 control patients with scleroderma but without a history of cancer.
• Serum tested via line blot and enzyme-linked immunosorbent assay for an array of scleroderma autoantibodies.
• Examined association between autoantibodies and overall cancer risk.

TAKEAWAYS:

• Anti-POLR3 and monospecific anti-Ro52 were associated with significantly increased overall cancer risk.
• Anti-centromere and anti-U1RNP were associated with a decreased cancer risk.
• These associations remained when looking specifically at cancer-associated scleroderma.
• Patients positive for anti-Ro52 in combination with either anti-U1RNP or anti-Th/To had a decreased risk of cancer, compared with those who had anti-Ro52 alone.

IN PRACTICE:

This study is too preliminary to have practice application.

SOURCE:

Ji Soo Kim, PhD, of John Hopkins University, Baltimore, was the first author of the study, published in Arthritis & Rheumatology on July 24, 2023. Fellow Johns Hopkins researchers Livia Casciola-Rosen, PhD, and Ami A. Shah, MD, were joint senior authors.

DISCLOSURES:

The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Donald B. and Dorothy L. Stabler Foundation, the Jerome L. Greene Foundation, the Chresanthe Staurulakis Memorial Discovery Fund, the Martha McCrory Professorship, and the Johns Hopkins inHealth initiative. The authors disclosed the following patents or patent applications: Autoimmune Antigens and Cancer, Materials and Methods for Assessing Cancer Risk and Treating Cancer.

A version of this article appeared on Medscape.com.

Most people hear “firm handshake” and automatically think “business world.” A cursory search reveals articles with titles like “Seven Super-Revealing Things Your Handshake Said About You” (Forbes) and “How a Handshake Can Tell You Everything You Need to Know About a Person” (Inc).

Those in the know, however, understand what a handshake really reveals: Current health and vitality. The amount of force that can be generated by the hand is a valid proxy for total-body strength. And total-body strength is one key to healthy aging.

Body temperature, weight, heart rate, and blood pressure inform any patient appointment. Should physicians include grip strength in that group?

Grip-strength testing is easy, fast, and noninvasive. It can be monitored over time. All it requires is a handgrip dynamometer, a tool that may cost less than a stethoscope, and a chair.

“Many studies have looked at strength as a predictor of positive health and weakness as a predictor of negative health outcomes,” said Mark Peterson, PhD, an associate professor at the University of Michigan, Ann Arbor, who’s worked on dozens of those studies.

Among the health risks associated with low grip strength: type 2 diabetes, heart disease, cancer, dementia and Alzheimer’s disease, depression, functional disability, osteoporosis, and premature death from any cause.

The prognostic merits of grip strength have been documented across continents and cultures. Although most of those studies have focused on older adults, they aren’t the only age group researchers have looked at.

“We have several papers on the value of grip strength for predicting diabetes and cardiovascular disease in children and adolescents,” Dr. Peterson said.
 

Survival of the strongest

The first thing to understand about grip-strength testing is that it’s only partially about grip. It’s mostly about strength. That’s what attracted Dr. Peterson to this line of research.

“I’m a former strength coach, so I wanted to make a case for why strength was important across populations, not just athletes,” he said. “I strongly believe in strength preservation and healthy living as a predictor for longevity.”

Consider a classic study of Swedish army recruits. Because of Sweden’s post–World War II conscription policy, virtually every young male in the country underwent a physical examination to see if they were fit for military service – an exam that included a grip-strength test.

That gave the researchers a database with more than a million participants. They followed up on them decades later through publicly available records.

What they found: The men with the weakest grip strength in their late teens were 20% more likely to have died by their mid-50s, compared with those with moderate to high grip strength. Even suicide rates were 20%-30% higher for the weakest recruits.

There’s a brutal Darwinian logic to the idea that a stronger person with a more powerful grip would enjoy a longer, healthier life. To our ancient ancestors, stronger hands meant they were probably better at everything that aided survival: hunting, fighting, building shelter, as well as bearing, transporting, and rearing children.

Fast forward to the 21st century where we must force ourselves to engage in physical activity. The old rules still apply: Strength aids survival.
 

Grip strength and the aging process

Some of the earliest grip-strength studies used it as a proxy for nutritional status in elderly men and women. Nourishment, in turn, predicted their ability to survive an illness or surgery.

Which makes sense; if an older person isn’t eating enough to maintain their health and vitality, their strength would decline. Declining strength would make them more susceptible to infections, hospitalizations, and postsurgical complications, leading to longer hospital stays, loss of independence, and ultimately a higher risk of death from any cause.

Along those lines, Dr. Peterson’s research team at the University of Michigan found that low grip strength is correlated with faster aging at the cellular level.

The study looked at DNA methylation, which Peterson describes as “a reflection of someone’s exposure to life events.”

For example, someone who smokes will have altered methylation patterns, compared with someone who doesn’t. Same with someone who’s had more exposure to environmental pollution.

Accelerated DNA methylation “means you’re essentially at higher risk for what are traditionally considered age-related chronic conditions,” Dr. Peterson said. Those conditions include Alzheimer’s, type 2 diabetes, chronic inflammation, and a higher risk for premature mortality.

Those things are also linked to low grip strength, which is linked to higher DNA methylation and faster biological aging.

But there’s still a missing piece of the puzzle: Why, exactly, would the strength of one’s grip be associated with so many health outcomes?
 

Grip strength and muscle function

“Declining muscle function is the first step of the disabling process,” said Ryan McGrath, PhD, an assistant professor at North Dakota State University, Fargo. “That’s what you can measure with a handgrip test. It helps you identify individuals at risk for the next step of the process, which is declines in physical performance.”

Dr. McGrath got involved in grip-strength research as a postdoctoral fellow at the University of Michigan, where he worked with Peterson. Like his mentor, he’s published multiple studies using data obtained with a handgrip dynamometer.

“It can be a nice tool for assessing muscle function and muscle strength,” he explained. Because the test is so easy to administer – you sit in a chair with your arm at your side and your elbow bent 90 degrees, and squeeze the device as hard as you can – researchers can work with large groups of study participants and come away with statistically powerful data.

“There are a lot of health outcomes it’s associated with,” Dr. McGrath added, “which is one of its greatest strengths and at the same time one of its key limitations.”

He compared the dynamometer with a tire gauge. Just as a tire gauge can alert you to a loss of air pressure without revealing the source of the leak, a dynamometer can’t tell you why your grip strength is deflated.

“It’s hard to specify the prognostic value,” he said. “You don’t know the next steps to take. As a standalone measurement, that’s a concern.”

That’s why his current research goes beyond simple tests of maximum grip strength to more sophisticated measurements of the rate of force development (how fast you can express strength), repeatability (how much your strength declines from your first to your second or third squeeze), and asymmetry (how big a gap there is between your right- and left-hand strength).

Any of those measures could detect a potential neural or neuromuscular issue.

In a 2020 study, for example, Dr. McGrath and his team at NDSU showed that older adults with both weakness and asymmetry in grip-strength tests were nearly four times more likely to experience functional limitations. Those limitations could affect their ability to do anything from routine chores to keeping themselves clean and fed.
 

Waging war on weakness

Using dynamometer readings, the generally accepted cutoffs for low grip strength are 26 kg for an adult male and 16 kg for a female.

But that’s way too simple, Dr. Peterson said.

For one thing, age matters. Grip strength typically peaks for men in their late 20s and declines rapidly in middle age and beyond. For women, it plateaus in their 20s and gently declines until their 50s. So, at minimum, the age-based standards included with a dynamometer should be consulted.

Another caveat: Dr. Peterson said grip strength tests aren’t very meaningful for people who actively train for strength, though he suggests dedicated athletes make up a relatively small percentage of the population – even as low as 10%.

The size of the person taking the test is also important.

“You absolutely must account for body mass in the context of understanding how grip strength, or any strength measure, is reflective of health and function,” Dr. Peterson said.

To calculate strength-weight ratio, which Dr. Peterson calls “normalized grip strength,” divide grip strength in kilograms by body weight in kilograms. For men, a ratio greater than 0.70 puts them in the higher percentiles. For women it’s 0.50.

And if the results suggest that the person in question is objectively weak? “For me, that’s easy,” Dr. Peterson said. “They need to exercise.”

Common sense suggests doing a lot of forearm exercises for grip strength. Not so, said Dr. Peterson. The strength of hand and forearm muscles reflects what they can do along with all other muscles moving together.

A 2019 study found that, for older adults, a variety of exercise programs can lead to modest but meaningful increases in participants’ grip strength – and they don’t necessarily have to include actual gripping exercises. The programs ranged from tai chi to water aerobics to walking, stretching, and all kinds of resistance training.

Dr. Peterson’s advice to everyone is pretty straightforward: Get stronger. It doesn’t really matter how you do it, or how much strength you ultimately gain. Even a little more strength means a little less weakness, and a little more life.

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

Most people hear “firm handshake” and automatically think “business world.” A cursory search reveals articles with titles like “Seven Super-Revealing Things Your Handshake Said About You” (Forbes) and “How a Handshake Can Tell You Everything You Need to Know About a Person” (Inc).

Those in the know, however, understand what a handshake really reveals: Current health and vitality. The amount of force that can be generated by the hand is a valid proxy for total-body strength. And total-body strength is one key to healthy aging.

Body temperature, weight, heart rate, and blood pressure inform any patient appointment. Should physicians include grip strength in that group?

Grip-strength testing is easy, fast, and noninvasive. It can be monitored over time. All it requires is a handgrip dynamometer, a tool that may cost less than a stethoscope, and a chair.

“Many studies have looked at strength as a predictor of positive health and weakness as a predictor of negative health outcomes,” said Mark Peterson, PhD, an associate professor at the University of Michigan, Ann Arbor, who’s worked on dozens of those studies.

Among the health risks associated with low grip strength: type 2 diabetes, heart disease, cancer, dementia and Alzheimer’s disease, depression, functional disability, osteoporosis, and premature death from any cause.

The prognostic merits of grip strength have been documented across continents and cultures. Although most of those studies have focused on older adults, they aren’t the only age group researchers have looked at.

“We have several papers on the value of grip strength for predicting diabetes and cardiovascular disease in children and adolescents,” Dr. Peterson said.
 

Survival of the strongest

The first thing to understand about grip-strength testing is that it’s only partially about grip. It’s mostly about strength. That’s what attracted Dr. Peterson to this line of research.

“I’m a former strength coach, so I wanted to make a case for why strength was important across populations, not just athletes,” he said. “I strongly believe in strength preservation and healthy living as a predictor for longevity.”

Consider a classic study of Swedish army recruits. Because of Sweden’s post–World War II conscription policy, virtually every young male in the country underwent a physical examination to see if they were fit for military service – an exam that included a grip-strength test.

That gave the researchers a database with more than a million participants. They followed up on them decades later through publicly available records.

What they found: The men with the weakest grip strength in their late teens were 20% more likely to have died by their mid-50s, compared with those with moderate to high grip strength. Even suicide rates were 20%-30% higher for the weakest recruits.

There’s a brutal Darwinian logic to the idea that a stronger person with a more powerful grip would enjoy a longer, healthier life. To our ancient ancestors, stronger hands meant they were probably better at everything that aided survival: hunting, fighting, building shelter, as well as bearing, transporting, and rearing children.

Fast forward to the 21st century where we must force ourselves to engage in physical activity. The old rules still apply: Strength aids survival.
 

Grip strength and the aging process

Some of the earliest grip-strength studies used it as a proxy for nutritional status in elderly men and women. Nourishment, in turn, predicted their ability to survive an illness or surgery.

Which makes sense; if an older person isn’t eating enough to maintain their health and vitality, their strength would decline. Declining strength would make them more susceptible to infections, hospitalizations, and postsurgical complications, leading to longer hospital stays, loss of independence, and ultimately a higher risk of death from any cause.

Along those lines, Dr. Peterson’s research team at the University of Michigan found that low grip strength is correlated with faster aging at the cellular level.

The study looked at DNA methylation, which Peterson describes as “a reflection of someone’s exposure to life events.”

For example, someone who smokes will have altered methylation patterns, compared with someone who doesn’t. Same with someone who’s had more exposure to environmental pollution.

Accelerated DNA methylation “means you’re essentially at higher risk for what are traditionally considered age-related chronic conditions,” Dr. Peterson said. Those conditions include Alzheimer’s, type 2 diabetes, chronic inflammation, and a higher risk for premature mortality.

Those things are also linked to low grip strength, which is linked to higher DNA methylation and faster biological aging.

But there’s still a missing piece of the puzzle: Why, exactly, would the strength of one’s grip be associated with so many health outcomes?
 

Grip strength and muscle function

“Declining muscle function is the first step of the disabling process,” said Ryan McGrath, PhD, an assistant professor at North Dakota State University, Fargo. “That’s what you can measure with a handgrip test. It helps you identify individuals at risk for the next step of the process, which is declines in physical performance.”

Dr. McGrath got involved in grip-strength research as a postdoctoral fellow at the University of Michigan, where he worked with Peterson. Like his mentor, he’s published multiple studies using data obtained with a handgrip dynamometer.

“It can be a nice tool for assessing muscle function and muscle strength,” he explained. Because the test is so easy to administer – you sit in a chair with your arm at your side and your elbow bent 90 degrees, and squeeze the device as hard as you can – researchers can work with large groups of study participants and come away with statistically powerful data.

“There are a lot of health outcomes it’s associated with,” Dr. McGrath added, “which is one of its greatest strengths and at the same time one of its key limitations.”

He compared the dynamometer with a tire gauge. Just as a tire gauge can alert you to a loss of air pressure without revealing the source of the leak, a dynamometer can’t tell you why your grip strength is deflated.

“It’s hard to specify the prognostic value,” he said. “You don’t know the next steps to take. As a standalone measurement, that’s a concern.”

That’s why his current research goes beyond simple tests of maximum grip strength to more sophisticated measurements of the rate of force development (how fast you can express strength), repeatability (how much your strength declines from your first to your second or third squeeze), and asymmetry (how big a gap there is between your right- and left-hand strength).

Any of those measures could detect a potential neural or neuromuscular issue.

In a 2020 study, for example, Dr. McGrath and his team at NDSU showed that older adults with both weakness and asymmetry in grip-strength tests were nearly four times more likely to experience functional limitations. Those limitations could affect their ability to do anything from routine chores to keeping themselves clean and fed.
 

Waging war on weakness

Using dynamometer readings, the generally accepted cutoffs for low grip strength are 26 kg for an adult male and 16 kg for a female.

But that’s way too simple, Dr. Peterson said.

For one thing, age matters. Grip strength typically peaks for men in their late 20s and declines rapidly in middle age and beyond. For women, it plateaus in their 20s and gently declines until their 50s. So, at minimum, the age-based standards included with a dynamometer should be consulted.

Another caveat: Dr. Peterson said grip strength tests aren’t very meaningful for people who actively train for strength, though he suggests dedicated athletes make up a relatively small percentage of the population – even as low as 10%.

The size of the person taking the test is also important.

“You absolutely must account for body mass in the context of understanding how grip strength, or any strength measure, is reflective of health and function,” Dr. Peterson said.

To calculate strength-weight ratio, which Dr. Peterson calls “normalized grip strength,” divide grip strength in kilograms by body weight in kilograms. For men, a ratio greater than 0.70 puts them in the higher percentiles. For women it’s 0.50.

And if the results suggest that the person in question is objectively weak? “For me, that’s easy,” Dr. Peterson said. “They need to exercise.”

Common sense suggests doing a lot of forearm exercises for grip strength. Not so, said Dr. Peterson. The strength of hand and forearm muscles reflects what they can do along with all other muscles moving together.

A 2019 study found that, for older adults, a variety of exercise programs can lead to modest but meaningful increases in participants’ grip strength – and they don’t necessarily have to include actual gripping exercises. The programs ranged from tai chi to water aerobics to walking, stretching, and all kinds of resistance training.

Dr. Peterson’s advice to everyone is pretty straightforward: Get stronger. It doesn’t really matter how you do it, or how much strength you ultimately gain. Even a little more strength means a little less weakness, and a little more life.

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

Most people hear “firm handshake” and automatically think “business world.” A cursory search reveals articles with titles like “Seven Super-Revealing Things Your Handshake Said About You” (Forbes) and “How a Handshake Can Tell You Everything You Need to Know About a Person” (Inc).

Those in the know, however, understand what a handshake really reveals: Current health and vitality. The amount of force that can be generated by the hand is a valid proxy for total-body strength. And total-body strength is one key to healthy aging.

Body temperature, weight, heart rate, and blood pressure inform any patient appointment. Should physicians include grip strength in that group?

Grip-strength testing is easy, fast, and noninvasive. It can be monitored over time. All it requires is a handgrip dynamometer, a tool that may cost less than a stethoscope, and a chair.

“Many studies have looked at strength as a predictor of positive health and weakness as a predictor of negative health outcomes,” said Mark Peterson, PhD, an associate professor at the University of Michigan, Ann Arbor, who’s worked on dozens of those studies.

Among the health risks associated with low grip strength: type 2 diabetes, heart disease, cancer, dementia and Alzheimer’s disease, depression, functional disability, osteoporosis, and premature death from any cause.

The prognostic merits of grip strength have been documented across continents and cultures. Although most of those studies have focused on older adults, they aren’t the only age group researchers have looked at.

“We have several papers on the value of grip strength for predicting diabetes and cardiovascular disease in children and adolescents,” Dr. Peterson said.
 

Survival of the strongest

The first thing to understand about grip-strength testing is that it’s only partially about grip. It’s mostly about strength. That’s what attracted Dr. Peterson to this line of research.

“I’m a former strength coach, so I wanted to make a case for why strength was important across populations, not just athletes,” he said. “I strongly believe in strength preservation and healthy living as a predictor for longevity.”

Consider a classic study of Swedish army recruits. Because of Sweden’s post–World War II conscription policy, virtually every young male in the country underwent a physical examination to see if they were fit for military service – an exam that included a grip-strength test.

That gave the researchers a database with more than a million participants. They followed up on them decades later through publicly available records.

What they found: The men with the weakest grip strength in their late teens were 20% more likely to have died by their mid-50s, compared with those with moderate to high grip strength. Even suicide rates were 20%-30% higher for the weakest recruits.

There’s a brutal Darwinian logic to the idea that a stronger person with a more powerful grip would enjoy a longer, healthier life. To our ancient ancestors, stronger hands meant they were probably better at everything that aided survival: hunting, fighting, building shelter, as well as bearing, transporting, and rearing children.

Fast forward to the 21st century where we must force ourselves to engage in physical activity. The old rules still apply: Strength aids survival.
 

Grip strength and the aging process

Some of the earliest grip-strength studies used it as a proxy for nutritional status in elderly men and women. Nourishment, in turn, predicted their ability to survive an illness or surgery.

Which makes sense; if an older person isn’t eating enough to maintain their health and vitality, their strength would decline. Declining strength would make them more susceptible to infections, hospitalizations, and postsurgical complications, leading to longer hospital stays, loss of independence, and ultimately a higher risk of death from any cause.

Along those lines, Dr. Peterson’s research team at the University of Michigan found that low grip strength is correlated with faster aging at the cellular level.

The study looked at DNA methylation, which Peterson describes as “a reflection of someone’s exposure to life events.”

For example, someone who smokes will have altered methylation patterns, compared with someone who doesn’t. Same with someone who’s had more exposure to environmental pollution.

Accelerated DNA methylation “means you’re essentially at higher risk for what are traditionally considered age-related chronic conditions,” Dr. Peterson said. Those conditions include Alzheimer’s, type 2 diabetes, chronic inflammation, and a higher risk for premature mortality.

Those things are also linked to low grip strength, which is linked to higher DNA methylation and faster biological aging.

But there’s still a missing piece of the puzzle: Why, exactly, would the strength of one’s grip be associated with so many health outcomes?
 

Grip strength and muscle function

“Declining muscle function is the first step of the disabling process,” said Ryan McGrath, PhD, an assistant professor at North Dakota State University, Fargo. “That’s what you can measure with a handgrip test. It helps you identify individuals at risk for the next step of the process, which is declines in physical performance.”

Dr. McGrath got involved in grip-strength research as a postdoctoral fellow at the University of Michigan, where he worked with Peterson. Like his mentor, he’s published multiple studies using data obtained with a handgrip dynamometer.

“It can be a nice tool for assessing muscle function and muscle strength,” he explained. Because the test is so easy to administer – you sit in a chair with your arm at your side and your elbow bent 90 degrees, and squeeze the device as hard as you can – researchers can work with large groups of study participants and come away with statistically powerful data.

“There are a lot of health outcomes it’s associated with,” Dr. McGrath added, “which is one of its greatest strengths and at the same time one of its key limitations.”

He compared the dynamometer with a tire gauge. Just as a tire gauge can alert you to a loss of air pressure without revealing the source of the leak, a dynamometer can’t tell you why your grip strength is deflated.

“It’s hard to specify the prognostic value,” he said. “You don’t know the next steps to take. As a standalone measurement, that’s a concern.”

That’s why his current research goes beyond simple tests of maximum grip strength to more sophisticated measurements of the rate of force development (how fast you can express strength), repeatability (how much your strength declines from your first to your second or third squeeze), and asymmetry (how big a gap there is between your right- and left-hand strength).

Any of those measures could detect a potential neural or neuromuscular issue.

In a 2020 study, for example, Dr. McGrath and his team at NDSU showed that older adults with both weakness and asymmetry in grip-strength tests were nearly four times more likely to experience functional limitations. Those limitations could affect their ability to do anything from routine chores to keeping themselves clean and fed.
 

Waging war on weakness

Using dynamometer readings, the generally accepted cutoffs for low grip strength are 26 kg for an adult male and 16 kg for a female.

But that’s way too simple, Dr. Peterson said.

For one thing, age matters. Grip strength typically peaks for men in their late 20s and declines rapidly in middle age and beyond. For women, it plateaus in their 20s and gently declines until their 50s. So, at minimum, the age-based standards included with a dynamometer should be consulted.

Another caveat: Dr. Peterson said grip strength tests aren’t very meaningful for people who actively train for strength, though he suggests dedicated athletes make up a relatively small percentage of the population – even as low as 10%.

The size of the person taking the test is also important.

“You absolutely must account for body mass in the context of understanding how grip strength, or any strength measure, is reflective of health and function,” Dr. Peterson said.

To calculate strength-weight ratio, which Dr. Peterson calls “normalized grip strength,” divide grip strength in kilograms by body weight in kilograms. For men, a ratio greater than 0.70 puts them in the higher percentiles. For women it’s 0.50.

And if the results suggest that the person in question is objectively weak? “For me, that’s easy,” Dr. Peterson said. “They need to exercise.”

Common sense suggests doing a lot of forearm exercises for grip strength. Not so, said Dr. Peterson. The strength of hand and forearm muscles reflects what they can do along with all other muscles moving together.

A 2019 study found that, for older adults, a variety of exercise programs can lead to modest but meaningful increases in participants’ grip strength – and they don’t necessarily have to include actual gripping exercises. The programs ranged from tai chi to water aerobics to walking, stretching, and all kinds of resistance training.

Dr. Peterson’s advice to everyone is pretty straightforward: Get stronger. It doesn’t really matter how you do it, or how much strength you ultimately gain. Even a little more strength means a little less weakness, and a little more life.

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.