Obesity

Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) given to adolescents with obesity was associated with a one-third decreased risk for suicidal ideation and suicide attempts compared with lifestyle intervention alone, a large international retrospective study found.

A study published in JAMA Pediatrics suggested that GLP-1 RAs such as semaglutide, liraglutide, and tirzepatide, which are widely used to treat type 2 diabetes (T2D), have a favorable psychiatric safety profile and open up potential avenues for prospective studies of psychiatric outcomes in adolescents with obesity.

Investigators Liya Kerem, MD, MSc, and Joshua Stokar, MD, of Hadassah University Medical Center in Jerusalem, Israel, reported that the reduced risk in GLP-1 RA recipients was maintained up to 3 years follow-up compared with propensity score–matched controls treated with behavioral interventions alone.

“These findings support the notion that childhood obesity does not result from lack of willpower and shed light on underlying mechanisms that can be targeted by pharmacotherapy.” Kerem and Stokar wrote.

Other research has suggested these agents have neurobiologic effects unrelated to weight loss that positively affect mood and mental health.
 

Study Details

The analysis included data from December 2019 to June 2024, drawn from 120 international healthcare organizations, mainly in the United States. A total of 4052 racially and ethnically diverse adolescents with obesity (aged 12-18 years [mean age, about 15.5 years]) being treated with an anti-obesity intervention were identified for the GLP-1 RA cohort and 50,112 for the control cohort. The arms were balanced for baseline demographic characteristics, psychiatric medications and comorbidities, and diagnoses associated with socioeconomic status and healthcare access.

Propensity score matching (PSM) resulted in 3456 participants in each of two balanced cohorts.

Before PSM, intervention patients were older (mean age, 15.5 vs 14.7 years), were more likely to be female (59% vs 49%), and had a higher body mass index (41.9 vs 33.8). They also had a higher prevalence of diabetes (40% vs 4%) and treatment with antidiabetic medications.

GLP-1 RA recipients also had a history of psychiatric diagnoses (17% vs 9% for mood disorders) and psychiatric medications (18% vs 7% for antidepressants). Previous use of non–GLP-1 RA anti-obesity medications was uncommon in the cohort overall, although more common in the GLP-1 RA cohort (2.5% vs 0.2% for phentermine).

Prescription of GLP-1 RA was associated with a 33% reduced risk for suicidal ideation or attempts over 12 months of follow-up: 1.45% vs 2.26% (hazard ratio [HR], 0.67; 95% CI, 0.47-0.95; P = .02). It was also associated with a higher rate of gastrointestinal symptoms: 6.9% vs 5.4% (HR, 1.41; 95% CI, 1.12-1.78; P = .003). There was no difference in rates of upper respiratory tract infections (URTIs), although some research suggests these agents reduce URTIs.
 

Mechanisms

The etiology of childhood obesity is complex and multifactorial, the authors wrote, and genetic predisposition to adiposity, an obesogenic environment, and a sedentary lifestyle synergistically contribute to its development. Variants in genes active in the hypothalamic appetite-regulation neurocircuitry appear to be associated with the development of childhood and adolescent obesity.

The authors noted that adolescence carries an increased risk for psychiatric disorders and suicidal ideation. “The amelioration of obesity could indirectly improve these psychiatric comorbidities,” they wrote. In addition, preclinical studies suggested that GLP-1 RA may improve depression-related neuropathology, including neuroinflammation and neurotransmitter imbalance, and may promote neurogenesis.

A recent meta-analysis found that adults with T2D treated with GLP-1 RA showed significant reduction in depression scale scores compared with those treated with non-GLP-1 RA antidiabetic medications.

Commenting on the study but not involved in it, psychiatrist Robert H. Dicker, MD, associate director of child and adolescent psychiatry at Northwell Zucker Hillside Hospital in Glen Oaks, New York, cautioned that these are preliminary data limited by a retrospective review, not a prospective double-blind, placebo-controlled study.

“The mechanism is unknown — is it a direct effect on weight loss with an improvement of quality of life, more positive feedback by the community, enhanced ability to exercise, and a decrease in depressive symptoms?” he asked.

Dicker suggested an alternative hypothesis: Does the GLP-1 RA have a direct effect on neurotransmitters and inflammation and, thus, an impact on mood, emotional regulation, impulse control, and suicide?

“To further answer these questions, prospective studies must be conducted. It is far too early to conclude that these medications are effective in treating mood disorders in our youth,” Dicker said. “But it is promising that these treatments do not appear to increase suicidal ideas and behavior.”

Adding another outsider’s perspective on the study, Suzanne E. Cuda, MD, FOMA, FAAP, a pediatrician who treats childhood obesity in San Antonio, said that while there was no risk for increased psychiatric disease and a suggestion that GLP-1 RAs may reduce suicidal ideation or attempts, “I don’t think this translates to a treatment for depression in adolescents. Nor does this study indicate there could be a decrease in depression due specifically to the use of GLP1Rs. If the results in this study are replicated, however, it would be reassuring to know that adolescents would not be at risk for an increase in suicidal ideation or attempts.”

This study had no external funding. Kerem reported receiving personal fees from Novo Nordisk for lectures on childhood obesity outside of the submitted work. No other disclosures were reported. Dicker and Cuda had no competing interests relevant to their comments.

A version of this article appeared on Medscape.com.

Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) given to adolescents with obesity was associated with a one-third decreased risk for suicidal ideation and suicide attempts compared with lifestyle intervention alone, a large international retrospective study found.

A study published in JAMA Pediatrics suggested that GLP-1 RAs such as semaglutide, liraglutide, and tirzepatide, which are widely used to treat type 2 diabetes (T2D), have a favorable psychiatric safety profile and open up potential avenues for prospective studies of psychiatric outcomes in adolescents with obesity.

Investigators Liya Kerem, MD, MSc, and Joshua Stokar, MD, of Hadassah University Medical Center in Jerusalem, Israel, reported that the reduced risk in GLP-1 RA recipients was maintained up to 3 years follow-up compared with propensity score–matched controls treated with behavioral interventions alone.

“These findings support the notion that childhood obesity does not result from lack of willpower and shed light on underlying mechanisms that can be targeted by pharmacotherapy.” Kerem and Stokar wrote.

Other research has suggested these agents have neurobiologic effects unrelated to weight loss that positively affect mood and mental health.
 

Study Details

The analysis included data from December 2019 to June 2024, drawn from 120 international healthcare organizations, mainly in the United States. A total of 4052 racially and ethnically diverse adolescents with obesity (aged 12-18 years [mean age, about 15.5 years]) being treated with an anti-obesity intervention were identified for the GLP-1 RA cohort and 50,112 for the control cohort. The arms were balanced for baseline demographic characteristics, psychiatric medications and comorbidities, and diagnoses associated with socioeconomic status and healthcare access.

Propensity score matching (PSM) resulted in 3456 participants in each of two balanced cohorts.

Before PSM, intervention patients were older (mean age, 15.5 vs 14.7 years), were more likely to be female (59% vs 49%), and had a higher body mass index (41.9 vs 33.8). They also had a higher prevalence of diabetes (40% vs 4%) and treatment with antidiabetic medications.

GLP-1 RA recipients also had a history of psychiatric diagnoses (17% vs 9% for mood disorders) and psychiatric medications (18% vs 7% for antidepressants). Previous use of non–GLP-1 RA anti-obesity medications was uncommon in the cohort overall, although more common in the GLP-1 RA cohort (2.5% vs 0.2% for phentermine).

Prescription of GLP-1 RA was associated with a 33% reduced risk for suicidal ideation or attempts over 12 months of follow-up: 1.45% vs 2.26% (hazard ratio [HR], 0.67; 95% CI, 0.47-0.95; P = .02). It was also associated with a higher rate of gastrointestinal symptoms: 6.9% vs 5.4% (HR, 1.41; 95% CI, 1.12-1.78; P = .003). There was no difference in rates of upper respiratory tract infections (URTIs), although some research suggests these agents reduce URTIs.
 

Mechanisms

The etiology of childhood obesity is complex and multifactorial, the authors wrote, and genetic predisposition to adiposity, an obesogenic environment, and a sedentary lifestyle synergistically contribute to its development. Variants in genes active in the hypothalamic appetite-regulation neurocircuitry appear to be associated with the development of childhood and adolescent obesity.

The authors noted that adolescence carries an increased risk for psychiatric disorders and suicidal ideation. “The amelioration of obesity could indirectly improve these psychiatric comorbidities,” they wrote. In addition, preclinical studies suggested that GLP-1 RA may improve depression-related neuropathology, including neuroinflammation and neurotransmitter imbalance, and may promote neurogenesis.

A recent meta-analysis found that adults with T2D treated with GLP-1 RA showed significant reduction in depression scale scores compared with those treated with non-GLP-1 RA antidiabetic medications.

Commenting on the study but not involved in it, psychiatrist Robert H. Dicker, MD, associate director of child and adolescent psychiatry at Northwell Zucker Hillside Hospital in Glen Oaks, New York, cautioned that these are preliminary data limited by a retrospective review, not a prospective double-blind, placebo-controlled study.

“The mechanism is unknown — is it a direct effect on weight loss with an improvement of quality of life, more positive feedback by the community, enhanced ability to exercise, and a decrease in depressive symptoms?” he asked.

Dicker suggested an alternative hypothesis: Does the GLP-1 RA have a direct effect on neurotransmitters and inflammation and, thus, an impact on mood, emotional regulation, impulse control, and suicide?

“To further answer these questions, prospective studies must be conducted. It is far too early to conclude that these medications are effective in treating mood disorders in our youth,” Dicker said. “But it is promising that these treatments do not appear to increase suicidal ideas and behavior.”

Adding another outsider’s perspective on the study, Suzanne E. Cuda, MD, FOMA, FAAP, a pediatrician who treats childhood obesity in San Antonio, said that while there was no risk for increased psychiatric disease and a suggestion that GLP-1 RAs may reduce suicidal ideation or attempts, “I don’t think this translates to a treatment for depression in adolescents. Nor does this study indicate there could be a decrease in depression due specifically to the use of GLP1Rs. If the results in this study are replicated, however, it would be reassuring to know that adolescents would not be at risk for an increase in suicidal ideation or attempts.”

This study had no external funding. Kerem reported receiving personal fees from Novo Nordisk for lectures on childhood obesity outside of the submitted work. No other disclosures were reported. Dicker and Cuda had no competing interests relevant to their comments.

A version of this article appeared on Medscape.com.

Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) given to adolescents with obesity was associated with a one-third decreased risk for suicidal ideation and suicide attempts compared with lifestyle intervention alone, a large international retrospective study found.

A study published in JAMA Pediatrics suggested that GLP-1 RAs such as semaglutide, liraglutide, and tirzepatide, which are widely used to treat type 2 diabetes (T2D), have a favorable psychiatric safety profile and open up potential avenues for prospective studies of psychiatric outcomes in adolescents with obesity.

Investigators Liya Kerem, MD, MSc, and Joshua Stokar, MD, of Hadassah University Medical Center in Jerusalem, Israel, reported that the reduced risk in GLP-1 RA recipients was maintained up to 3 years follow-up compared with propensity score–matched controls treated with behavioral interventions alone.

“These findings support the notion that childhood obesity does not result from lack of willpower and shed light on underlying mechanisms that can be targeted by pharmacotherapy.” Kerem and Stokar wrote.

Other research has suggested these agents have neurobiologic effects unrelated to weight loss that positively affect mood and mental health.
 

Study Details

The analysis included data from December 2019 to June 2024, drawn from 120 international healthcare organizations, mainly in the United States. A total of 4052 racially and ethnically diverse adolescents with obesity (aged 12-18 years [mean age, about 15.5 years]) being treated with an anti-obesity intervention were identified for the GLP-1 RA cohort and 50,112 for the control cohort. The arms were balanced for baseline demographic characteristics, psychiatric medications and comorbidities, and diagnoses associated with socioeconomic status and healthcare access.

Propensity score matching (PSM) resulted in 3456 participants in each of two balanced cohorts.

Before PSM, intervention patients were older (mean age, 15.5 vs 14.7 years), were more likely to be female (59% vs 49%), and had a higher body mass index (41.9 vs 33.8). They also had a higher prevalence of diabetes (40% vs 4%) and treatment with antidiabetic medications.

GLP-1 RA recipients also had a history of psychiatric diagnoses (17% vs 9% for mood disorders) and psychiatric medications (18% vs 7% for antidepressants). Previous use of non–GLP-1 RA anti-obesity medications was uncommon in the cohort overall, although more common in the GLP-1 RA cohort (2.5% vs 0.2% for phentermine).

Prescription of GLP-1 RA was associated with a 33% reduced risk for suicidal ideation or attempts over 12 months of follow-up: 1.45% vs 2.26% (hazard ratio [HR], 0.67; 95% CI, 0.47-0.95; P = .02). It was also associated with a higher rate of gastrointestinal symptoms: 6.9% vs 5.4% (HR, 1.41; 95% CI, 1.12-1.78; P = .003). There was no difference in rates of upper respiratory tract infections (URTIs), although some research suggests these agents reduce URTIs.
 

Mechanisms

The etiology of childhood obesity is complex and multifactorial, the authors wrote, and genetic predisposition to adiposity, an obesogenic environment, and a sedentary lifestyle synergistically contribute to its development. Variants in genes active in the hypothalamic appetite-regulation neurocircuitry appear to be associated with the development of childhood and adolescent obesity.

The authors noted that adolescence carries an increased risk for psychiatric disorders and suicidal ideation. “The amelioration of obesity could indirectly improve these psychiatric comorbidities,” they wrote. In addition, preclinical studies suggested that GLP-1 RA may improve depression-related neuropathology, including neuroinflammation and neurotransmitter imbalance, and may promote neurogenesis.

A recent meta-analysis found that adults with T2D treated with GLP-1 RA showed significant reduction in depression scale scores compared with those treated with non-GLP-1 RA antidiabetic medications.

Commenting on the study but not involved in it, psychiatrist Robert H. Dicker, MD, associate director of child and adolescent psychiatry at Northwell Zucker Hillside Hospital in Glen Oaks, New York, cautioned that these are preliminary data limited by a retrospective review, not a prospective double-blind, placebo-controlled study.

“The mechanism is unknown — is it a direct effect on weight loss with an improvement of quality of life, more positive feedback by the community, enhanced ability to exercise, and a decrease in depressive symptoms?” he asked.

Dicker suggested an alternative hypothesis: Does the GLP-1 RA have a direct effect on neurotransmitters and inflammation and, thus, an impact on mood, emotional regulation, impulse control, and suicide?

“To further answer these questions, prospective studies must be conducted. It is far too early to conclude that these medications are effective in treating mood disorders in our youth,” Dicker said. “But it is promising that these treatments do not appear to increase suicidal ideas and behavior.”

Adding another outsider’s perspective on the study, Suzanne E. Cuda, MD, FOMA, FAAP, a pediatrician who treats childhood obesity in San Antonio, said that while there was no risk for increased psychiatric disease and a suggestion that GLP-1 RAs may reduce suicidal ideation or attempts, “I don’t think this translates to a treatment for depression in adolescents. Nor does this study indicate there could be a decrease in depression due specifically to the use of GLP1Rs. If the results in this study are replicated, however, it would be reassuring to know that adolescents would not be at risk for an increase in suicidal ideation or attempts.”

This study had no external funding. Kerem reported receiving personal fees from Novo Nordisk for lectures on childhood obesity outside of the submitted work. No other disclosures were reported. Dicker and Cuda had no competing interests relevant to their comments.

A version of this article appeared on Medscape.com.

Losses of muscle and strength are inescapable effects of the aging process. Left unchecked, these progressive losses will start to impair physical function. 

Once a certain level of impairment occurs, an individual can be diagnosed with sarcopenia, which comes from the Greek words “sarco” (flesh) and “penia” (poverty). Individuals with sarcopenia have a significant increase in the risk for falls and death, as well as diminished quality of life.

Muscle mass losses generally occur with weight loss, and the increasing use of glucagon-like peptide 1 (GLP-1) medications may lead to greater incidence and prevalence of sarcopenia in the years to come.

A recent meta-analysis of 56 studies (mean participant age, 50 years) found a twofold greater risk for mortality in those with sarcopenia vs those without. Despite its health consequences, sarcopenia tends to be underdiagnosed and, consequently, undertreated at a population and individual level. Part of the reason probably stems from the lack of health insurance reimbursement for individual clinicians and hospital systems to perform sarcopenia screening assessments. 

In aging and obesity, it appears justified to include and emphasize a recommendation for sarcopenia screening in medical society guidelines; however, individual patients and clinicians do not need to wait for updated guidelines to implement sarcopenia screening, treatment, and prevention strategies in their own lives and/or clinical practice. 
 

Simple Prevention and Treatment Strategy

Much can be done to help prevent sarcopenia. The primary strategy, unsurprisingly, is engaging in frequent strength training. But that doesn’t mean hours in the gym every week. 

With just one session per week over 10 weeks, lean body mass (LBM), a common proxy for muscle mass, increased by 0.33 kg, according to a study which evaluated LBM improvements across different strength training frequencies. Adding a second weekly session was significantly better. In the twice-weekly group, LBM increased by 1.4 kg over 10 weeks, resulting in an increase in LBM more than four times greater than the once-a-week group. (There was no greater improvement in LBM by adding a third weekly session vs two weekly sessions.) 

Although that particular study didn’t identify greater benefit at three times a week, compared with twice a week, the specific training routines and lack of a protein consumption assessment may have played a role in that finding. 

Underlying the diminishing benefits, a different study found a marginally greater benefit in favor of performing ≥ five sets per major muscle group per week, compared with < five sets per week for increasing muscle in the legs, arms, back, chest, and shoulders. 

Expensive gym memberships and fancy equipment are not necessary. While the use of strength training machines and free weights have been viewed by many as the optimal approach, a recent systematic review and meta-analysis found that comparable improvements to strength can be achieved with workouts using resistance bands. For those who struggle to find the time to go to a gym, or for whom gym fees are not financially affordable, resistance bands are a cheaper and more convenient alternative. 

Lucas, Assistant Professor of Clinical Medicine, Comprehensive Weight Control Center, Weill Cornell Medicine, New York City, disclosed ties with Measured (Better Health Labs).

A version of this article appeared on Medscape.com.

Losses of muscle and strength are inescapable effects of the aging process. Left unchecked, these progressive losses will start to impair physical function. 

Once a certain level of impairment occurs, an individual can be diagnosed with sarcopenia, which comes from the Greek words “sarco” (flesh) and “penia” (poverty). Individuals with sarcopenia have a significant increase in the risk for falls and death, as well as diminished quality of life.

Muscle mass losses generally occur with weight loss, and the increasing use of glucagon-like peptide 1 (GLP-1) medications may lead to greater incidence and prevalence of sarcopenia in the years to come.

A recent meta-analysis of 56 studies (mean participant age, 50 years) found a twofold greater risk for mortality in those with sarcopenia vs those without. Despite its health consequences, sarcopenia tends to be underdiagnosed and, consequently, undertreated at a population and individual level. Part of the reason probably stems from the lack of health insurance reimbursement for individual clinicians and hospital systems to perform sarcopenia screening assessments. 

In aging and obesity, it appears justified to include and emphasize a recommendation for sarcopenia screening in medical society guidelines; however, individual patients and clinicians do not need to wait for updated guidelines to implement sarcopenia screening, treatment, and prevention strategies in their own lives and/or clinical practice. 
 

Simple Prevention and Treatment Strategy

Much can be done to help prevent sarcopenia. The primary strategy, unsurprisingly, is engaging in frequent strength training. But that doesn’t mean hours in the gym every week. 

With just one session per week over 10 weeks, lean body mass (LBM), a common proxy for muscle mass, increased by 0.33 kg, according to a study which evaluated LBM improvements across different strength training frequencies. Adding a second weekly session was significantly better. In the twice-weekly group, LBM increased by 1.4 kg over 10 weeks, resulting in an increase in LBM more than four times greater than the once-a-week group. (There was no greater improvement in LBM by adding a third weekly session vs two weekly sessions.) 

Although that particular study didn’t identify greater benefit at three times a week, compared with twice a week, the specific training routines and lack of a protein consumption assessment may have played a role in that finding. 

Underlying the diminishing benefits, a different study found a marginally greater benefit in favor of performing ≥ five sets per major muscle group per week, compared with < five sets per week for increasing muscle in the legs, arms, back, chest, and shoulders. 

Expensive gym memberships and fancy equipment are not necessary. While the use of strength training machines and free weights have been viewed by many as the optimal approach, a recent systematic review and meta-analysis found that comparable improvements to strength can be achieved with workouts using resistance bands. For those who struggle to find the time to go to a gym, or for whom gym fees are not financially affordable, resistance bands are a cheaper and more convenient alternative. 

Lucas, Assistant Professor of Clinical Medicine, Comprehensive Weight Control Center, Weill Cornell Medicine, New York City, disclosed ties with Measured (Better Health Labs).

A version of this article appeared on Medscape.com.

Losses of muscle and strength are inescapable effects of the aging process. Left unchecked, these progressive losses will start to impair physical function. 

Once a certain level of impairment occurs, an individual can be diagnosed with sarcopenia, which comes from the Greek words “sarco” (flesh) and “penia” (poverty). Individuals with sarcopenia have a significant increase in the risk for falls and death, as well as diminished quality of life.

Muscle mass losses generally occur with weight loss, and the increasing use of glucagon-like peptide 1 (GLP-1) medications may lead to greater incidence and prevalence of sarcopenia in the years to come.

A recent meta-analysis of 56 studies (mean participant age, 50 years) found a twofold greater risk for mortality in those with sarcopenia vs those without. Despite its health consequences, sarcopenia tends to be underdiagnosed and, consequently, undertreated at a population and individual level. Part of the reason probably stems from the lack of health insurance reimbursement for individual clinicians and hospital systems to perform sarcopenia screening assessments. 

In aging and obesity, it appears justified to include and emphasize a recommendation for sarcopenia screening in medical society guidelines; however, individual patients and clinicians do not need to wait for updated guidelines to implement sarcopenia screening, treatment, and prevention strategies in their own lives and/or clinical practice. 
 

Simple Prevention and Treatment Strategy

Much can be done to help prevent sarcopenia. The primary strategy, unsurprisingly, is engaging in frequent strength training. But that doesn’t mean hours in the gym every week. 

With just one session per week over 10 weeks, lean body mass (LBM), a common proxy for muscle mass, increased by 0.33 kg, according to a study which evaluated LBM improvements across different strength training frequencies. Adding a second weekly session was significantly better. In the twice-weekly group, LBM increased by 1.4 kg over 10 weeks, resulting in an increase in LBM more than four times greater than the once-a-week group. (There was no greater improvement in LBM by adding a third weekly session vs two weekly sessions.) 

Although that particular study didn’t identify greater benefit at three times a week, compared with twice a week, the specific training routines and lack of a protein consumption assessment may have played a role in that finding. 

Underlying the diminishing benefits, a different study found a marginally greater benefit in favor of performing ≥ five sets per major muscle group per week, compared with < five sets per week for increasing muscle in the legs, arms, back, chest, and shoulders. 

Expensive gym memberships and fancy equipment are not necessary. While the use of strength training machines and free weights have been viewed by many as the optimal approach, a recent systematic review and meta-analysis found that comparable improvements to strength can be achieved with workouts using resistance bands. For those who struggle to find the time to go to a gym, or for whom gym fees are not financially affordable, resistance bands are a cheaper and more convenient alternative. 

Lucas, Assistant Professor of Clinical Medicine, Comprehensive Weight Control Center, Weill Cornell Medicine, New York City, disclosed ties with Measured (Better Health Labs).

A version of this article appeared on Medscape.com.

“Obesity only recently caught the public’s attention as a disease,” Matthias Blüher, MD, professor of medicine at the Leipzig University and director of the Helmholtz Institute for Metabolism, Obesity and Vascular Research, Leipzig, Germany, told attendees in a thought-provoking presentation at the European Association for the Study of Diabetes (EASD) 2024 Annual Meeting.

Even though the attitudes around how obesity is perceived may be relatively new, Blüher believes they are nonetheless significant. As a sign of how the cultural headwinds have shifted, he noted the 2022 film The Whale, which focuses on a character struggling with obesity. As Blüher pointed out, not only did the film’s star, Brendan Fraser, receive an Academy Award for his portrayal but he also theorized that the majority of celebrities in the audience were likely taking new weight loss medications.

“I strongly believe that in the future, obesity treatment will carry less stigma. It will be considered not as a cosmetic problem, but as a progressive disease.”

He sees several changes in the management of obesity likely to occur on the near horizon, beginning with when interventions directed at treating it will begin.

Obesity treatment should start at a young age, he said, because if you have overweight at ages 3-6 years, the likelihood of becoming an adult with obesity is approximately 90%. “Looking ahead, shouldn’t we put more emphasis on this age group?”

Furthermore, he hopes that clinical trials will move beyond body weight and body mass index (BMI) as their main outcome parameters. Instead, “we should talk about fat distribution, fat or adipose tissue function, muscle loss, body composition, and severity of disease.”

Blüher pointed to the recently published framework for the diagnosis, staging, and management of obesity in adults put forward by the European Association for the Study of Obesity. It states that obesity should be staged not based on BMI or body weight alone but also on an individual›s medical, functional, and psychological (eg, mental health and eating behavior) status.

“The causes of obesity are too complex to be individually targeted,” he continued, unlike examples such as hypercholesterolemia or smoking cessation, where clinicians may have one target to address.

“But overeating, slow metabolism, and low physical activity involve socio-cultural factors, global food marketing, and many other factors. Therefore, clinicians should be setting health targets, such as improving sleep apnea and improving physical functioning, rather than a kilogram number.”
 

Three Pillars of Treatment

Right now, clinicians have three pillars of treatments available, Blüher said. The first is behavioral intervention, including strategies such as counseling, diet, exercise, self-monitoring, stress management, and sleep management.

“We know that these behavioral aspects typically lack adherence and effect size, but they’re important, and for a certain group of people, they may be the best and safest treatment.”

The second pillar is pharmacotherapy, and the third is surgery.

Each pillar poses questions for future research, he explained.

“First, do we really need more evidence that behavioral interventions typically fail in the long run and are prone to rebound of body weight and health issues? No. Or which diet is best? We have hundreds of diet interventions, all of which basically show very similar outcomes. They lead to an average weight loss of 3% to 5% and do improve health conditions associated with obesity.”

When it comes to pharmacotherapies, Blüher does believe clinicians need more options.

Depending on affordability and access, glucagon-like peptide 1 (GLP-1) semaglutide will likely become the first-line therapy for most people living with obesity who want to take medications, he suggested. The dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 tirzepatide will be reserved for those with more severe conditions.

“But this is not the end of the story,” he said. “The pipelines for obesity pharmacotherapies are full, and they have different categories. We are optimistic that we will have more therapies not only for type 2 diabetes (T2D) but also for obesity. Combinations such as CagriSema (cagrilintide + semaglutide, currently indicated for T2D) may outperform the monotherapies. We have to see if they’re as safe, and we have to wait for phase 3 trials and long-term outcomes.”

“The field is open for many combinations, ideas and interactions among the incretin-based signaling systems, but personally, I think that the triple agonists have a very bright future,” Blüher said.

For example, retatrutide, an agonist of the GIP, GLP-1, and glucagon receptors, showed promise in a phase 2 trial. Although that was not a comparative study, “the average changes in body weight suggest that in a dose-dependent manner, you can expect even more weight loss than with tirzepatide.”
 

Treating the Causes

The future of obesity therapy might also be directed at the originating factors that cause it, Blüher suggested, adding that “treating the causes is a dream of mine.”

One example of treating the cause is leptin therapy, as shown in a 1999 study of recombinant leptin in a child with congenital leptin deficiency. A more recent example is setmelanotide treatment for proopiomelanocortin deficiency.

“We are at the beginning for these causative treatments of obesity, and I hope that the future will hold much more of these insights and targets, as in cancer therapy.”

“Finally,” he said, “We eat with our brain. And so in the future, we also will be better able to use our knowledge about the complex neural circuits that are obesogenic, and how to target them. In doing so, we can learn from surgeons because obesity surgery is very effective in changing the anatomy, and we also observe hormonal changes. We see that ghrelin, GLP-1, peptide YY, and many others are affected when the anatomy changes. Why can’t we use that knowledge to design drugs that resemble or mimic the effect size of bariatric surgery?”

And that goes to the third pillar of treatment and the question of whether the new weight loss drugs may replace surgery, which also was the topic of another EASD session.

Blüher doesn’t see that happening for at least a decade, given that there is still an effect-size gap between tirzepatide and surgery, especially for individuals with T2D. In addition, he noted, there will still be nonresponders to drugs, and clinicians are not treating to target yet. Looking ahead, he foresees a combination of surgery and multi-receptor agonists.

“I believe that obesity won’t be cured in the future, but we will have increasingly better lifelong management with a multidisciplinary approach, although behavioral interventions still will not be as successful as pharmacotherapy and bariatric surgery,” he concluded.
 

Q&A

During the question-and-answer session following his lecture, several attendees asked Blüher for his thoughts around other emerging areas in this field. One wanted to know whether microbiome changes might be a future target for obesity treatment.

“So far, we don’t really understand which bacteria, which composition, at which age, and at which part of the intestine need to be targeted,” Blüher responded. “Before we know that mechanistically, I think it would be difficult, but it could be an avenue to go for, though I’m a little less optimistic about it compared to other approaches.”

Given that obesity is not one disease, are there cluster subtypes, as for T2D — eg, the hungry brain, the hungry gut, low metabolism — that might benefit from individualized treatment, another attendee asked.

“We do try to subcluster people living with obesity,” Blüher said. “We did that based on adipose tissue expression signatures, and indeed there is large heterogeneity. But we are far from addressing the root causes and all subtypes of the disease, and that would be a requirement before we could personalize treatment in that way.”

Next, an attendee asked what is responsible for the differential weight loss in people with diabetes and people without? Blüher responded that although he doesn’t have the answer, he does have hypotheses.

“One could be that the disease process — eg, deterioration of beta cell function, of the balance of hormones such as insulin and leptin, of inflammatory parameters, of insulin resistance — is much more advanced in diseases such as T2D and sleep apnea. Maybe it then takes more to address comorbid conditions such as inflammation and insulin resistance. Therefore, combining current therapies with insulin sensitizers, for example, could produce better results.”

What about using continuous glucose monitoring to help people stick to their diet?

“That’s an important question that speaks to personalized treatment,” he said. “It applies not only to continuous glucose monitoring but also to nutrition and other modes of self-monitoring, which seem to be among the most successful tools for long-term weight maintenance.”

Blüher finished by saying, “As we look into the future, I hope that there will be better approaches for all aspects of personalized medicine, whether it is nutrition, exercise, pharmacotherapy, or even surgical procedures.”

Blüher received honoraria for lectures and/or served as a consultant to Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Daiichi Sankyo, Eli Lilly, Novo Nordisk, Novartis, Pfizer, and Sanofi.
 

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

“Obesity only recently caught the public’s attention as a disease,” Matthias Blüher, MD, professor of medicine at the Leipzig University and director of the Helmholtz Institute for Metabolism, Obesity and Vascular Research, Leipzig, Germany, told attendees in a thought-provoking presentation at the European Association for the Study of Diabetes (EASD) 2024 Annual Meeting.

Even though the attitudes around how obesity is perceived may be relatively new, Blüher believes they are nonetheless significant. As a sign of how the cultural headwinds have shifted, he noted the 2022 film The Whale, which focuses on a character struggling with obesity. As Blüher pointed out, not only did the film’s star, Brendan Fraser, receive an Academy Award for his portrayal but he also theorized that the majority of celebrities in the audience were likely taking new weight loss medications.

“I strongly believe that in the future, obesity treatment will carry less stigma. It will be considered not as a cosmetic problem, but as a progressive disease.”

He sees several changes in the management of obesity likely to occur on the near horizon, beginning with when interventions directed at treating it will begin.

Obesity treatment should start at a young age, he said, because if you have overweight at ages 3-6 years, the likelihood of becoming an adult with obesity is approximately 90%. “Looking ahead, shouldn’t we put more emphasis on this age group?”

Furthermore, he hopes that clinical trials will move beyond body weight and body mass index (BMI) as their main outcome parameters. Instead, “we should talk about fat distribution, fat or adipose tissue function, muscle loss, body composition, and severity of disease.”

Blüher pointed to the recently published framework for the diagnosis, staging, and management of obesity in adults put forward by the European Association for the Study of Obesity. It states that obesity should be staged not based on BMI or body weight alone but also on an individual›s medical, functional, and psychological (eg, mental health and eating behavior) status.

“The causes of obesity are too complex to be individually targeted,” he continued, unlike examples such as hypercholesterolemia or smoking cessation, where clinicians may have one target to address.

“But overeating, slow metabolism, and low physical activity involve socio-cultural factors, global food marketing, and many other factors. Therefore, clinicians should be setting health targets, such as improving sleep apnea and improving physical functioning, rather than a kilogram number.”
 

Three Pillars of Treatment

Right now, clinicians have three pillars of treatments available, Blüher said. The first is behavioral intervention, including strategies such as counseling, diet, exercise, self-monitoring, stress management, and sleep management.

“We know that these behavioral aspects typically lack adherence and effect size, but they’re important, and for a certain group of people, they may be the best and safest treatment.”

The second pillar is pharmacotherapy, and the third is surgery.

Each pillar poses questions for future research, he explained.

“First, do we really need more evidence that behavioral interventions typically fail in the long run and are prone to rebound of body weight and health issues? No. Or which diet is best? We have hundreds of diet interventions, all of which basically show very similar outcomes. They lead to an average weight loss of 3% to 5% and do improve health conditions associated with obesity.”

When it comes to pharmacotherapies, Blüher does believe clinicians need more options.

Depending on affordability and access, glucagon-like peptide 1 (GLP-1) semaglutide will likely become the first-line therapy for most people living with obesity who want to take medications, he suggested. The dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 tirzepatide will be reserved for those with more severe conditions.

“But this is not the end of the story,” he said. “The pipelines for obesity pharmacotherapies are full, and they have different categories. We are optimistic that we will have more therapies not only for type 2 diabetes (T2D) but also for obesity. Combinations such as CagriSema (cagrilintide + semaglutide, currently indicated for T2D) may outperform the monotherapies. We have to see if they’re as safe, and we have to wait for phase 3 trials and long-term outcomes.”

“The field is open for many combinations, ideas and interactions among the incretin-based signaling systems, but personally, I think that the triple agonists have a very bright future,” Blüher said.

For example, retatrutide, an agonist of the GIP, GLP-1, and glucagon receptors, showed promise in a phase 2 trial. Although that was not a comparative study, “the average changes in body weight suggest that in a dose-dependent manner, you can expect even more weight loss than with tirzepatide.”
 

Treating the Causes

The future of obesity therapy might also be directed at the originating factors that cause it, Blüher suggested, adding that “treating the causes is a dream of mine.”

One example of treating the cause is leptin therapy, as shown in a 1999 study of recombinant leptin in a child with congenital leptin deficiency. A more recent example is setmelanotide treatment for proopiomelanocortin deficiency.

“We are at the beginning for these causative treatments of obesity, and I hope that the future will hold much more of these insights and targets, as in cancer therapy.”

“Finally,” he said, “We eat with our brain. And so in the future, we also will be better able to use our knowledge about the complex neural circuits that are obesogenic, and how to target them. In doing so, we can learn from surgeons because obesity surgery is very effective in changing the anatomy, and we also observe hormonal changes. We see that ghrelin, GLP-1, peptide YY, and many others are affected when the anatomy changes. Why can’t we use that knowledge to design drugs that resemble or mimic the effect size of bariatric surgery?”

And that goes to the third pillar of treatment and the question of whether the new weight loss drugs may replace surgery, which also was the topic of another EASD session.

Blüher doesn’t see that happening for at least a decade, given that there is still an effect-size gap between tirzepatide and surgery, especially for individuals with T2D. In addition, he noted, there will still be nonresponders to drugs, and clinicians are not treating to target yet. Looking ahead, he foresees a combination of surgery and multi-receptor agonists.

“I believe that obesity won’t be cured in the future, but we will have increasingly better lifelong management with a multidisciplinary approach, although behavioral interventions still will not be as successful as pharmacotherapy and bariatric surgery,” he concluded.
 

Q&A

During the question-and-answer session following his lecture, several attendees asked Blüher for his thoughts around other emerging areas in this field. One wanted to know whether microbiome changes might be a future target for obesity treatment.

“So far, we don’t really understand which bacteria, which composition, at which age, and at which part of the intestine need to be targeted,” Blüher responded. “Before we know that mechanistically, I think it would be difficult, but it could be an avenue to go for, though I’m a little less optimistic about it compared to other approaches.”

Given that obesity is not one disease, are there cluster subtypes, as for T2D — eg, the hungry brain, the hungry gut, low metabolism — that might benefit from individualized treatment, another attendee asked.

“We do try to subcluster people living with obesity,” Blüher said. “We did that based on adipose tissue expression signatures, and indeed there is large heterogeneity. But we are far from addressing the root causes and all subtypes of the disease, and that would be a requirement before we could personalize treatment in that way.”

Next, an attendee asked what is responsible for the differential weight loss in people with diabetes and people without? Blüher responded that although he doesn’t have the answer, he does have hypotheses.

“One could be that the disease process — eg, deterioration of beta cell function, of the balance of hormones such as insulin and leptin, of inflammatory parameters, of insulin resistance — is much more advanced in diseases such as T2D and sleep apnea. Maybe it then takes more to address comorbid conditions such as inflammation and insulin resistance. Therefore, combining current therapies with insulin sensitizers, for example, could produce better results.”

What about using continuous glucose monitoring to help people stick to their diet?

“That’s an important question that speaks to personalized treatment,” he said. “It applies not only to continuous glucose monitoring but also to nutrition and other modes of self-monitoring, which seem to be among the most successful tools for long-term weight maintenance.”

Blüher finished by saying, “As we look into the future, I hope that there will be better approaches for all aspects of personalized medicine, whether it is nutrition, exercise, pharmacotherapy, or even surgical procedures.”

Blüher received honoraria for lectures and/or served as a consultant to Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Daiichi Sankyo, Eli Lilly, Novo Nordisk, Novartis, Pfizer, and Sanofi.
 

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

“Obesity only recently caught the public’s attention as a disease,” Matthias Blüher, MD, professor of medicine at the Leipzig University and director of the Helmholtz Institute for Metabolism, Obesity and Vascular Research, Leipzig, Germany, told attendees in a thought-provoking presentation at the European Association for the Study of Diabetes (EASD) 2024 Annual Meeting.

Even though the attitudes around how obesity is perceived may be relatively new, Blüher believes they are nonetheless significant. As a sign of how the cultural headwinds have shifted, he noted the 2022 film The Whale, which focuses on a character struggling with obesity. As Blüher pointed out, not only did the film’s star, Brendan Fraser, receive an Academy Award for his portrayal but he also theorized that the majority of celebrities in the audience were likely taking new weight loss medications.

“I strongly believe that in the future, obesity treatment will carry less stigma. It will be considered not as a cosmetic problem, but as a progressive disease.”

He sees several changes in the management of obesity likely to occur on the near horizon, beginning with when interventions directed at treating it will begin.

Obesity treatment should start at a young age, he said, because if you have overweight at ages 3-6 years, the likelihood of becoming an adult with obesity is approximately 90%. “Looking ahead, shouldn’t we put more emphasis on this age group?”

Furthermore, he hopes that clinical trials will move beyond body weight and body mass index (BMI) as their main outcome parameters. Instead, “we should talk about fat distribution, fat or adipose tissue function, muscle loss, body composition, and severity of disease.”

Blüher pointed to the recently published framework for the diagnosis, staging, and management of obesity in adults put forward by the European Association for the Study of Obesity. It states that obesity should be staged not based on BMI or body weight alone but also on an individual›s medical, functional, and psychological (eg, mental health and eating behavior) status.

“The causes of obesity are too complex to be individually targeted,” he continued, unlike examples such as hypercholesterolemia or smoking cessation, where clinicians may have one target to address.

“But overeating, slow metabolism, and low physical activity involve socio-cultural factors, global food marketing, and many other factors. Therefore, clinicians should be setting health targets, such as improving sleep apnea and improving physical functioning, rather than a kilogram number.”
 

Three Pillars of Treatment

Right now, clinicians have three pillars of treatments available, Blüher said. The first is behavioral intervention, including strategies such as counseling, diet, exercise, self-monitoring, stress management, and sleep management.

“We know that these behavioral aspects typically lack adherence and effect size, but they’re important, and for a certain group of people, they may be the best and safest treatment.”

The second pillar is pharmacotherapy, and the third is surgery.

Each pillar poses questions for future research, he explained.

“First, do we really need more evidence that behavioral interventions typically fail in the long run and are prone to rebound of body weight and health issues? No. Or which diet is best? We have hundreds of diet interventions, all of which basically show very similar outcomes. They lead to an average weight loss of 3% to 5% and do improve health conditions associated with obesity.”

When it comes to pharmacotherapies, Blüher does believe clinicians need more options.

Depending on affordability and access, glucagon-like peptide 1 (GLP-1) semaglutide will likely become the first-line therapy for most people living with obesity who want to take medications, he suggested. The dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 tirzepatide will be reserved for those with more severe conditions.

“But this is not the end of the story,” he said. “The pipelines for obesity pharmacotherapies are full, and they have different categories. We are optimistic that we will have more therapies not only for type 2 diabetes (T2D) but also for obesity. Combinations such as CagriSema (cagrilintide + semaglutide, currently indicated for T2D) may outperform the monotherapies. We have to see if they’re as safe, and we have to wait for phase 3 trials and long-term outcomes.”

“The field is open for many combinations, ideas and interactions among the incretin-based signaling systems, but personally, I think that the triple agonists have a very bright future,” Blüher said.

For example, retatrutide, an agonist of the GIP, GLP-1, and glucagon receptors, showed promise in a phase 2 trial. Although that was not a comparative study, “the average changes in body weight suggest that in a dose-dependent manner, you can expect even more weight loss than with tirzepatide.”
 

Treating the Causes

The future of obesity therapy might also be directed at the originating factors that cause it, Blüher suggested, adding that “treating the causes is a dream of mine.”

One example of treating the cause is leptin therapy, as shown in a 1999 study of recombinant leptin in a child with congenital leptin deficiency. A more recent example is setmelanotide treatment for proopiomelanocortin deficiency.

“We are at the beginning for these causative treatments of obesity, and I hope that the future will hold much more of these insights and targets, as in cancer therapy.”

“Finally,” he said, “We eat with our brain. And so in the future, we also will be better able to use our knowledge about the complex neural circuits that are obesogenic, and how to target them. In doing so, we can learn from surgeons because obesity surgery is very effective in changing the anatomy, and we also observe hormonal changes. We see that ghrelin, GLP-1, peptide YY, and many others are affected when the anatomy changes. Why can’t we use that knowledge to design drugs that resemble or mimic the effect size of bariatric surgery?”

And that goes to the third pillar of treatment and the question of whether the new weight loss drugs may replace surgery, which also was the topic of another EASD session.

Blüher doesn’t see that happening for at least a decade, given that there is still an effect-size gap between tirzepatide and surgery, especially for individuals with T2D. In addition, he noted, there will still be nonresponders to drugs, and clinicians are not treating to target yet. Looking ahead, he foresees a combination of surgery and multi-receptor agonists.

“I believe that obesity won’t be cured in the future, but we will have increasingly better lifelong management with a multidisciplinary approach, although behavioral interventions still will not be as successful as pharmacotherapy and bariatric surgery,” he concluded.
 

Q&A

During the question-and-answer session following his lecture, several attendees asked Blüher for his thoughts around other emerging areas in this field. One wanted to know whether microbiome changes might be a future target for obesity treatment.

“So far, we don’t really understand which bacteria, which composition, at which age, and at which part of the intestine need to be targeted,” Blüher responded. “Before we know that mechanistically, I think it would be difficult, but it could be an avenue to go for, though I’m a little less optimistic about it compared to other approaches.”

Given that obesity is not one disease, are there cluster subtypes, as for T2D — eg, the hungry brain, the hungry gut, low metabolism — that might benefit from individualized treatment, another attendee asked.

“We do try to subcluster people living with obesity,” Blüher said. “We did that based on adipose tissue expression signatures, and indeed there is large heterogeneity. But we are far from addressing the root causes and all subtypes of the disease, and that would be a requirement before we could personalize treatment in that way.”

Next, an attendee asked what is responsible for the differential weight loss in people with diabetes and people without? Blüher responded that although he doesn’t have the answer, he does have hypotheses.

“One could be that the disease process — eg, deterioration of beta cell function, of the balance of hormones such as insulin and leptin, of inflammatory parameters, of insulin resistance — is much more advanced in diseases such as T2D and sleep apnea. Maybe it then takes more to address comorbid conditions such as inflammation and insulin resistance. Therefore, combining current therapies with insulin sensitizers, for example, could produce better results.”

What about using continuous glucose monitoring to help people stick to their diet?

“That’s an important question that speaks to personalized treatment,” he said. “It applies not only to continuous glucose monitoring but also to nutrition and other modes of self-monitoring, which seem to be among the most successful tools for long-term weight maintenance.”

Blüher finished by saying, “As we look into the future, I hope that there will be better approaches for all aspects of personalized medicine, whether it is nutrition, exercise, pharmacotherapy, or even surgical procedures.”

Blüher received honoraria for lectures and/or served as a consultant to Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Daiichi Sankyo, Eli Lilly, Novo Nordisk, Novartis, Pfizer, and Sanofi.
 

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

Editor's Note: This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Editor's Note: This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Editor's Note: This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

TOPLINE:

VIENNA, AUSTRIA — Participants with type 2 diabetes who were able to stop insulin for up to 12 months after receiving the novel recellularization via electroporation therapy (ReCET) procedure in combination with treatment with semaglutide maintained their response at 24 months.

METHODOLOGY:

• ReCET technology, manufactured by Endogenex, uses a specialized catheter that ablates the duodenal mucosa with electroporation, enhancing sensitivity to endogenous insulin.
• In the first-in-human study, a total of 14 participants (aged 28-75 years; body mass index, 24-40) underwent the ReCET procedure. They then followed a 2-week isocaloric liquid diet, after which they were initiated on semaglutide and gradually titrated up to 1 mg/wk.
• Patients were followed for a total of 24 months.

TAKEAWAY:

• Of the 14 participants, 12 (86%) no longer required insulin at the 6- and 12-month follow-ups.
• At the 24-month follow-up, 11 patients were still insulin-free while maintaining A1c levels below 7.5%. (One patient withdrew consent at 18 months.)
• Semaglutide at the maximum dose was well-tolerated by 93% of participants. One patient experienced nausea that limited titration to the maximum dose. There were no serious adverse events to the ReCET procedure.
• Researchers have started the EMINENT-2 trial that will compare the use of ReCET with a sham procedure. All patients will still receive semaglutide.

IN PRACTICE:

• “These findings are very encouraging, suggesting that ReCET is a safe and feasible procedure that, when combined with semaglutide, can effectively eliminate the need for insulin therapy,” said the study’s lead author.
• It’s a novel way of treating type 2 diabetes using a single endoscopic procedure instead of repeated insulin injections, Busch explained. “But we do need to consider whether repeat treatment will be necessary because I don’t believe this will be forever.”

SOURCE:

This study was led by Celine Busch, MBBS, a PhD candidate in gastroenterology at Amsterdam University Medical Center, Amsterdam, the Netherlands, and was presented (abstract OP049) at the United European Gastroenterology (UEG) Week 2024 in Vienna, Austria, on October 14, 2024.

LIMITATIONS:

Limitations included the small sample size, uncontrolled nature, and bias due to combination therapy.

DISCLOSURES:

This study received an unrestricted research grant from Endogenex. No other relevant disclosures were declared.

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

TOPLINE:

VIENNA, AUSTRIA — Participants with type 2 diabetes who were able to stop insulin for up to 12 months after receiving the novel recellularization via electroporation therapy (ReCET) procedure in combination with treatment with semaglutide maintained their response at 24 months.

METHODOLOGY:

• ReCET technology, manufactured by Endogenex, uses a specialized catheter that ablates the duodenal mucosa with electroporation, enhancing sensitivity to endogenous insulin.
• In the first-in-human study, a total of 14 participants (aged 28-75 years; body mass index, 24-40) underwent the ReCET procedure. They then followed a 2-week isocaloric liquid diet, after which they were initiated on semaglutide and gradually titrated up to 1 mg/wk.
• Patients were followed for a total of 24 months.

TAKEAWAY:

• Of the 14 participants, 12 (86%) no longer required insulin at the 6- and 12-month follow-ups.
• At the 24-month follow-up, 11 patients were still insulin-free while maintaining A1c levels below 7.5%. (One patient withdrew consent at 18 months.)
• Semaglutide at the maximum dose was well-tolerated by 93% of participants. One patient experienced nausea that limited titration to the maximum dose. There were no serious adverse events to the ReCET procedure.
• Researchers have started the EMINENT-2 trial that will compare the use of ReCET with a sham procedure. All patients will still receive semaglutide.

IN PRACTICE:

• “These findings are very encouraging, suggesting that ReCET is a safe and feasible procedure that, when combined with semaglutide, can effectively eliminate the need for insulin therapy,” said the study’s lead author.
• It’s a novel way of treating type 2 diabetes using a single endoscopic procedure instead of repeated insulin injections, Busch explained. “But we do need to consider whether repeat treatment will be necessary because I don’t believe this will be forever.”

SOURCE:

This study was led by Celine Busch, MBBS, a PhD candidate in gastroenterology at Amsterdam University Medical Center, Amsterdam, the Netherlands, and was presented (abstract OP049) at the United European Gastroenterology (UEG) Week 2024 in Vienna, Austria, on October 14, 2024.

LIMITATIONS:

Limitations included the small sample size, uncontrolled nature, and bias due to combination therapy.

DISCLOSURES:

This study received an unrestricted research grant from Endogenex. No other relevant disclosures were declared.

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

TOPLINE:

VIENNA, AUSTRIA — Participants with type 2 diabetes who were able to stop insulin for up to 12 months after receiving the novel recellularization via electroporation therapy (ReCET) procedure in combination with treatment with semaglutide maintained their response at 24 months.

METHODOLOGY:

• ReCET technology, manufactured by Endogenex, uses a specialized catheter that ablates the duodenal mucosa with electroporation, enhancing sensitivity to endogenous insulin.
• In the first-in-human study, a total of 14 participants (aged 28-75 years; body mass index, 24-40) underwent the ReCET procedure. They then followed a 2-week isocaloric liquid diet, after which they were initiated on semaglutide and gradually titrated up to 1 mg/wk.
• Patients were followed for a total of 24 months.

TAKEAWAY:

• Of the 14 participants, 12 (86%) no longer required insulin at the 6- and 12-month follow-ups.
• At the 24-month follow-up, 11 patients were still insulin-free while maintaining A1c levels below 7.5%. (One patient withdrew consent at 18 months.)
• Semaglutide at the maximum dose was well-tolerated by 93% of participants. One patient experienced nausea that limited titration to the maximum dose. There were no serious adverse events to the ReCET procedure.
• Researchers have started the EMINENT-2 trial that will compare the use of ReCET with a sham procedure. All patients will still receive semaglutide.

IN PRACTICE:

• “These findings are very encouraging, suggesting that ReCET is a safe and feasible procedure that, when combined with semaglutide, can effectively eliminate the need for insulin therapy,” said the study’s lead author.
• It’s a novel way of treating type 2 diabetes using a single endoscopic procedure instead of repeated insulin injections, Busch explained. “But we do need to consider whether repeat treatment will be necessary because I don’t believe this will be forever.”

SOURCE:

This study was led by Celine Busch, MBBS, a PhD candidate in gastroenterology at Amsterdam University Medical Center, Amsterdam, the Netherlands, and was presented (abstract OP049) at the United European Gastroenterology (UEG) Week 2024 in Vienna, Austria, on October 14, 2024.

LIMITATIONS:

Limitations included the small sample size, uncontrolled nature, and bias due to combination therapy.

DISCLOSURES:

This study received an unrestricted research grant from Endogenex. No other relevant disclosures were declared.

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

TOPLINE:

Eating more eggs is linked to weight gain in postmenopausal women, especially those with a high intake of Western foods such as processed and red meat, French fries, sweets, and deserts. Genetic predisposition for a high body mass index (BMI) also influences weight gain with higher egg intake.

METHODOLOGY:

• Egg consumption and elevated body weight are each linked to an increased risk for serious chronic diseases; however, whether elevated body weight mediates the association between egg intake and an elevated risk for serious chronic diseases needs further assessment.
• To investigate the association between eating eggs and weight gain, as well as the role of genetic susceptibility to an elevated BMI, researchers conducted a prospective study including 4439 postmenopausal women of European descent from the Women’s Health Initiative (WHI).
• They measured the participants’ consumption of egg and egg nutrients using a self-administered food frequency questionnaire.
• Changes in the consumption of eggs and egg nutrients such as cholesterol, choline, and betaine were assessed between baseline and follow-up visits at 1, 3, 6, and 9 years.
• The primary outcome was the change in body weight between baseline and each follow-up visit. Furthermore, an exploratory analysis evaluated how eating Western foods and genetic predisposition for a high BMI (assessed through a polygenic score) influenced weight change.

TAKEAWAY:

• An increased consumption of eggs was associated with weight gain, showing a positive linear trend at 1, 2, 3, and 6 years. By the third year, women whose egg consumption had increased by two eggs per week gained 0.70 kg more weight (P = .0002) than women whose egg consumption was reduced by 2.4 eggs per week (P-linear < .0001).
• An increase in the consumption of nutrients obtained from eggs, including cholesterol (P-linear < .0001) and choline (P-linear < .02), was positively associated with weight gain.
• Women with a higher consumption of Western foods showed significant associations between changes in egg, cholesterol, and choline intake and weight gain.
• A significant association was found between the BMI polygenic score and changes in body weight, with women most genetically predisposed to a higher BMI showing greater weight gain when their egg consumption increased by an average of 3.5 eggs per week.

IN PRACTICE:

“These results suggest that even relatively small increases or decreases in egg consumption could cause increases or decreases, respectively, in body weight among postmenopausal women, unless there are adequate compensating changes in factors such as dietary energy intake or physical activity,” the authors wrote. “Our results require confirmation,” they added.

SOURCE:

This study, led by James A. Greenberg, Department of Health and Nutrition Sciences, Brooklyn College, The City University of New York, was published online in Clinical Nutrition.

LIMITATIONS: 

This observational study was susceptible to residual confounding, which suggests that the observed associations may not have established causality. Additionally, the results were according to data from a group of postmenopausal American women of European descent, which limited the generalizability to other populations.

DISCLOSURES:

The WHI program was funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health & Human Services. The authors declared no conflicts of interest.

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

TOPLINE:

Eating more eggs is linked to weight gain in postmenopausal women, especially those with a high intake of Western foods such as processed and red meat, French fries, sweets, and deserts. Genetic predisposition for a high body mass index (BMI) also influences weight gain with higher egg intake.

METHODOLOGY:

• Egg consumption and elevated body weight are each linked to an increased risk for serious chronic diseases; however, whether elevated body weight mediates the association between egg intake and an elevated risk for serious chronic diseases needs further assessment.
• To investigate the association between eating eggs and weight gain, as well as the role of genetic susceptibility to an elevated BMI, researchers conducted a prospective study including 4439 postmenopausal women of European descent from the Women’s Health Initiative (WHI).
• They measured the participants’ consumption of egg and egg nutrients using a self-administered food frequency questionnaire.
• Changes in the consumption of eggs and egg nutrients such as cholesterol, choline, and betaine were assessed between baseline and follow-up visits at 1, 3, 6, and 9 years.
• The primary outcome was the change in body weight between baseline and each follow-up visit. Furthermore, an exploratory analysis evaluated how eating Western foods and genetic predisposition for a high BMI (assessed through a polygenic score) influenced weight change.

TAKEAWAY:

• An increased consumption of eggs was associated with weight gain, showing a positive linear trend at 1, 2, 3, and 6 years. By the third year, women whose egg consumption had increased by two eggs per week gained 0.70 kg more weight (P = .0002) than women whose egg consumption was reduced by 2.4 eggs per week (P-linear < .0001).
• An increase in the consumption of nutrients obtained from eggs, including cholesterol (P-linear < .0001) and choline (P-linear < .02), was positively associated with weight gain.
• Women with a higher consumption of Western foods showed significant associations between changes in egg, cholesterol, and choline intake and weight gain.
• A significant association was found between the BMI polygenic score and changes in body weight, with women most genetically predisposed to a higher BMI showing greater weight gain when their egg consumption increased by an average of 3.5 eggs per week.

IN PRACTICE:

“These results suggest that even relatively small increases or decreases in egg consumption could cause increases or decreases, respectively, in body weight among postmenopausal women, unless there are adequate compensating changes in factors such as dietary energy intake or physical activity,” the authors wrote. “Our results require confirmation,” they added.

SOURCE:

This study, led by James A. Greenberg, Department of Health and Nutrition Sciences, Brooklyn College, The City University of New York, was published online in Clinical Nutrition.

LIMITATIONS: 

This observational study was susceptible to residual confounding, which suggests that the observed associations may not have established causality. Additionally, the results were according to data from a group of postmenopausal American women of European descent, which limited the generalizability to other populations.

DISCLOSURES:

The WHI program was funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health & Human Services. The authors declared no conflicts of interest.

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

TOPLINE:

Eating more eggs is linked to weight gain in postmenopausal women, especially those with a high intake of Western foods such as processed and red meat, French fries, sweets, and deserts. Genetic predisposition for a high body mass index (BMI) also influences weight gain with higher egg intake.

METHODOLOGY:

• Egg consumption and elevated body weight are each linked to an increased risk for serious chronic diseases; however, whether elevated body weight mediates the association between egg intake and an elevated risk for serious chronic diseases needs further assessment.
• To investigate the association between eating eggs and weight gain, as well as the role of genetic susceptibility to an elevated BMI, researchers conducted a prospective study including 4439 postmenopausal women of European descent from the Women’s Health Initiative (WHI).
• They measured the participants’ consumption of egg and egg nutrients using a self-administered food frequency questionnaire.
• Changes in the consumption of eggs and egg nutrients such as cholesterol, choline, and betaine were assessed between baseline and follow-up visits at 1, 3, 6, and 9 years.
• The primary outcome was the change in body weight between baseline and each follow-up visit. Furthermore, an exploratory analysis evaluated how eating Western foods and genetic predisposition for a high BMI (assessed through a polygenic score) influenced weight change.

TAKEAWAY:

• An increased consumption of eggs was associated with weight gain, showing a positive linear trend at 1, 2, 3, and 6 years. By the third year, women whose egg consumption had increased by two eggs per week gained 0.70 kg more weight (P = .0002) than women whose egg consumption was reduced by 2.4 eggs per week (P-linear < .0001).
• An increase in the consumption of nutrients obtained from eggs, including cholesterol (P-linear < .0001) and choline (P-linear < .02), was positively associated with weight gain.
• Women with a higher consumption of Western foods showed significant associations between changes in egg, cholesterol, and choline intake and weight gain.
• A significant association was found between the BMI polygenic score and changes in body weight, with women most genetically predisposed to a higher BMI showing greater weight gain when their egg consumption increased by an average of 3.5 eggs per week.

IN PRACTICE:

“These results suggest that even relatively small increases or decreases in egg consumption could cause increases or decreases, respectively, in body weight among postmenopausal women, unless there are adequate compensating changes in factors such as dietary energy intake or physical activity,” the authors wrote. “Our results require confirmation,” they added.

SOURCE:

This study, led by James A. Greenberg, Department of Health and Nutrition Sciences, Brooklyn College, The City University of New York, was published online in Clinical Nutrition.

LIMITATIONS: 

This observational study was susceptible to residual confounding, which suggests that the observed associations may not have established causality. Additionally, the results were according to data from a group of postmenopausal American women of European descent, which limited the generalizability to other populations.

DISCLOSURES:

The WHI program was funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health & Human Services. The authors declared no conflicts of interest.

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

TOPLINE:

Cancer survivors who had overweight or obesity at the time of their initial cancer diagnosis have a higher risk for a second primary cancer, particularly an obesity-related cancer, a new analysis found.

METHODOLOGY:

• Cancer survivors have an increased risk for another primary cancer. Studies suggest that lifestyle factors, such as excess body weight, may contribute to the risk for a second cancer; however, prospective long-term data on this association remain limited.
• Researchers evaluated 26,894 participants (mean age at first cancer diagnosis, 72.2 years; 97.6% White) from the Cancer Prevention Study II Nutrition cohort, who were diagnosed with a first nonmetastatic primary cancer between 1992 and 2015.
• Body mass index (BMI) was calculated from self-reported data at the time of the first primary cancer diagnosis; 10,713 participants had a normal BMI (18.5 to < 25.0), 11,497 had overweight (25.0 to < 30.0), and 4684 had obesity (≥ 30.0). Participants were followed through 2017.
• The study outcomes were the incidences of any second primary cancer and obesity-related second cancers.
• The most common first primary cancers were prostate (35.0%), breast (19.1%), and colorectal (9.5%) cancers; almost 40% of all first primary cancers were related to obesity.

TAKEAWAY:

• Overall, 13.9% participants (3749 of 26,894) were diagnosed with a second cancer over a median of 7.9 years; 33.2% of these cancers were related to obesity.
• Compared with participants with a normal BMI, those who had overweight had a 15% higher risk for any second cancer (adjusted hazard ratio [aHR], 1.15) and a 40% higher risk for an obesity-related second cancer (aHR, 1.40). Additionally, those with obesity had a 34% higher risk for any second cancer and a 78% higher risk for an obesity-related second cancer.
• For every 5-unit increase in BMI, the risk for an obesity-related cancer (aHR, 1.28) was considerably higher than the risk for any second cancer (aHR, 1.13).
• Among all survivors, every 5-unit increase in BMI was associated with a 42% increased risk for colorectal cancer as a second cancer (aHR, 1.42) and a 70% higher risk for kidney cancer as a second cancer (aHR, 1.70).

IN PRACTICE:

“In this cohort study of older survivors of nonmetastatic cancer, those who had overweight or obesity at the time of their first cancer diagnosis were at higher risk of developing a second cancer, especially obesity-related cancers,” the authors wrote. “These findings have important public health implications and may inform evidence-based survivorship guidelines to reduce the risk of second primary cancers among cancer survivors.”

SOURCE:

This study, led by Clara Bodelon, PhD, MS, American Cancer Society, Atlanta, was published online in JAMA Network Open.

LIMITATIONS:

The exclusion of multiple primary cancers in the same site could have underestimated the magnitude of the association of excess body weight with the risk for second primary cancers. BMI was used as a measure of excess body fat in this study, which does not differentiate between fat and lean mass. Unmeasured or residual confounding factors might be present.

DISCLOSURES:

The study was supported by grants from the Centers for Disease Control and Prevention’s National Program of Cancer Registries and cancer registries supported by the National Cancer Institute’s Surveillance, Epidemiology, and End Results Program. No relevant conflicts of interest were disclosed by the authors.

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

TOPLINE:

Cancer survivors who had overweight or obesity at the time of their initial cancer diagnosis have a higher risk for a second primary cancer, particularly an obesity-related cancer, a new analysis found.

METHODOLOGY:

• Cancer survivors have an increased risk for another primary cancer. Studies suggest that lifestyle factors, such as excess body weight, may contribute to the risk for a second cancer; however, prospective long-term data on this association remain limited.
• Researchers evaluated 26,894 participants (mean age at first cancer diagnosis, 72.2 years; 97.6% White) from the Cancer Prevention Study II Nutrition cohort, who were diagnosed with a first nonmetastatic primary cancer between 1992 and 2015.
• Body mass index (BMI) was calculated from self-reported data at the time of the first primary cancer diagnosis; 10,713 participants had a normal BMI (18.5 to < 25.0), 11,497 had overweight (25.0 to < 30.0), and 4684 had obesity (≥ 30.0). Participants were followed through 2017.
• The study outcomes were the incidences of any second primary cancer and obesity-related second cancers.
• The most common first primary cancers were prostate (35.0%), breast (19.1%), and colorectal (9.5%) cancers; almost 40% of all first primary cancers were related to obesity.

TAKEAWAY:

• Overall, 13.9% participants (3749 of 26,894) were diagnosed with a second cancer over a median of 7.9 years; 33.2% of these cancers were related to obesity.
• Compared with participants with a normal BMI, those who had overweight had a 15% higher risk for any second cancer (adjusted hazard ratio [aHR], 1.15) and a 40% higher risk for an obesity-related second cancer (aHR, 1.40). Additionally, those with obesity had a 34% higher risk for any second cancer and a 78% higher risk for an obesity-related second cancer.
• For every 5-unit increase in BMI, the risk for an obesity-related cancer (aHR, 1.28) was considerably higher than the risk for any second cancer (aHR, 1.13).
• Among all survivors, every 5-unit increase in BMI was associated with a 42% increased risk for colorectal cancer as a second cancer (aHR, 1.42) and a 70% higher risk for kidney cancer as a second cancer (aHR, 1.70).

IN PRACTICE:

“In this cohort study of older survivors of nonmetastatic cancer, those who had overweight or obesity at the time of their first cancer diagnosis were at higher risk of developing a second cancer, especially obesity-related cancers,” the authors wrote. “These findings have important public health implications and may inform evidence-based survivorship guidelines to reduce the risk of second primary cancers among cancer survivors.”

SOURCE:

This study, led by Clara Bodelon, PhD, MS, American Cancer Society, Atlanta, was published online in JAMA Network Open.

LIMITATIONS:

The exclusion of multiple primary cancers in the same site could have underestimated the magnitude of the association of excess body weight with the risk for second primary cancers. BMI was used as a measure of excess body fat in this study, which does not differentiate between fat and lean mass. Unmeasured or residual confounding factors might be present.

DISCLOSURES:

The study was supported by grants from the Centers for Disease Control and Prevention’s National Program of Cancer Registries and cancer registries supported by the National Cancer Institute’s Surveillance, Epidemiology, and End Results Program. No relevant conflicts of interest were disclosed by the authors.

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

TOPLINE:

Cancer survivors who had overweight or obesity at the time of their initial cancer diagnosis have a higher risk for a second primary cancer, particularly an obesity-related cancer, a new analysis found.

METHODOLOGY:

• Cancer survivors have an increased risk for another primary cancer. Studies suggest that lifestyle factors, such as excess body weight, may contribute to the risk for a second cancer; however, prospective long-term data on this association remain limited.
• Researchers evaluated 26,894 participants (mean age at first cancer diagnosis, 72.2 years; 97.6% White) from the Cancer Prevention Study II Nutrition cohort, who were diagnosed with a first nonmetastatic primary cancer between 1992 and 2015.
• Body mass index (BMI) was calculated from self-reported data at the time of the first primary cancer diagnosis; 10,713 participants had a normal BMI (18.5 to < 25.0), 11,497 had overweight (25.0 to < 30.0), and 4684 had obesity (≥ 30.0). Participants were followed through 2017.
• The study outcomes were the incidences of any second primary cancer and obesity-related second cancers.
• The most common first primary cancers were prostate (35.0%), breast (19.1%), and colorectal (9.5%) cancers; almost 40% of all first primary cancers were related to obesity.

TAKEAWAY:

• Overall, 13.9% participants (3749 of 26,894) were diagnosed with a second cancer over a median of 7.9 years; 33.2% of these cancers were related to obesity.
• Compared with participants with a normal BMI, those who had overweight had a 15% higher risk for any second cancer (adjusted hazard ratio [aHR], 1.15) and a 40% higher risk for an obesity-related second cancer (aHR, 1.40). Additionally, those with obesity had a 34% higher risk for any second cancer and a 78% higher risk for an obesity-related second cancer.
• For every 5-unit increase in BMI, the risk for an obesity-related cancer (aHR, 1.28) was considerably higher than the risk for any second cancer (aHR, 1.13).
• Among all survivors, every 5-unit increase in BMI was associated with a 42% increased risk for colorectal cancer as a second cancer (aHR, 1.42) and a 70% higher risk for kidney cancer as a second cancer (aHR, 1.70).

IN PRACTICE:

“In this cohort study of older survivors of nonmetastatic cancer, those who had overweight or obesity at the time of their first cancer diagnosis were at higher risk of developing a second cancer, especially obesity-related cancers,” the authors wrote. “These findings have important public health implications and may inform evidence-based survivorship guidelines to reduce the risk of second primary cancers among cancer survivors.”

SOURCE:

This study, led by Clara Bodelon, PhD, MS, American Cancer Society, Atlanta, was published online in JAMA Network Open.

LIMITATIONS:

The exclusion of multiple primary cancers in the same site could have underestimated the magnitude of the association of excess body weight with the risk for second primary cancers. BMI was used as a measure of excess body fat in this study, which does not differentiate between fat and lean mass. Unmeasured or residual confounding factors might be present.

DISCLOSURES:

The study was supported by grants from the Centers for Disease Control and Prevention’s National Program of Cancer Registries and cancer registries supported by the National Cancer Institute’s Surveillance, Epidemiology, and End Results Program. No relevant conflicts of interest were disclosed by the authors.

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

Obesity is a chronic disease affecting more than 20% of adults in the United States. In 2022, prevalence was 20.5% among those aged 18 to 24 and 39.9% among those aged 45 to 54 years. This patient meets criteria for obesity (BMI ≥ 30), and it is likely that her obesity contributed to development of T2D, hypertension, osteoarthritis, and joint edema (as shown in the image). 

Patients with obesity are at high risk of developing cardiometabolic disease and osteoarthritis. Obesity is a key driver of T2D and cardiovascular disease development through its influence on insulin and lipid metabolism and proinflammatory changes. Factors associated with obesity that foster arthritis development include the erosive effects of adiponectin and leptin on cartilage and direct inflammation in joint tissues. 

It is important for patients with obesity and comorbid T2D and hypertension to receive multidisciplinary care designed to address all aspects of their health and minimize their risk for progression. The primary goal for this patient should be to promote weight loss safely while also improving her glycemic control and blood pressure. For patients with obesity and comorbid T2D, the American Diabetes Association recommends glucagon-like peptide-1 receptor agonists (GLP-1 RAs; semaglutide or liraglutide) or the dual gastric inhibitory polypeptide (GIP)/GLP-1 RA tirzepatide. The GLP-1 RA drugs reduce the risk for major cardiovascular events for patients with T2D while also providing substantial reductions in glucose levels without increasing hypoglycemia risk. They are available in higher doses (semaglutide 2.4 mg weekly, liraglutide 3.0 mg daily) for patients with obesity. These drugs also have salubrious effects on cardiorenal health and reduce progression of kidney disease. Tirzepatide produced greater reductions in A1c vs semaglutide in patients with T2D in the SURPASS-2 trial. It also has been shown to reduce atherosclerotic cardiovascular events in patients with overweight or obesity (without diabetes) in a post hoc analysis of the SURMOUNT-1 trial. Its effect on a broad set of cardiac, renal, and metabolic outcomes is being studied in the ongoing SURMOUNT-MMO trial. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). 

Pharmacologic interventions for osteoarthritis include nonsteroidal anti-inflammatory drugs, including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib. These may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical nonsteroidal anti-inflammatory drugs also may be useful. For more intractable joint pain, options include injecting corticosteroid or sodium hyaluronate into the affected joints or joint replacement.

In addition, comprehensive care includes lifestyle modifications designed to promote weight loss, reduce sodium, and increase exercise and intake of healthy foods. While maintaining intensive lifestyle modifications can be challenging, achieving weight loss of ≥ 5% can improve cardiometabolic risk factors in patients with obesity and T2D. Greater benefit is seen with greater reductions in body weight. Other interventions include behavioral modification and encouragement of increased physical activity to the extent of the patient's ability. Achieving substantial weight loss also could help relieve stress on the patient's joints, improve physical function, and mitigate osteoarthritis-related pain. The patient also may benefit from nonpharmacologic approaches to joint pain, including hot or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Obesity is a chronic disease affecting more than 20% of adults in the United States. In 2022, prevalence was 20.5% among those aged 18 to 24 and 39.9% among those aged 45 to 54 years. This patient meets criteria for obesity (BMI ≥ 30), and it is likely that her obesity contributed to development of T2D, hypertension, osteoarthritis, and joint edema (as shown in the image). 

Patients with obesity are at high risk of developing cardiometabolic disease and osteoarthritis. Obesity is a key driver of T2D and cardiovascular disease development through its influence on insulin and lipid metabolism and proinflammatory changes. Factors associated with obesity that foster arthritis development include the erosive effects of adiponectin and leptin on cartilage and direct inflammation in joint tissues. 

It is important for patients with obesity and comorbid T2D and hypertension to receive multidisciplinary care designed to address all aspects of their health and minimize their risk for progression. The primary goal for this patient should be to promote weight loss safely while also improving her glycemic control and blood pressure. For patients with obesity and comorbid T2D, the American Diabetes Association recommends glucagon-like peptide-1 receptor agonists (GLP-1 RAs; semaglutide or liraglutide) or the dual gastric inhibitory polypeptide (GIP)/GLP-1 RA tirzepatide. The GLP-1 RA drugs reduce the risk for major cardiovascular events for patients with T2D while also providing substantial reductions in glucose levels without increasing hypoglycemia risk. They are available in higher doses (semaglutide 2.4 mg weekly, liraglutide 3.0 mg daily) for patients with obesity. These drugs also have salubrious effects on cardiorenal health and reduce progression of kidney disease. Tirzepatide produced greater reductions in A1c vs semaglutide in patients with T2D in the SURPASS-2 trial. It also has been shown to reduce atherosclerotic cardiovascular events in patients with overweight or obesity (without diabetes) in a post hoc analysis of the SURMOUNT-1 trial. Its effect on a broad set of cardiac, renal, and metabolic outcomes is being studied in the ongoing SURMOUNT-MMO trial. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). 

Pharmacologic interventions for osteoarthritis include nonsteroidal anti-inflammatory drugs, including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib. These may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical nonsteroidal anti-inflammatory drugs also may be useful. For more intractable joint pain, options include injecting corticosteroid or sodium hyaluronate into the affected joints or joint replacement.

In addition, comprehensive care includes lifestyle modifications designed to promote weight loss, reduce sodium, and increase exercise and intake of healthy foods. While maintaining intensive lifestyle modifications can be challenging, achieving weight loss of ≥ 5% can improve cardiometabolic risk factors in patients with obesity and T2D. Greater benefit is seen with greater reductions in body weight. Other interventions include behavioral modification and encouragement of increased physical activity to the extent of the patient's ability. Achieving substantial weight loss also could help relieve stress on the patient's joints, improve physical function, and mitigate osteoarthritis-related pain. The patient also may benefit from nonpharmacologic approaches to joint pain, including hot or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Obesity is a chronic disease affecting more than 20% of adults in the United States. In 2022, prevalence was 20.5% among those aged 18 to 24 and 39.9% among those aged 45 to 54 years. This patient meets criteria for obesity (BMI ≥ 30), and it is likely that her obesity contributed to development of T2D, hypertension, osteoarthritis, and joint edema (as shown in the image). 

Patients with obesity are at high risk of developing cardiometabolic disease and osteoarthritis. Obesity is a key driver of T2D and cardiovascular disease development through its influence on insulin and lipid metabolism and proinflammatory changes. Factors associated with obesity that foster arthritis development include the erosive effects of adiponectin and leptin on cartilage and direct inflammation in joint tissues. 

It is important for patients with obesity and comorbid T2D and hypertension to receive multidisciplinary care designed to address all aspects of their health and minimize their risk for progression. The primary goal for this patient should be to promote weight loss safely while also improving her glycemic control and blood pressure. For patients with obesity and comorbid T2D, the American Diabetes Association recommends glucagon-like peptide-1 receptor agonists (GLP-1 RAs; semaglutide or liraglutide) or the dual gastric inhibitory polypeptide (GIP)/GLP-1 RA tirzepatide. The GLP-1 RA drugs reduce the risk for major cardiovascular events for patients with T2D while also providing substantial reductions in glucose levels without increasing hypoglycemia risk. They are available in higher doses (semaglutide 2.4 mg weekly, liraglutide 3.0 mg daily) for patients with obesity. These drugs also have salubrious effects on cardiorenal health and reduce progression of kidney disease. Tirzepatide produced greater reductions in A1c vs semaglutide in patients with T2D in the SURPASS-2 trial. It also has been shown to reduce atherosclerotic cardiovascular events in patients with overweight or obesity (without diabetes) in a post hoc analysis of the SURMOUNT-1 trial. Its effect on a broad set of cardiac, renal, and metabolic outcomes is being studied in the ongoing SURMOUNT-MMO trial. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). 

Pharmacologic interventions for osteoarthritis include nonsteroidal anti-inflammatory drugs, including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib. These may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical nonsteroidal anti-inflammatory drugs also may be useful. For more intractable joint pain, options include injecting corticosteroid or sodium hyaluronate into the affected joints or joint replacement.

In addition, comprehensive care includes lifestyle modifications designed to promote weight loss, reduce sodium, and increase exercise and intake of healthy foods. While maintaining intensive lifestyle modifications can be challenging, achieving weight loss of ≥ 5% can improve cardiometabolic risk factors in patients with obesity and T2D. Greater benefit is seen with greater reductions in body weight. Other interventions include behavioral modification and encouragement of increased physical activity to the extent of the patient's ability. Achieving substantial weight loss also could help relieve stress on the patient's joints, improve physical function, and mitigate osteoarthritis-related pain. The patient also may benefit from nonpharmacologic approaches to joint pain, including hot or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Many people who lose weight, whether through diet and lifestyle changes, medication, or bariatric surgery, recognize their body has changed. While they also experience improvements in quality of life and psychosocial areas, that’s not true for everyone. Some patients don’t “see” they’ve lost weight — a phenomenon referred to as “phantom fat,” “ghost fat,” or “vestigial body image.”

“Most people are happy with their appearance, or at least their body shape, after weight loss — although some are unhappy with the loose, sagging skin that can follow weight loss and seek plastic surgery to remedy that,” David B. Sarwer, PhD, director of the Center for Obesity Research and Education and professor of social and behavioral sciences, Temple University College of Public Health, Philadelphia, told this news organization. “There’s a subset of people who remain dissatisfied with their body image, including their shape.”

This body dissatisfaction of people who lose weight may be long-standing, predating the weight loss, or may be new because weight loss has catalyzed a host of previously unaddressed psychosocial issues. Some may show up at assessments on treatment onset, while others may be detected by monitoring changes during or after weight loss. “Mental health counseling after bariatric surgery is greatly underutilized,” Dr. Sarwer observed.
 

Ghost Fat

Research has corroborated the lingering self-perception of being “obese” vs “ex-obese.” In one study, patients who had undergone bariatric surgery reported being unable to see the difference in their size and shape 18-30 months following their procedure, despite substantial weight loss.

Some research suggests that rapid weight loss (eg, through bariatric surgery) is more likely to generate the perception of “phantom fat,” but additional research is needed to investigate whether the mode and speed of weight loss affect subsequent body image.

Being habituated to one’s former appearance may play a role, Dr. Sarwer suggested. “We see this not only with weight loss but with other body-altering procedures. It takes the brain time to catch up to the new appearance. In rhinoplasty, for example, it may take patients a while before they become accustomed to looking at their new face in the mirror after decades of looking at a more prominent nose.”
 

Years of Social Stigma

It may also take time for people to overcome years of enduring the stigma of obesity.

There are “pervasive” negative attitudes implying that individuals who are overweight and/or obese are “lazy, weak-willed, lacking in self-discipline and willpower” — a problem compounded by social media and media in general, which present unrealistic, glorified body images and disparaging messages about those with weight problems.

“Body image is a construct, rather than what you see in the mirror,” Sheethal Reddy, PhD, a psychologist at the Emory Bariatric Center, Emory University Hospital Midtown, Atlanta, told this news organization. “It’s the mental construct of our physical selves.”

According to Dr. Reddy, body image develops “within a broader societal context and is influenced by the person’s ethnic, racial, and cultural heritage.”

Adolescents are particularly vulnerable to body dissatisfaction. This is compounded in those with obesity, who often experience weight-based victimization and internalized weight-based stigma, compared with adolescents with lower weights. Weight stigma often takes the form of teasing and bullying.

“Appearance-related bullying and teasing during childhood and adolescence can reverberate into adulthood and persist throughout the lifespan,” Dr. Sarwer said. “When we see these patients and ask if they’ve ever been teased or bullied, not only do many say yes but it takes them back to those moments, to that origin story, and they remember someone saying something mean, cruel, and hurtful.”

Stigmatizing experiences can affect subjective body image, even after the weight has been lost and the person’s body is objectively thinner. Research comparing individuals who were overweight and lost weight to individuals who are currently overweight and haven’t lost weight and individuals who were never overweight suggests that “vestigial” body disparagement may persist following weight loss — especially in those with early-onset obesity.
 

The Role of Genetics

Genetics may contribute to people’s self-perception and body dissatisfaction, both before and after weight loss. A study of 827 community-based adolescents examined the association between polygenic risk scores (PRS) for body mass index (BMI) and type 2 diabetes and symptoms of body dissatisfaction and depression.

“Given the significant genetic role in BMI, we wanted to explore whether genetic risk for BMI might also predict body dissatisfaction,” lead author Krista Ekberg, MS, a doctoral candidate in clinical psychology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, told this news organization.

Genetic influences on BMI, as measured by PRS, were significantly associated with both phenotypic BMI and body dissatisfaction. “The association between PRS and body dissatisfaction was largely explained by BMI, suggesting that BMI itself accounts for much of the link between genetic risk and body dissatisfaction.”
 

Psychiatric History and Trauma

Adverse experiences, particularly sexual or physical abuse, may also account for body dissatisfaction after weight loss. “When some people with a history of this type of abuse lose a large amount of weight — typically after bariatric surgery — they often go through a period of emotional turbulence,” Dr. Sarwer said.

Childhood maltreatment can also be associated with body image disturbances in adulthood, according to a meta-analysis of 12 studies, encompassing 15,481 participants. Sexual abuse is “surprisingly common” among patients with obesity, according to Dr. Sarwer. A chart review of 131 patients revealed that 60% of those who reported a history of rape or sexual molestation were ≥ 50 pounds overweight vs only 28% of age- and sex-matched controls without a history of abuse. Other studies have corroborated these findings.

Excess weight can serve an “adaptive function,” Dr. Sarwer noted. It can be a self-protective mechanism that “insulates” them from sexual advances by potential romantic partners or abusers. Some may find that, after weight loss, repressed memories of a sexual assault surface as a result of the newer, more “attractive” appearance. Feeling vulnerable in their thinner bodies, they may need to regard themselves as overweight to maintain that feeling of “protection.” Weight loss may also trigger memories, flashbacks, or nightmares, as people return to a weight at which they were abused.

Dissociation is another mechanism linking trauma with post–weight loss body dysmorphia, Supatra Tovar, PsyD, RD, a clinical psychologist and registered dietitian with a practice in California, told this news organization. Dissociation from the body is often a coping mechanism for dealing with an overwhelming traumatic experience.

Individuals with a history of depression, anxiety, or posttraumatic stress disorder have higher levels of body dysmorphia, both before and after weight loss. One study found that patients undergoing bariatric surgery who had some type of psychopathology and other psychological risk factors were significantly more likely to report body image concerns 3 months after the surgery. Body image concerns were also more common in patients with preoperative depression, current psychotropic medication use, and a history of outpatient therapy or psychotropic medication use.

“Depression, anxiety, and trauma play a role in how you see yourself and how you carry yourself,” Dr. Reddy said. “This is wrapped up in any type of psychopathology. Being depressed is like looking at yourself through a cloud. It’s the opposite of ‘rose-colored glasses’ and instead, looking at yourself through a negative lens.”
 

Diagnosis and Interventions

Some helpful tools to assess the presence and extent of weight dissatisfaction and body dysmorphia include the Eating Disorder Inventory — Body Dissatisfaction Subscale and the Body Shape Questionnaire. It’s also important to take into account “the extent to which people are invested in their appearance psychologically,” Dr. Sarwer advised. The AO subscale of the Multidimensional Body-Self Relations Questionnaire generally assesses this. The Body Image Quality of Life Inventory assesses how and to what extent the perceived body image affects the person’s quality of life.

Experts recommend cognitive behavioral therapy (CBT) as an evidence-based intervention for body image issues, including those following weight loss.

“There’s an extensive CBT body image therapy program specifically tailored to the needs of overweight and obese individuals,” Dr. Sarwer said. “We don’t ignore historical variables that may have contributed to the problem, like early bullying, but we encourage people to think about what’s going on in their day-to-day life today. We drill down not only into the maladaptive behaviors but also the cognition and beliefs that may be erroneous but underlie these behaviors.”

The aim of CBT is to “modify irrational and dysfunctional thoughts, emotions, and behaviors through techniques such as self-monitoring, cognitive structuring, psychoeducation, desensitization, and exposure and response prevention.” The program laid out in Cash’s body image workbook includes eight steps. (Figure).

Weight Loss Doesn’t Automatically Equate With Happiness

Another realistic expectation runs counter to a common misperception that becoming thin will automatically translate into becoming happier. That’s not always the case, according to Dr. Tovar.

“If you haven’t worked deeply on addressing self-compassion and understanding that who you are at the core has nothing to do with your physical appearance, you can have an empty feeling once you’ve reached this point,” she said. “You still don’t know who you are and what you’re contributing to the world [because] you’ve been so focused on losing weight.”

Weight loss can also “unmask” questions about self-worth, even when receiving compliments about one’s “improved” appearance. “Praise and compliments after weight loss can be a double-edged sword,” Dr. Tovar observed. “You might think, ‘I wasn’t accepted or praised when I was overweight. The only way to be acceptable or validated is by losing weight, so I have to continue losing weight.’ ” This fuels fear of regaining the weight and can lead to continuing to see oneself as overweight, perhaps as a way to stay motivated to continue with weight loss. “Feeling that one’s value depends on remaining thin hampers body satisfaction,” she said.

Dr. Tovar, author of the book Deprogram Diet Culture: Rethink Your Relationship with Food, Heal Your Mind, and Live a Diet-Free Life, encourages people to shift the emphasis from weight loss to a holistic focus on self-worth and to explore obstacles to those feelings both before and after weight loss.

Endocrinologists and other medical professionals can help by not engaging in “weight and body shaming,” Dr. Tovar said.

She recommends physicians “encourage patients to tune in to their own bodies, helping them become more aware of how different foods affect their physical and emotional well-being.”

Set realistic expectations through “open, nonjudgmental conversations about the complexities of metabolism, weight, and health.”

Dr. Tovar advises rather than focusing on weight loss as the primary goal, physicians should focus on health markers such as blood glucose, energy levels, mental well-being, and physical fitness.

Prioritize “listening over lecturing.” Begin with empathy, asking questions such as “How do you feel about your health right now? What changes have you noticed in your body lately?” Doing this “creates space for the patient to express their concerns without feeling judged or shamed.”

Refer patients to a mental health professional when a patient exhibits signs of disordered eating or poor body image or when emotional factors are playing a significant role in the relationship with food and weight. “If a patient is caught in a cycle of dieting and weight gain, struggles with binge eating, or displays symptoms of depression or anxiety related to body, then psychological help is crucial.”

Ultimately, the goal of treatment “should be to provide a safe, supportive environment where patients can heal — not just physically but also emotionally and mentally,” Dr. Tovar added.

Dr. Tovar, Ms. Ekberg, and Dr. Reddy reported no relevant financial relationships. Dr. Sarwer received grant funding from the National Institute of Dental and Craniofacial Research and National Institute of Diabetes and Digestive and Kidney Diseases. He has consulting relationships with Novo Nordisk and Twenty30 Health. He is an associate editor for Obesity Surgery and editor in chief of Obesity Science & Practice.
 

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

Many people who lose weight, whether through diet and lifestyle changes, medication, or bariatric surgery, recognize their body has changed. While they also experience improvements in quality of life and psychosocial areas, that’s not true for everyone. Some patients don’t “see” they’ve lost weight — a phenomenon referred to as “phantom fat,” “ghost fat,” or “vestigial body image.”

“Most people are happy with their appearance, or at least their body shape, after weight loss — although some are unhappy with the loose, sagging skin that can follow weight loss and seek plastic surgery to remedy that,” David B. Sarwer, PhD, director of the Center for Obesity Research and Education and professor of social and behavioral sciences, Temple University College of Public Health, Philadelphia, told this news organization. “There’s a subset of people who remain dissatisfied with their body image, including their shape.”

This body dissatisfaction of people who lose weight may be long-standing, predating the weight loss, or may be new because weight loss has catalyzed a host of previously unaddressed psychosocial issues. Some may show up at assessments on treatment onset, while others may be detected by monitoring changes during or after weight loss. “Mental health counseling after bariatric surgery is greatly underutilized,” Dr. Sarwer observed.
 

Ghost Fat

Research has corroborated the lingering self-perception of being “obese” vs “ex-obese.” In one study, patients who had undergone bariatric surgery reported being unable to see the difference in their size and shape 18-30 months following their procedure, despite substantial weight loss.

Some research suggests that rapid weight loss (eg, through bariatric surgery) is more likely to generate the perception of “phantom fat,” but additional research is needed to investigate whether the mode and speed of weight loss affect subsequent body image.

Being habituated to one’s former appearance may play a role, Dr. Sarwer suggested. “We see this not only with weight loss but with other body-altering procedures. It takes the brain time to catch up to the new appearance. In rhinoplasty, for example, it may take patients a while before they become accustomed to looking at their new face in the mirror after decades of looking at a more prominent nose.”
 

Years of Social Stigma

It may also take time for people to overcome years of enduring the stigma of obesity.

There are “pervasive” negative attitudes implying that individuals who are overweight and/or obese are “lazy, weak-willed, lacking in self-discipline and willpower” — a problem compounded by social media and media in general, which present unrealistic, glorified body images and disparaging messages about those with weight problems.

“Body image is a construct, rather than what you see in the mirror,” Sheethal Reddy, PhD, a psychologist at the Emory Bariatric Center, Emory University Hospital Midtown, Atlanta, told this news organization. “It’s the mental construct of our physical selves.”

According to Dr. Reddy, body image develops “within a broader societal context and is influenced by the person’s ethnic, racial, and cultural heritage.”

Adolescents are particularly vulnerable to body dissatisfaction. This is compounded in those with obesity, who often experience weight-based victimization and internalized weight-based stigma, compared with adolescents with lower weights. Weight stigma often takes the form of teasing and bullying.

“Appearance-related bullying and teasing during childhood and adolescence can reverberate into adulthood and persist throughout the lifespan,” Dr. Sarwer said. “When we see these patients and ask if they’ve ever been teased or bullied, not only do many say yes but it takes them back to those moments, to that origin story, and they remember someone saying something mean, cruel, and hurtful.”

Stigmatizing experiences can affect subjective body image, even after the weight has been lost and the person’s body is objectively thinner. Research comparing individuals who were overweight and lost weight to individuals who are currently overweight and haven’t lost weight and individuals who were never overweight suggests that “vestigial” body disparagement may persist following weight loss — especially in those with early-onset obesity.
 

The Role of Genetics

Genetics may contribute to people’s self-perception and body dissatisfaction, both before and after weight loss. A study of 827 community-based adolescents examined the association between polygenic risk scores (PRS) for body mass index (BMI) and type 2 diabetes and symptoms of body dissatisfaction and depression.

“Given the significant genetic role in BMI, we wanted to explore whether genetic risk for BMI might also predict body dissatisfaction,” lead author Krista Ekberg, MS, a doctoral candidate in clinical psychology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, told this news organization.

Genetic influences on BMI, as measured by PRS, were significantly associated with both phenotypic BMI and body dissatisfaction. “The association between PRS and body dissatisfaction was largely explained by BMI, suggesting that BMI itself accounts for much of the link between genetic risk and body dissatisfaction.”
 

Psychiatric History and Trauma

Adverse experiences, particularly sexual or physical abuse, may also account for body dissatisfaction after weight loss. “When some people with a history of this type of abuse lose a large amount of weight — typically after bariatric surgery — they often go through a period of emotional turbulence,” Dr. Sarwer said.

Childhood maltreatment can also be associated with body image disturbances in adulthood, according to a meta-analysis of 12 studies, encompassing 15,481 participants. Sexual abuse is “surprisingly common” among patients with obesity, according to Dr. Sarwer. A chart review of 131 patients revealed that 60% of those who reported a history of rape or sexual molestation were ≥ 50 pounds overweight vs only 28% of age- and sex-matched controls without a history of abuse. Other studies have corroborated these findings.

Excess weight can serve an “adaptive function,” Dr. Sarwer noted. It can be a self-protective mechanism that “insulates” them from sexual advances by potential romantic partners or abusers. Some may find that, after weight loss, repressed memories of a sexual assault surface as a result of the newer, more “attractive” appearance. Feeling vulnerable in their thinner bodies, they may need to regard themselves as overweight to maintain that feeling of “protection.” Weight loss may also trigger memories, flashbacks, or nightmares, as people return to a weight at which they were abused.

Dissociation is another mechanism linking trauma with post–weight loss body dysmorphia, Supatra Tovar, PsyD, RD, a clinical psychologist and registered dietitian with a practice in California, told this news organization. Dissociation from the body is often a coping mechanism for dealing with an overwhelming traumatic experience.

Individuals with a history of depression, anxiety, or posttraumatic stress disorder have higher levels of body dysmorphia, both before and after weight loss. One study found that patients undergoing bariatric surgery who had some type of psychopathology and other psychological risk factors were significantly more likely to report body image concerns 3 months after the surgery. Body image concerns were also more common in patients with preoperative depression, current psychotropic medication use, and a history of outpatient therapy or psychotropic medication use.

“Depression, anxiety, and trauma play a role in how you see yourself and how you carry yourself,” Dr. Reddy said. “This is wrapped up in any type of psychopathology. Being depressed is like looking at yourself through a cloud. It’s the opposite of ‘rose-colored glasses’ and instead, looking at yourself through a negative lens.”
 

Diagnosis and Interventions

Some helpful tools to assess the presence and extent of weight dissatisfaction and body dysmorphia include the Eating Disorder Inventory — Body Dissatisfaction Subscale and the Body Shape Questionnaire. It’s also important to take into account “the extent to which people are invested in their appearance psychologically,” Dr. Sarwer advised. The AO subscale of the Multidimensional Body-Self Relations Questionnaire generally assesses this. The Body Image Quality of Life Inventory assesses how and to what extent the perceived body image affects the person’s quality of life.

Experts recommend cognitive behavioral therapy (CBT) as an evidence-based intervention for body image issues, including those following weight loss.

“There’s an extensive CBT body image therapy program specifically tailored to the needs of overweight and obese individuals,” Dr. Sarwer said. “We don’t ignore historical variables that may have contributed to the problem, like early bullying, but we encourage people to think about what’s going on in their day-to-day life today. We drill down not only into the maladaptive behaviors but also the cognition and beliefs that may be erroneous but underlie these behaviors.”

The aim of CBT is to “modify irrational and dysfunctional thoughts, emotions, and behaviors through techniques such as self-monitoring, cognitive structuring, psychoeducation, desensitization, and exposure and response prevention.” The program laid out in Cash’s body image workbook includes eight steps. (Figure).

Weight Loss Doesn’t Automatically Equate With Happiness

Another realistic expectation runs counter to a common misperception that becoming thin will automatically translate into becoming happier. That’s not always the case, according to Dr. Tovar.

“If you haven’t worked deeply on addressing self-compassion and understanding that who you are at the core has nothing to do with your physical appearance, you can have an empty feeling once you’ve reached this point,” she said. “You still don’t know who you are and what you’re contributing to the world [because] you’ve been so focused on losing weight.”

Weight loss can also “unmask” questions about self-worth, even when receiving compliments about one’s “improved” appearance. “Praise and compliments after weight loss can be a double-edged sword,” Dr. Tovar observed. “You might think, ‘I wasn’t accepted or praised when I was overweight. The only way to be acceptable or validated is by losing weight, so I have to continue losing weight.’ ” This fuels fear of regaining the weight and can lead to continuing to see oneself as overweight, perhaps as a way to stay motivated to continue with weight loss. “Feeling that one’s value depends on remaining thin hampers body satisfaction,” she said.

Dr. Tovar, author of the book Deprogram Diet Culture: Rethink Your Relationship with Food, Heal Your Mind, and Live a Diet-Free Life, encourages people to shift the emphasis from weight loss to a holistic focus on self-worth and to explore obstacles to those feelings both before and after weight loss.

Endocrinologists and other medical professionals can help by not engaging in “weight and body shaming,” Dr. Tovar said.

She recommends physicians “encourage patients to tune in to their own bodies, helping them become more aware of how different foods affect their physical and emotional well-being.”

Set realistic expectations through “open, nonjudgmental conversations about the complexities of metabolism, weight, and health.”

Dr. Tovar advises rather than focusing on weight loss as the primary goal, physicians should focus on health markers such as blood glucose, energy levels, mental well-being, and physical fitness.

Prioritize “listening over lecturing.” Begin with empathy, asking questions such as “How do you feel about your health right now? What changes have you noticed in your body lately?” Doing this “creates space for the patient to express their concerns without feeling judged or shamed.”

Refer patients to a mental health professional when a patient exhibits signs of disordered eating or poor body image or when emotional factors are playing a significant role in the relationship with food and weight. “If a patient is caught in a cycle of dieting and weight gain, struggles with binge eating, or displays symptoms of depression or anxiety related to body, then psychological help is crucial.”

Ultimately, the goal of treatment “should be to provide a safe, supportive environment where patients can heal — not just physically but also emotionally and mentally,” Dr. Tovar added.

Dr. Tovar, Ms. Ekberg, and Dr. Reddy reported no relevant financial relationships. Dr. Sarwer received grant funding from the National Institute of Dental and Craniofacial Research and National Institute of Diabetes and Digestive and Kidney Diseases. He has consulting relationships with Novo Nordisk and Twenty30 Health. He is an associate editor for Obesity Surgery and editor in chief of Obesity Science & Practice.
 

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

Many people who lose weight, whether through diet and lifestyle changes, medication, or bariatric surgery, recognize their body has changed. While they also experience improvements in quality of life and psychosocial areas, that’s not true for everyone. Some patients don’t “see” they’ve lost weight — a phenomenon referred to as “phantom fat,” “ghost fat,” or “vestigial body image.”

“Most people are happy with their appearance, or at least their body shape, after weight loss — although some are unhappy with the loose, sagging skin that can follow weight loss and seek plastic surgery to remedy that,” David B. Sarwer, PhD, director of the Center for Obesity Research and Education and professor of social and behavioral sciences, Temple University College of Public Health, Philadelphia, told this news organization. “There’s a subset of people who remain dissatisfied with their body image, including their shape.”

This body dissatisfaction of people who lose weight may be long-standing, predating the weight loss, or may be new because weight loss has catalyzed a host of previously unaddressed psychosocial issues. Some may show up at assessments on treatment onset, while others may be detected by monitoring changes during or after weight loss. “Mental health counseling after bariatric surgery is greatly underutilized,” Dr. Sarwer observed.
 

Ghost Fat

Research has corroborated the lingering self-perception of being “obese” vs “ex-obese.” In one study, patients who had undergone bariatric surgery reported being unable to see the difference in their size and shape 18-30 months following their procedure, despite substantial weight loss.

Some research suggests that rapid weight loss (eg, through bariatric surgery) is more likely to generate the perception of “phantom fat,” but additional research is needed to investigate whether the mode and speed of weight loss affect subsequent body image.

Being habituated to one’s former appearance may play a role, Dr. Sarwer suggested. “We see this not only with weight loss but with other body-altering procedures. It takes the brain time to catch up to the new appearance. In rhinoplasty, for example, it may take patients a while before they become accustomed to looking at their new face in the mirror after decades of looking at a more prominent nose.”
 

Years of Social Stigma

It may also take time for people to overcome years of enduring the stigma of obesity.

There are “pervasive” negative attitudes implying that individuals who are overweight and/or obese are “lazy, weak-willed, lacking in self-discipline and willpower” — a problem compounded by social media and media in general, which present unrealistic, glorified body images and disparaging messages about those with weight problems.

“Body image is a construct, rather than what you see in the mirror,” Sheethal Reddy, PhD, a psychologist at the Emory Bariatric Center, Emory University Hospital Midtown, Atlanta, told this news organization. “It’s the mental construct of our physical selves.”

According to Dr. Reddy, body image develops “within a broader societal context and is influenced by the person’s ethnic, racial, and cultural heritage.”

Adolescents are particularly vulnerable to body dissatisfaction. This is compounded in those with obesity, who often experience weight-based victimization and internalized weight-based stigma, compared with adolescents with lower weights. Weight stigma often takes the form of teasing and bullying.

“Appearance-related bullying and teasing during childhood and adolescence can reverberate into adulthood and persist throughout the lifespan,” Dr. Sarwer said. “When we see these patients and ask if they’ve ever been teased or bullied, not only do many say yes but it takes them back to those moments, to that origin story, and they remember someone saying something mean, cruel, and hurtful.”

Stigmatizing experiences can affect subjective body image, even after the weight has been lost and the person’s body is objectively thinner. Research comparing individuals who were overweight and lost weight to individuals who are currently overweight and haven’t lost weight and individuals who were never overweight suggests that “vestigial” body disparagement may persist following weight loss — especially in those with early-onset obesity.
 

The Role of Genetics

Genetics may contribute to people’s self-perception and body dissatisfaction, both before and after weight loss. A study of 827 community-based adolescents examined the association between polygenic risk scores (PRS) for body mass index (BMI) and type 2 diabetes and symptoms of body dissatisfaction and depression.

“Given the significant genetic role in BMI, we wanted to explore whether genetic risk for BMI might also predict body dissatisfaction,” lead author Krista Ekberg, MS, a doctoral candidate in clinical psychology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, told this news organization.

Genetic influences on BMI, as measured by PRS, were significantly associated with both phenotypic BMI and body dissatisfaction. “The association between PRS and body dissatisfaction was largely explained by BMI, suggesting that BMI itself accounts for much of the link between genetic risk and body dissatisfaction.”
 

Psychiatric History and Trauma

Adverse experiences, particularly sexual or physical abuse, may also account for body dissatisfaction after weight loss. “When some people with a history of this type of abuse lose a large amount of weight — typically after bariatric surgery — they often go through a period of emotional turbulence,” Dr. Sarwer said.

Childhood maltreatment can also be associated with body image disturbances in adulthood, according to a meta-analysis of 12 studies, encompassing 15,481 participants. Sexual abuse is “surprisingly common” among patients with obesity, according to Dr. Sarwer. A chart review of 131 patients revealed that 60% of those who reported a history of rape or sexual molestation were ≥ 50 pounds overweight vs only 28% of age- and sex-matched controls without a history of abuse. Other studies have corroborated these findings.

Excess weight can serve an “adaptive function,” Dr. Sarwer noted. It can be a self-protective mechanism that “insulates” them from sexual advances by potential romantic partners or abusers. Some may find that, after weight loss, repressed memories of a sexual assault surface as a result of the newer, more “attractive” appearance. Feeling vulnerable in their thinner bodies, they may need to regard themselves as overweight to maintain that feeling of “protection.” Weight loss may also trigger memories, flashbacks, or nightmares, as people return to a weight at which they were abused.

Dissociation is another mechanism linking trauma with post–weight loss body dysmorphia, Supatra Tovar, PsyD, RD, a clinical psychologist and registered dietitian with a practice in California, told this news organization. Dissociation from the body is often a coping mechanism for dealing with an overwhelming traumatic experience.

Individuals with a history of depression, anxiety, or posttraumatic stress disorder have higher levels of body dysmorphia, both before and after weight loss. One study found that patients undergoing bariatric surgery who had some type of psychopathology and other psychological risk factors were significantly more likely to report body image concerns 3 months after the surgery. Body image concerns were also more common in patients with preoperative depression, current psychotropic medication use, and a history of outpatient therapy or psychotropic medication use.

“Depression, anxiety, and trauma play a role in how you see yourself and how you carry yourself,” Dr. Reddy said. “This is wrapped up in any type of psychopathology. Being depressed is like looking at yourself through a cloud. It’s the opposite of ‘rose-colored glasses’ and instead, looking at yourself through a negative lens.”
 

Diagnosis and Interventions

Some helpful tools to assess the presence and extent of weight dissatisfaction and body dysmorphia include the Eating Disorder Inventory — Body Dissatisfaction Subscale and the Body Shape Questionnaire. It’s also important to take into account “the extent to which people are invested in their appearance psychologically,” Dr. Sarwer advised. The AO subscale of the Multidimensional Body-Self Relations Questionnaire generally assesses this. The Body Image Quality of Life Inventory assesses how and to what extent the perceived body image affects the person’s quality of life.

Experts recommend cognitive behavioral therapy (CBT) as an evidence-based intervention for body image issues, including those following weight loss.

“There’s an extensive CBT body image therapy program specifically tailored to the needs of overweight and obese individuals,” Dr. Sarwer said. “We don’t ignore historical variables that may have contributed to the problem, like early bullying, but we encourage people to think about what’s going on in their day-to-day life today. We drill down not only into the maladaptive behaviors but also the cognition and beliefs that may be erroneous but underlie these behaviors.”

The aim of CBT is to “modify irrational and dysfunctional thoughts, emotions, and behaviors through techniques such as self-monitoring, cognitive structuring, psychoeducation, desensitization, and exposure and response prevention.” The program laid out in Cash’s body image workbook includes eight steps. (Figure).

Weight Loss Doesn’t Automatically Equate With Happiness

Another realistic expectation runs counter to a common misperception that becoming thin will automatically translate into becoming happier. That’s not always the case, according to Dr. Tovar.

“If you haven’t worked deeply on addressing self-compassion and understanding that who you are at the core has nothing to do with your physical appearance, you can have an empty feeling once you’ve reached this point,” she said. “You still don’t know who you are and what you’re contributing to the world [because] you’ve been so focused on losing weight.”

Weight loss can also “unmask” questions about self-worth, even when receiving compliments about one’s “improved” appearance. “Praise and compliments after weight loss can be a double-edged sword,” Dr. Tovar observed. “You might think, ‘I wasn’t accepted or praised when I was overweight. The only way to be acceptable or validated is by losing weight, so I have to continue losing weight.’ ” This fuels fear of regaining the weight and can lead to continuing to see oneself as overweight, perhaps as a way to stay motivated to continue with weight loss. “Feeling that one’s value depends on remaining thin hampers body satisfaction,” she said.

Dr. Tovar, author of the book Deprogram Diet Culture: Rethink Your Relationship with Food, Heal Your Mind, and Live a Diet-Free Life, encourages people to shift the emphasis from weight loss to a holistic focus on self-worth and to explore obstacles to those feelings both before and after weight loss.

Endocrinologists and other medical professionals can help by not engaging in “weight and body shaming,” Dr. Tovar said.

She recommends physicians “encourage patients to tune in to their own bodies, helping them become more aware of how different foods affect their physical and emotional well-being.”

Set realistic expectations through “open, nonjudgmental conversations about the complexities of metabolism, weight, and health.”

Dr. Tovar advises rather than focusing on weight loss as the primary goal, physicians should focus on health markers such as blood glucose, energy levels, mental well-being, and physical fitness.

Prioritize “listening over lecturing.” Begin with empathy, asking questions such as “How do you feel about your health right now? What changes have you noticed in your body lately?” Doing this “creates space for the patient to express their concerns without feeling judged or shamed.”

Refer patients to a mental health professional when a patient exhibits signs of disordered eating or poor body image or when emotional factors are playing a significant role in the relationship with food and weight. “If a patient is caught in a cycle of dieting and weight gain, struggles with binge eating, or displays symptoms of depression or anxiety related to body, then psychological help is crucial.”

Ultimately, the goal of treatment “should be to provide a safe, supportive environment where patients can heal — not just physically but also emotionally and mentally,” Dr. Tovar added.

Dr. Tovar, Ms. Ekberg, and Dr. Reddy reported no relevant financial relationships. Dr. Sarwer received grant funding from the National Institute of Dental and Craniofacial Research and National Institute of Diabetes and Digestive and Kidney Diseases. He has consulting relationships with Novo Nordisk and Twenty30 Health. He is an associate editor for Obesity Surgery and editor in chief of Obesity Science & Practice.
 

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

On October 2, the Food and Drug Administration (FDA)’s Drug Shortage Database showed that the tirzepatide injection (Zepbound, Mounjaro/Lilly) shortage is now “resolved.” The agency wrote in a clarification aimed at compounders that Lilly said it can meet the “present and projected national demand” and that compounders are restricted from making the products. 

Nevertheless, patients and prescribers may still see “intermittent localized supply disruptions as the products move through the supply chain,” the FDA noted.

The Alliance for Pharmacy Compounding (APC) responded swiftly, alerting its members and the public to the resolved shortage and stating that compounders “must immediately cease preparing and dispensing compounded copies” of the two drugs.

However, APC CEO Scott Brunner added it often takes a long time for FDA-approved versions of the drug to become widely available to wholesalers, hospitals, and clinics. Even after Lilly announced greater availability for the drugs, including in a new vial format for low doses, “for most pharmacies, they’re lucky to get two or three boxes of Zepbound a day from their wholesaler — for a patient waiting list that can number in the hundreds.”

“We have already heard this morning from APC members that they are unable to fill orders for their patients,” he said.

Furthermore, he contended, “I suspect plenty of patients taking compounded tirzepatide are going to be caught flat-footed by this. They are being cut off cold turkey, their prescription no longer fillable. They’ll need to get in to see their provider to get a new prescription, and that will take some time. It’s possible that so many patients presently taking compounded GLP-1s [glucagon-like peptide 1] will be eventually switched to the FDA-approved versions — if they can afford them, of course — that it will push tirzepatide injection back into shortage.”

Commenting on the shortage resolution, endocrinologist Beverly Tchang, MD, DABOM, an assistant professor of clinical medicine at Weill Cornell Medicine in New York City told this news organization, “we are not yet experiencing relief from the shortages, but I hope this resolves at least one barrier to access for our patients.”

“I don’t think it will create confusion,” she said. “Fortunately or unfortunately, patients and clinicians are adept by now with therapeutic transitions because we’ve been forced to do so whenever insurance withdraws coverage or a shortage recurs or a coupon expires. It’s obviously not ideal but patients are motivated and clinicians don’t give up.”

This news organization has previously reported on the impact of the shortages and how endocrinologists and obesity medicine specialists were handling them, in light of concerns about compounding pharmacies that may or may not be well founded. 

Dr. Tchang declared that she is an adviser to Novo Nordisk.

A version of this article appeared on Medscape.com.

On October 2, the Food and Drug Administration (FDA)’s Drug Shortage Database showed that the tirzepatide injection (Zepbound, Mounjaro/Lilly) shortage is now “resolved.” The agency wrote in a clarification aimed at compounders that Lilly said it can meet the “present and projected national demand” and that compounders are restricted from making the products. 

Nevertheless, patients and prescribers may still see “intermittent localized supply disruptions as the products move through the supply chain,” the FDA noted.

The Alliance for Pharmacy Compounding (APC) responded swiftly, alerting its members and the public to the resolved shortage and stating that compounders “must immediately cease preparing and dispensing compounded copies” of the two drugs.

However, APC CEO Scott Brunner added it often takes a long time for FDA-approved versions of the drug to become widely available to wholesalers, hospitals, and clinics. Even after Lilly announced greater availability for the drugs, including in a new vial format for low doses, “for most pharmacies, they’re lucky to get two or three boxes of Zepbound a day from their wholesaler — for a patient waiting list that can number in the hundreds.”

“We have already heard this morning from APC members that they are unable to fill orders for their patients,” he said.

Furthermore, he contended, “I suspect plenty of patients taking compounded tirzepatide are going to be caught flat-footed by this. They are being cut off cold turkey, their prescription no longer fillable. They’ll need to get in to see their provider to get a new prescription, and that will take some time. It’s possible that so many patients presently taking compounded GLP-1s [glucagon-like peptide 1] will be eventually switched to the FDA-approved versions — if they can afford them, of course — that it will push tirzepatide injection back into shortage.”

Commenting on the shortage resolution, endocrinologist Beverly Tchang, MD, DABOM, an assistant professor of clinical medicine at Weill Cornell Medicine in New York City told this news organization, “we are not yet experiencing relief from the shortages, but I hope this resolves at least one barrier to access for our patients.”

“I don’t think it will create confusion,” she said. “Fortunately or unfortunately, patients and clinicians are adept by now with therapeutic transitions because we’ve been forced to do so whenever insurance withdraws coverage or a shortage recurs or a coupon expires. It’s obviously not ideal but patients are motivated and clinicians don’t give up.”

This news organization has previously reported on the impact of the shortages and how endocrinologists and obesity medicine specialists were handling them, in light of concerns about compounding pharmacies that may or may not be well founded. 

Dr. Tchang declared that she is an adviser to Novo Nordisk.

A version of this article appeared on Medscape.com.

On October 2, the Food and Drug Administration (FDA)’s Drug Shortage Database showed that the tirzepatide injection (Zepbound, Mounjaro/Lilly) shortage is now “resolved.” The agency wrote in a clarification aimed at compounders that Lilly said it can meet the “present and projected national demand” and that compounders are restricted from making the products. 

Nevertheless, patients and prescribers may still see “intermittent localized supply disruptions as the products move through the supply chain,” the FDA noted.

The Alliance for Pharmacy Compounding (APC) responded swiftly, alerting its members and the public to the resolved shortage and stating that compounders “must immediately cease preparing and dispensing compounded copies” of the two drugs.

However, APC CEO Scott Brunner added it often takes a long time for FDA-approved versions of the drug to become widely available to wholesalers, hospitals, and clinics. Even after Lilly announced greater availability for the drugs, including in a new vial format for low doses, “for most pharmacies, they’re lucky to get two or three boxes of Zepbound a day from their wholesaler — for a patient waiting list that can number in the hundreds.”

“We have already heard this morning from APC members that they are unable to fill orders for their patients,” he said.

Furthermore, he contended, “I suspect plenty of patients taking compounded tirzepatide are going to be caught flat-footed by this. They are being cut off cold turkey, their prescription no longer fillable. They’ll need to get in to see their provider to get a new prescription, and that will take some time. It’s possible that so many patients presently taking compounded GLP-1s [glucagon-like peptide 1] will be eventually switched to the FDA-approved versions — if they can afford them, of course — that it will push tirzepatide injection back into shortage.”

Commenting on the shortage resolution, endocrinologist Beverly Tchang, MD, DABOM, an assistant professor of clinical medicine at Weill Cornell Medicine in New York City told this news organization, “we are not yet experiencing relief from the shortages, but I hope this resolves at least one barrier to access for our patients.”

“I don’t think it will create confusion,” she said. “Fortunately or unfortunately, patients and clinicians are adept by now with therapeutic transitions because we’ve been forced to do so whenever insurance withdraws coverage or a shortage recurs or a coupon expires. It’s obviously not ideal but patients are motivated and clinicians don’t give up.”

This news organization has previously reported on the impact of the shortages and how endocrinologists and obesity medicine specialists were handling them, in light of concerns about compounding pharmacies that may or may not be well founded. 

Dr. Tchang declared that she is an adviser to Novo Nordisk.

A version of this article appeared on Medscape.com.