Obesity

After bariatric surgery in 2014, Kristal Hartman still struggled to manage her weight long term. It took her over a year to lose 100 pounds, a loss she initially maintained, but then gradually her body mass index (BMI) started creeping up again.

“The body kind of has a set point, and you have to constantly trick it because it is going to start to gain weight again,” Ms. Hartman, who is on the national board of directors for the Obesity Action Coalition, said in an interview.

So, 2.5 years after her surgery, Ms. Hartman began weekly subcutaneous injections of the glucagonlike peptide–1 (GLP-1) agonist semaglutide, a medication that is now almost infamous because of its popularity among celebrities and social media influencers.

Branded as Ozempic for type 2 diabetes and Wegovy for obesity, both contain semaglutide but in slightly different doses. The popularity of the medication has led to shortages for those living with type 2 diabetes and/or obesity. And other medications are waiting in the wings that work on GLP-1 and other hormones that regulate appetite, such as the twincretin tirzepatide (Mounjaro), another weekly injection, approved by the Food and Drug Administration in May 2022 for type 2 diabetes and awaiting approval for obesity.

Ms. Hartman said taking semaglutide helped her not only lose weight but also “curb [her] obsessive thoughts over food.” To maintain a BMI within the healthy range, as well as taking the GLP-1 agonist, Ms. Hartman relies on other strategies, including exercise, and mental health support.

“Physicians really need to be open to these FDA-approved medications as one of many tools in the toolbox for patients with obesity. It’s just like any other chronic disease state, when they are thinking of using these, they need to think about long-term use ... in patients who have obesity, not just [among those people] who just want to lose 5-10 pounds. That’s not what these drugs are designed for. They are for people who are actually living with the chronic disease of obesity every day of their lives,” she emphasized.

On average, patients lose 25%-40% of their total body weight following bariatric surgery, said Teresa LeMasters, MD, president of the American Society for Metabolic & Bariatric Surgery. However, there typically is a “small” weight regain after surgery.

“For most patients, it is a small 5-10 pounds, but for some others, it can be significant,” said Dr. LeMasters, a bariatric surgeon at UnityPoint Clinic, Des Moines, Iowa.

“We do still see some patients– anywhere from 10% to 30% – who will have some [significant] weight regain, and so then we will look at that,” she noted. In those cases, the disease of obesity “is definitely still present.”
 

Medications can counter weight regain after surgery

For patients who don’t reach their weight loss goals after bariatric surgery, Dr. LeMasters said it’s appropriate to consider adding an anti-obesity medication. The newer GLP-1 agonists can lead to a loss of around 15% of body weight in some patients.

“The GLP-1 agonists have been very helpful for treating patients who’ve had bariatric surgery and had some weight regain, or even just to optimize their initial response to surgery if they are starting at a very, very severe point of disease,” she explained.

She noted, however, that some patients shouldn’t be prescribed GLP-1 agonists, including those with a history of thyroid cancer or pancreatitis.

Caroline M. Apovian, MD, codirector of the center for weight management and wellness and professor of medicine at Harvard Medical School, Boston, said in an interview that the physiology behind bariatric surgery and that of the newer obesity medications is somewhat aligned.

“In order to reduce ... body weight permanently you need adjustments. We learned that you need the adjustments of the hormones [that affect appetite, such as GLP-1], and that’s why bariatric surgery works because ... [it] provides the most durable and the most effective treatment for obesity ... because [with surgery] you are adjusting the secretion and timing of many of the hormones that regulate body weight,” she explained.

So, when people are taking GLP-1 agonists for obesity, with or without surgery, these medications “are meant and were approved by the FDA to be taken indefinitely. They are not [for the] short term,” Dr. Apovian noted.

Benjamin O’Donnell, MD, an associate professor at Ohio State University Wexner Medical Center, Columbus, agreed that the newer anti-obesity medications can be very effective; however, he expressed uncertainty about prescribing these medications for years and years.

“If somebody has obesity, they need medicine to help them manage appetite and maintain a lower, healthier weight. It would make sense that they would just stay on the medicine,” he noted.

But he qualified: “I have a hard time committing to saying that someone should take this medication for the rest of their life. Part of my hesitation is that the medications are expensive, so we’ve had a hard time with people staying on them, mostly because of insurance formulary changes.”
 

Why stop the medications? Side effects and lack of insurance coverage

Many people have to discontinue these newer medications for that exact reason.

When Ms. Hartman’s insurance coverage lapsed, she had to go without semaglutide for a while.

“At that time, I absolutely gained weight back up into an abnormal BMI range,” Ms. Hartman said. When she was able to resume the medication, she lost weight again and her BMI returned to normal range.

These medications currently cost around $1,400 per month in the United States, unless patients can access initiatives such as company coupons. Some insurers, including state-subsidized Medicare and Medicaid, don’t cover the new medications.

Dr. O’Donnell said, “More accessibility for more people would help in the big picture.”

Other patients stop taking GLP-1 agonists because they experience side effects, such as nausea.

“Gastrointestinal complaints ... are the number one reason for people to come off the medication,” said Disha Narang, MD, an endocrinologist and obesity medicine specialist at Northwestern Medicine Lake Forest (Ill.) Hospital.

“It is an elective therapy, so it is not mandatory that someone take it. So if they are not feeling well or they are sick, then that’s a major reason for coming off of it,” she said.

Dan Bessesen, MD, professor of medicine at the University of Colorado at Denver, Aurora, and chief of endocrinology, agreed.

Patients are unlikely to stay on these medications if they feel nauseous or experience vomiting, he said. Although he noted there are options to try to counter this, such as starting patients on a very low dose of the drug and up-titrating slowly. This method requires good coordination between the patient and physician.

Goutham Rao, MD, a professor of medicine at Case Western Reserve University and head of the weight-loss initiative Fitter Me at University Hospitals, both in Cleveland, said that prior to prescribing GLP-1 agonists for weight loss, he sets four basic, nonnegotiable goals for patients: “to have breakfast within 30 minutes of getting up, to drink just water, no food or drink after 7:00 p.m. except for water, and 30 minutes of continuous exercise per day, which is typically, for older clientele, walking.”

This, he said, can help establish good habits because if “patients are not engaged psychologically in weight loss ... they expect the medication to do [all] the work.”
 

Most regain weight after stopping obesity medications

As Ms. Hartman’s story illustrates, discontinuing the medications often leads to weight regain.

“Without the medicine, there are a variety of things that will happen. Appetite will tend to increase, and so [patients] will gradually tend to eat more over time,” Dr. Bessesen noted.

“So it may take a long time for the weight regain to happen, but in every study where an obesity medicine has been used, and then it is stopped, the weight goes back to where it was on lifestyle alone,” he added.

In the STEP 1 trial, almost 2,000 patients who were either overweight or living with obesity were randomized 2:1 to semaglutide, titrated up to 2.4 mg each week by week 16, or placebo in addition to lifestyle modification. After 68 weeks, those in the semaglutide group had a mean weight loss of 14.9%, compared with 2.4% in the placebo group.

Patients were also followed in a 1-year extension of the trial, published in Diabetes, Obesity, and Metabolism.

Within 1 year of stopping treatment, participants regained two thirds of the weight they had initially lost.

Hence, Dr. Bessesen stressed that a total rethink of how obesity is approached is needed among most physicians.

“I think in the future treating obesity with medications should be like treating hypertension and diabetes, something most primary care doctors are comfortable doing, but that’s going to take a little work and practice on the part of clinicians to really have a comfortable conversation about risks, and benefits, with patients,” he said.

“I would encourage primary care doctors to learn more about the treatment of obesity, and learn more about bias and stigma, and think about how they can deliver care that is compassionate and competent,” he concluded.

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

After bariatric surgery in 2014, Kristal Hartman still struggled to manage her weight long term. It took her over a year to lose 100 pounds, a loss she initially maintained, but then gradually her body mass index (BMI) started creeping up again.

“The body kind of has a set point, and you have to constantly trick it because it is going to start to gain weight again,” Ms. Hartman, who is on the national board of directors for the Obesity Action Coalition, said in an interview.

So, 2.5 years after her surgery, Ms. Hartman began weekly subcutaneous injections of the glucagonlike peptide–1 (GLP-1) agonist semaglutide, a medication that is now almost infamous because of its popularity among celebrities and social media influencers.

Branded as Ozempic for type 2 diabetes and Wegovy for obesity, both contain semaglutide but in slightly different doses. The popularity of the medication has led to shortages for those living with type 2 diabetes and/or obesity. And other medications are waiting in the wings that work on GLP-1 and other hormones that regulate appetite, such as the twincretin tirzepatide (Mounjaro), another weekly injection, approved by the Food and Drug Administration in May 2022 for type 2 diabetes and awaiting approval for obesity.

Ms. Hartman said taking semaglutide helped her not only lose weight but also “curb [her] obsessive thoughts over food.” To maintain a BMI within the healthy range, as well as taking the GLP-1 agonist, Ms. Hartman relies on other strategies, including exercise, and mental health support.

“Physicians really need to be open to these FDA-approved medications as one of many tools in the toolbox for patients with obesity. It’s just like any other chronic disease state, when they are thinking of using these, they need to think about long-term use ... in patients who have obesity, not just [among those people] who just want to lose 5-10 pounds. That’s not what these drugs are designed for. They are for people who are actually living with the chronic disease of obesity every day of their lives,” she emphasized.

On average, patients lose 25%-40% of their total body weight following bariatric surgery, said Teresa LeMasters, MD, president of the American Society for Metabolic & Bariatric Surgery. However, there typically is a “small” weight regain after surgery.

“For most patients, it is a small 5-10 pounds, but for some others, it can be significant,” said Dr. LeMasters, a bariatric surgeon at UnityPoint Clinic, Des Moines, Iowa.

“We do still see some patients– anywhere from 10% to 30% – who will have some [significant] weight regain, and so then we will look at that,” she noted. In those cases, the disease of obesity “is definitely still present.”
 

Medications can counter weight regain after surgery

For patients who don’t reach their weight loss goals after bariatric surgery, Dr. LeMasters said it’s appropriate to consider adding an anti-obesity medication. The newer GLP-1 agonists can lead to a loss of around 15% of body weight in some patients.

“The GLP-1 agonists have been very helpful for treating patients who’ve had bariatric surgery and had some weight regain, or even just to optimize their initial response to surgery if they are starting at a very, very severe point of disease,” she explained.

She noted, however, that some patients shouldn’t be prescribed GLP-1 agonists, including those with a history of thyroid cancer or pancreatitis.

Caroline M. Apovian, MD, codirector of the center for weight management and wellness and professor of medicine at Harvard Medical School, Boston, said in an interview that the physiology behind bariatric surgery and that of the newer obesity medications is somewhat aligned.

“In order to reduce ... body weight permanently you need adjustments. We learned that you need the adjustments of the hormones [that affect appetite, such as GLP-1], and that’s why bariatric surgery works because ... [it] provides the most durable and the most effective treatment for obesity ... because [with surgery] you are adjusting the secretion and timing of many of the hormones that regulate body weight,” she explained.

So, when people are taking GLP-1 agonists for obesity, with or without surgery, these medications “are meant and were approved by the FDA to be taken indefinitely. They are not [for the] short term,” Dr. Apovian noted.

Benjamin O’Donnell, MD, an associate professor at Ohio State University Wexner Medical Center, Columbus, agreed that the newer anti-obesity medications can be very effective; however, he expressed uncertainty about prescribing these medications for years and years.

“If somebody has obesity, they need medicine to help them manage appetite and maintain a lower, healthier weight. It would make sense that they would just stay on the medicine,” he noted.

But he qualified: “I have a hard time committing to saying that someone should take this medication for the rest of their life. Part of my hesitation is that the medications are expensive, so we’ve had a hard time with people staying on them, mostly because of insurance formulary changes.”
 

Why stop the medications? Side effects and lack of insurance coverage

Many people have to discontinue these newer medications for that exact reason.

When Ms. Hartman’s insurance coverage lapsed, she had to go without semaglutide for a while.

“At that time, I absolutely gained weight back up into an abnormal BMI range,” Ms. Hartman said. When she was able to resume the medication, she lost weight again and her BMI returned to normal range.

These medications currently cost around $1,400 per month in the United States, unless patients can access initiatives such as company coupons. Some insurers, including state-subsidized Medicare and Medicaid, don’t cover the new medications.

Dr. O’Donnell said, “More accessibility for more people would help in the big picture.”

Other patients stop taking GLP-1 agonists because they experience side effects, such as nausea.

“Gastrointestinal complaints ... are the number one reason for people to come off the medication,” said Disha Narang, MD, an endocrinologist and obesity medicine specialist at Northwestern Medicine Lake Forest (Ill.) Hospital.

“It is an elective therapy, so it is not mandatory that someone take it. So if they are not feeling well or they are sick, then that’s a major reason for coming off of it,” she said.

Dan Bessesen, MD, professor of medicine at the University of Colorado at Denver, Aurora, and chief of endocrinology, agreed.

Patients are unlikely to stay on these medications if they feel nauseous or experience vomiting, he said. Although he noted there are options to try to counter this, such as starting patients on a very low dose of the drug and up-titrating slowly. This method requires good coordination between the patient and physician.

Goutham Rao, MD, a professor of medicine at Case Western Reserve University and head of the weight-loss initiative Fitter Me at University Hospitals, both in Cleveland, said that prior to prescribing GLP-1 agonists for weight loss, he sets four basic, nonnegotiable goals for patients: “to have breakfast within 30 minutes of getting up, to drink just water, no food or drink after 7:00 p.m. except for water, and 30 minutes of continuous exercise per day, which is typically, for older clientele, walking.”

This, he said, can help establish good habits because if “patients are not engaged psychologically in weight loss ... they expect the medication to do [all] the work.”
 

Most regain weight after stopping obesity medications

As Ms. Hartman’s story illustrates, discontinuing the medications often leads to weight regain.

“Without the medicine, there are a variety of things that will happen. Appetite will tend to increase, and so [patients] will gradually tend to eat more over time,” Dr. Bessesen noted.

“So it may take a long time for the weight regain to happen, but in every study where an obesity medicine has been used, and then it is stopped, the weight goes back to where it was on lifestyle alone,” he added.

In the STEP 1 trial, almost 2,000 patients who were either overweight or living with obesity were randomized 2:1 to semaglutide, titrated up to 2.4 mg each week by week 16, or placebo in addition to lifestyle modification. After 68 weeks, those in the semaglutide group had a mean weight loss of 14.9%, compared with 2.4% in the placebo group.

Patients were also followed in a 1-year extension of the trial, published in Diabetes, Obesity, and Metabolism.

Within 1 year of stopping treatment, participants regained two thirds of the weight they had initially lost.

Hence, Dr. Bessesen stressed that a total rethink of how obesity is approached is needed among most physicians.

“I think in the future treating obesity with medications should be like treating hypertension and diabetes, something most primary care doctors are comfortable doing, but that’s going to take a little work and practice on the part of clinicians to really have a comfortable conversation about risks, and benefits, with patients,” he said.

“I would encourage primary care doctors to learn more about the treatment of obesity, and learn more about bias and stigma, and think about how they can deliver care that is compassionate and competent,” he concluded.

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

After bariatric surgery in 2014, Kristal Hartman still struggled to manage her weight long term. It took her over a year to lose 100 pounds, a loss she initially maintained, but then gradually her body mass index (BMI) started creeping up again.

“The body kind of has a set point, and you have to constantly trick it because it is going to start to gain weight again,” Ms. Hartman, who is on the national board of directors for the Obesity Action Coalition, said in an interview.

So, 2.5 years after her surgery, Ms. Hartman began weekly subcutaneous injections of the glucagonlike peptide–1 (GLP-1) agonist semaglutide, a medication that is now almost infamous because of its popularity among celebrities and social media influencers.

Branded as Ozempic for type 2 diabetes and Wegovy for obesity, both contain semaglutide but in slightly different doses. The popularity of the medication has led to shortages for those living with type 2 diabetes and/or obesity. And other medications are waiting in the wings that work on GLP-1 and other hormones that regulate appetite, such as the twincretin tirzepatide (Mounjaro), another weekly injection, approved by the Food and Drug Administration in May 2022 for type 2 diabetes and awaiting approval for obesity.

Ms. Hartman said taking semaglutide helped her not only lose weight but also “curb [her] obsessive thoughts over food.” To maintain a BMI within the healthy range, as well as taking the GLP-1 agonist, Ms. Hartman relies on other strategies, including exercise, and mental health support.

“Physicians really need to be open to these FDA-approved medications as one of many tools in the toolbox for patients with obesity. It’s just like any other chronic disease state, when they are thinking of using these, they need to think about long-term use ... in patients who have obesity, not just [among those people] who just want to lose 5-10 pounds. That’s not what these drugs are designed for. They are for people who are actually living with the chronic disease of obesity every day of their lives,” she emphasized.

On average, patients lose 25%-40% of their total body weight following bariatric surgery, said Teresa LeMasters, MD, president of the American Society for Metabolic & Bariatric Surgery. However, there typically is a “small” weight regain after surgery.

“For most patients, it is a small 5-10 pounds, but for some others, it can be significant,” said Dr. LeMasters, a bariatric surgeon at UnityPoint Clinic, Des Moines, Iowa.

“We do still see some patients– anywhere from 10% to 30% – who will have some [significant] weight regain, and so then we will look at that,” she noted. In those cases, the disease of obesity “is definitely still present.”
 

Medications can counter weight regain after surgery

For patients who don’t reach their weight loss goals after bariatric surgery, Dr. LeMasters said it’s appropriate to consider adding an anti-obesity medication. The newer GLP-1 agonists can lead to a loss of around 15% of body weight in some patients.

“The GLP-1 agonists have been very helpful for treating patients who’ve had bariatric surgery and had some weight regain, or even just to optimize their initial response to surgery if they are starting at a very, very severe point of disease,” she explained.

She noted, however, that some patients shouldn’t be prescribed GLP-1 agonists, including those with a history of thyroid cancer or pancreatitis.

Caroline M. Apovian, MD, codirector of the center for weight management and wellness and professor of medicine at Harvard Medical School, Boston, said in an interview that the physiology behind bariatric surgery and that of the newer obesity medications is somewhat aligned.

“In order to reduce ... body weight permanently you need adjustments. We learned that you need the adjustments of the hormones [that affect appetite, such as GLP-1], and that’s why bariatric surgery works because ... [it] provides the most durable and the most effective treatment for obesity ... because [with surgery] you are adjusting the secretion and timing of many of the hormones that regulate body weight,” she explained.

So, when people are taking GLP-1 agonists for obesity, with or without surgery, these medications “are meant and were approved by the FDA to be taken indefinitely. They are not [for the] short term,” Dr. Apovian noted.

Benjamin O’Donnell, MD, an associate professor at Ohio State University Wexner Medical Center, Columbus, agreed that the newer anti-obesity medications can be very effective; however, he expressed uncertainty about prescribing these medications for years and years.

“If somebody has obesity, they need medicine to help them manage appetite and maintain a lower, healthier weight. It would make sense that they would just stay on the medicine,” he noted.

But he qualified: “I have a hard time committing to saying that someone should take this medication for the rest of their life. Part of my hesitation is that the medications are expensive, so we’ve had a hard time with people staying on them, mostly because of insurance formulary changes.”
 

Why stop the medications? Side effects and lack of insurance coverage

Many people have to discontinue these newer medications for that exact reason.

When Ms. Hartman’s insurance coverage lapsed, she had to go without semaglutide for a while.

“At that time, I absolutely gained weight back up into an abnormal BMI range,” Ms. Hartman said. When she was able to resume the medication, she lost weight again and her BMI returned to normal range.

These medications currently cost around $1,400 per month in the United States, unless patients can access initiatives such as company coupons. Some insurers, including state-subsidized Medicare and Medicaid, don’t cover the new medications.

Dr. O’Donnell said, “More accessibility for more people would help in the big picture.”

Other patients stop taking GLP-1 agonists because they experience side effects, such as nausea.

“Gastrointestinal complaints ... are the number one reason for people to come off the medication,” said Disha Narang, MD, an endocrinologist and obesity medicine specialist at Northwestern Medicine Lake Forest (Ill.) Hospital.

“It is an elective therapy, so it is not mandatory that someone take it. So if they are not feeling well or they are sick, then that’s a major reason for coming off of it,” she said.

Dan Bessesen, MD, professor of medicine at the University of Colorado at Denver, Aurora, and chief of endocrinology, agreed.

Patients are unlikely to stay on these medications if they feel nauseous or experience vomiting, he said. Although he noted there are options to try to counter this, such as starting patients on a very low dose of the drug and up-titrating slowly. This method requires good coordination between the patient and physician.

Goutham Rao, MD, a professor of medicine at Case Western Reserve University and head of the weight-loss initiative Fitter Me at University Hospitals, both in Cleveland, said that prior to prescribing GLP-1 agonists for weight loss, he sets four basic, nonnegotiable goals for patients: “to have breakfast within 30 minutes of getting up, to drink just water, no food or drink after 7:00 p.m. except for water, and 30 minutes of continuous exercise per day, which is typically, for older clientele, walking.”

This, he said, can help establish good habits because if “patients are not engaged psychologically in weight loss ... they expect the medication to do [all] the work.”
 

Most regain weight after stopping obesity medications

As Ms. Hartman’s story illustrates, discontinuing the medications often leads to weight regain.

“Without the medicine, there are a variety of things that will happen. Appetite will tend to increase, and so [patients] will gradually tend to eat more over time,” Dr. Bessesen noted.

“So it may take a long time for the weight regain to happen, but in every study where an obesity medicine has been used, and then it is stopped, the weight goes back to where it was on lifestyle alone,” he added.

In the STEP 1 trial, almost 2,000 patients who were either overweight or living with obesity were randomized 2:1 to semaglutide, titrated up to 2.4 mg each week by week 16, or placebo in addition to lifestyle modification. After 68 weeks, those in the semaglutide group had a mean weight loss of 14.9%, compared with 2.4% in the placebo group.

Patients were also followed in a 1-year extension of the trial, published in Diabetes, Obesity, and Metabolism.

Within 1 year of stopping treatment, participants regained two thirds of the weight they had initially lost.

Hence, Dr. Bessesen stressed that a total rethink of how obesity is approached is needed among most physicians.

“I think in the future treating obesity with medications should be like treating hypertension and diabetes, something most primary care doctors are comfortable doing, but that’s going to take a little work and practice on the part of clinicians to really have a comfortable conversation about risks, and benefits, with patients,” he said.

“I would encourage primary care doctors to learn more about the treatment of obesity, and learn more about bias and stigma, and think about how they can deliver care that is compassionate and competent,” he concluded.

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

Universal screening of all U.S. adults aged 35-70 years for prediabetes and type 2 diabetes, regardless of body mass index, would provide the fairest means of detection, according to a new analysis.

This would better detect prediabetes and diabetes in ethnic groups that have a higher risk of diabetes at lower cutoffs. Compared with White individuals, Black or Hispanic adults have a higher risk of developing type 2 diabetes at a younger age, and Asian, Hispanic, and Black Americans all have a higher risk of developing it at a lower BMI. 

In the new study, researchers examined six different screening scenarios in a nationally representative sample without diabetes.

They compared screening for prediabetes and type 2 diabetes using criteria from the 2021 U.S. Preventive Services Task Force (USPSTF) recommendations with the 2015 USPSTF recommendations, as well as four other screening thresholds with lower age or weight.

Universal screening for prediabetes and diabetes at age 35-70, regardless of BMI – which appears to be the sweet spot for most equitable detection in different races – may be easier to put into practice because it will mean clinicians don’t have to remember alternate cutoffs for different patient groups, the researchers suggested.

“All major racial and ethnic minority groups develop diabetes at lower weights than White adults, and it’s most pronounced for Asian Americans,” lead author Matthew J. O’Brien, MD, explained in a press release.

“If we make decisions about diabetes testing based on weight we will miss some people from racial and ethnic minority groups who are developing prediabetes and diabetes at lower weights,” said Dr. O’Brien, of Northwestern University, Chicago.

Going forward, to achieve equity in diagnosing prediabetes and diabetes “also requires addressing structural barriers [facing racial and ethnic minorities], which include not having a usual source of primary care, lacking health insurance, or having copays for screening tests based on insurance coverage,” the authors noted in their paper, published online in the American Journal of Preventive Medicine.

There is also a need for further study to examine the cost-effectiveness of any approach, and to study the impact of screening criteria on diagnosis, treatment, and outcomes in diverse populations.
 

Nationally representative sample, six screening scenarios

In the overall U.S. population, 81% of adults with prediabetes are unaware they have it, said Dr. O’Brien and colleagues, and 23% of diabetes cases are undiagnosed.

And Black, Hispanic, or Asian individuals have a nearly twofold higher prevalence of diabetes compared with White individuals.

The 2021 USPSTF recommendations state that clinicians should screen asymptomatic adults aged 35-70 years with overweight/obesity (BMI ≥ 25 kg/m²) and “should consider screening at an earlier age in persons from groups with disproportionately high incidence and prevalence (American Indian/Alaska Native, Asian American, Black, Hispanic/Latino, or Native Hawaiian/Pacific Islander persons) or in persons who have a family history of diabetes, a history of gestational diabetes, or a history of polycystic ovarian syndrome, and at a lower BMI in Asian American persons. Data suggest that a BMI of 23 or greater may be an appropriate cut point in Asian American persons.”

Dr. O’Brien and colleagues identified 3,243 nonpregnant adults without diagnosed diabetes who participated in the National Health and Nutrition Examination Survey (NHANES) in 2017-2020 and had an A1c blood test. (Half also had a fasting plasma glucose test.)

First, they compared screening using the more recent and earlier USPSTF criteria: BMI of at least 25 kg/m² and age 35-70 (2021 criteria) and BMI of at least 25 kg/m² and age 40-70 (2015 criteria).

They estimated that 13.9 million more adults would be eligible for screening using the 2021 versus the 2015 screening criteria.

The increases in screening eligibility were highest in Hispanic individuals (30.6%), followed by Asian individuals (17.9%), White individuals (14.0%), and Black individuals (13.9%).

Using the USPSTF 2021 versus 2015 screening criteria resulted in marginally higher sensitivity (58.6% vs. 52.9%) but lower specificity (69.3% vs. 76.4%) overall, as well as within each racial group.

Next, the researchers examined screening at two lower age cutoffs and two lower BMI cutoffs: BMI of at least 25 kg/m² and age 30-70, BMI of at least 25 kg/m² and age 18-70, age 35-70 and BMI of at least 23 kg/m², and age 35-70 and any BMI.

Screening at these lower age and weight thresholds resulted in even greater sensitivity and lower specificity than using the 2021 USPSTF criteria, especially among Hispanic, non-Hispanic Black, and Asian adults.

However, screening all adults aged 35-70 years regardless of BMI yielded the most equitable detection of prediabetes and diabetes – with a sensitivity of 67.8% and a specificity of 52.1% in the overall population, and a sensitivity of 70.1%, 70.4%, 68.4%, and 67.6%, and a specificity of 53.8%, 59.9%, 56.2%, and 48.9%, in the Asian, Black, Hispanic, and White subgroups, respectively.

The American Diabetes Association currently recommends screening all adults aged ≥ 35 years, or at any age if they have overweight/obesity and an additional diabetes risk factor, the researchers noted.

The study was partly funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. The authors have reported no relevant financial relationships.
 

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

Universal screening of all U.S. adults aged 35-70 years for prediabetes and type 2 diabetes, regardless of body mass index, would provide the fairest means of detection, according to a new analysis.

This would better detect prediabetes and diabetes in ethnic groups that have a higher risk of diabetes at lower cutoffs. Compared with White individuals, Black or Hispanic adults have a higher risk of developing type 2 diabetes at a younger age, and Asian, Hispanic, and Black Americans all have a higher risk of developing it at a lower BMI. 

In the new study, researchers examined six different screening scenarios in a nationally representative sample without diabetes.

They compared screening for prediabetes and type 2 diabetes using criteria from the 2021 U.S. Preventive Services Task Force (USPSTF) recommendations with the 2015 USPSTF recommendations, as well as four other screening thresholds with lower age or weight.

Universal screening for prediabetes and diabetes at age 35-70, regardless of BMI – which appears to be the sweet spot for most equitable detection in different races – may be easier to put into practice because it will mean clinicians don’t have to remember alternate cutoffs for different patient groups, the researchers suggested.

“All major racial and ethnic minority groups develop diabetes at lower weights than White adults, and it’s most pronounced for Asian Americans,” lead author Matthew J. O’Brien, MD, explained in a press release.

“If we make decisions about diabetes testing based on weight we will miss some people from racial and ethnic minority groups who are developing prediabetes and diabetes at lower weights,” said Dr. O’Brien, of Northwestern University, Chicago.

Going forward, to achieve equity in diagnosing prediabetes and diabetes “also requires addressing structural barriers [facing racial and ethnic minorities], which include not having a usual source of primary care, lacking health insurance, or having copays for screening tests based on insurance coverage,” the authors noted in their paper, published online in the American Journal of Preventive Medicine.

There is also a need for further study to examine the cost-effectiveness of any approach, and to study the impact of screening criteria on diagnosis, treatment, and outcomes in diverse populations.
 

Nationally representative sample, six screening scenarios

In the overall U.S. population, 81% of adults with prediabetes are unaware they have it, said Dr. O’Brien and colleagues, and 23% of diabetes cases are undiagnosed.

And Black, Hispanic, or Asian individuals have a nearly twofold higher prevalence of diabetes compared with White individuals.

The 2021 USPSTF recommendations state that clinicians should screen asymptomatic adults aged 35-70 years with overweight/obesity (BMI ≥ 25 kg/m²) and “should consider screening at an earlier age in persons from groups with disproportionately high incidence and prevalence (American Indian/Alaska Native, Asian American, Black, Hispanic/Latino, or Native Hawaiian/Pacific Islander persons) or in persons who have a family history of diabetes, a history of gestational diabetes, or a history of polycystic ovarian syndrome, and at a lower BMI in Asian American persons. Data suggest that a BMI of 23 or greater may be an appropriate cut point in Asian American persons.”

Dr. O’Brien and colleagues identified 3,243 nonpregnant adults without diagnosed diabetes who participated in the National Health and Nutrition Examination Survey (NHANES) in 2017-2020 and had an A1c blood test. (Half also had a fasting plasma glucose test.)

First, they compared screening using the more recent and earlier USPSTF criteria: BMI of at least 25 kg/m² and age 35-70 (2021 criteria) and BMI of at least 25 kg/m² and age 40-70 (2015 criteria).

They estimated that 13.9 million more adults would be eligible for screening using the 2021 versus the 2015 screening criteria.

The increases in screening eligibility were highest in Hispanic individuals (30.6%), followed by Asian individuals (17.9%), White individuals (14.0%), and Black individuals (13.9%).

Using the USPSTF 2021 versus 2015 screening criteria resulted in marginally higher sensitivity (58.6% vs. 52.9%) but lower specificity (69.3% vs. 76.4%) overall, as well as within each racial group.

Next, the researchers examined screening at two lower age cutoffs and two lower BMI cutoffs: BMI of at least 25 kg/m² and age 30-70, BMI of at least 25 kg/m² and age 18-70, age 35-70 and BMI of at least 23 kg/m², and age 35-70 and any BMI.

Screening at these lower age and weight thresholds resulted in even greater sensitivity and lower specificity than using the 2021 USPSTF criteria, especially among Hispanic, non-Hispanic Black, and Asian adults.

However, screening all adults aged 35-70 years regardless of BMI yielded the most equitable detection of prediabetes and diabetes – with a sensitivity of 67.8% and a specificity of 52.1% in the overall population, and a sensitivity of 70.1%, 70.4%, 68.4%, and 67.6%, and a specificity of 53.8%, 59.9%, 56.2%, and 48.9%, in the Asian, Black, Hispanic, and White subgroups, respectively.

The American Diabetes Association currently recommends screening all adults aged ≥ 35 years, or at any age if they have overweight/obesity and an additional diabetes risk factor, the researchers noted.

The study was partly funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. The authors have reported no relevant financial relationships.
 

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

Universal screening of all U.S. adults aged 35-70 years for prediabetes and type 2 diabetes, regardless of body mass index, would provide the fairest means of detection, according to a new analysis.

This would better detect prediabetes and diabetes in ethnic groups that have a higher risk of diabetes at lower cutoffs. Compared with White individuals, Black or Hispanic adults have a higher risk of developing type 2 diabetes at a younger age, and Asian, Hispanic, and Black Americans all have a higher risk of developing it at a lower BMI. 

In the new study, researchers examined six different screening scenarios in a nationally representative sample without diabetes.

They compared screening for prediabetes and type 2 diabetes using criteria from the 2021 U.S. Preventive Services Task Force (USPSTF) recommendations with the 2015 USPSTF recommendations, as well as four other screening thresholds with lower age or weight.

Universal screening for prediabetes and diabetes at age 35-70, regardless of BMI – which appears to be the sweet spot for most equitable detection in different races – may be easier to put into practice because it will mean clinicians don’t have to remember alternate cutoffs for different patient groups, the researchers suggested.

“All major racial and ethnic minority groups develop diabetes at lower weights than White adults, and it’s most pronounced for Asian Americans,” lead author Matthew J. O’Brien, MD, explained in a press release.

“If we make decisions about diabetes testing based on weight we will miss some people from racial and ethnic minority groups who are developing prediabetes and diabetes at lower weights,” said Dr. O’Brien, of Northwestern University, Chicago.

Going forward, to achieve equity in diagnosing prediabetes and diabetes “also requires addressing structural barriers [facing racial and ethnic minorities], which include not having a usual source of primary care, lacking health insurance, or having copays for screening tests based on insurance coverage,” the authors noted in their paper, published online in the American Journal of Preventive Medicine.

There is also a need for further study to examine the cost-effectiveness of any approach, and to study the impact of screening criteria on diagnosis, treatment, and outcomes in diverse populations.
 

Nationally representative sample, six screening scenarios

In the overall U.S. population, 81% of adults with prediabetes are unaware they have it, said Dr. O’Brien and colleagues, and 23% of diabetes cases are undiagnosed.

And Black, Hispanic, or Asian individuals have a nearly twofold higher prevalence of diabetes compared with White individuals.

The 2021 USPSTF recommendations state that clinicians should screen asymptomatic adults aged 35-70 years with overweight/obesity (BMI ≥ 25 kg/m²) and “should consider screening at an earlier age in persons from groups with disproportionately high incidence and prevalence (American Indian/Alaska Native, Asian American, Black, Hispanic/Latino, or Native Hawaiian/Pacific Islander persons) or in persons who have a family history of diabetes, a history of gestational diabetes, or a history of polycystic ovarian syndrome, and at a lower BMI in Asian American persons. Data suggest that a BMI of 23 or greater may be an appropriate cut point in Asian American persons.”

Dr. O’Brien and colleagues identified 3,243 nonpregnant adults without diagnosed diabetes who participated in the National Health and Nutrition Examination Survey (NHANES) in 2017-2020 and had an A1c blood test. (Half also had a fasting plasma glucose test.)

First, they compared screening using the more recent and earlier USPSTF criteria: BMI of at least 25 kg/m² and age 35-70 (2021 criteria) and BMI of at least 25 kg/m² and age 40-70 (2015 criteria).

They estimated that 13.9 million more adults would be eligible for screening using the 2021 versus the 2015 screening criteria.

The increases in screening eligibility were highest in Hispanic individuals (30.6%), followed by Asian individuals (17.9%), White individuals (14.0%), and Black individuals (13.9%).

Using the USPSTF 2021 versus 2015 screening criteria resulted in marginally higher sensitivity (58.6% vs. 52.9%) but lower specificity (69.3% vs. 76.4%) overall, as well as within each racial group.

Next, the researchers examined screening at two lower age cutoffs and two lower BMI cutoffs: BMI of at least 25 kg/m² and age 30-70, BMI of at least 25 kg/m² and age 18-70, age 35-70 and BMI of at least 23 kg/m², and age 35-70 and any BMI.

Screening at these lower age and weight thresholds resulted in even greater sensitivity and lower specificity than using the 2021 USPSTF criteria, especially among Hispanic, non-Hispanic Black, and Asian adults.

However, screening all adults aged 35-70 years regardless of BMI yielded the most equitable detection of prediabetes and diabetes – with a sensitivity of 67.8% and a specificity of 52.1% in the overall population, and a sensitivity of 70.1%, 70.4%, 68.4%, and 67.6%, and a specificity of 53.8%, 59.9%, 56.2%, and 48.9%, in the Asian, Black, Hispanic, and White subgroups, respectively.

The American Diabetes Association currently recommends screening all adults aged ≥ 35 years, or at any age if they have overweight/obesity and an additional diabetes risk factor, the researchers noted.

The study was partly funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. The authors have reported no relevant financial relationships.
 

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

A new compilation of nearly all research to date on the health impacts of sugar offers dozens of reasons to cut back.

Researchers from China and the United States rounded up 8,601 scientific studies on sugar and combined them to evaluate its impact on 83 health outcomes. The studies accounted for decades of research on the topic, stretching back to the beginning of the largest electronic databases for scientific papers.

The result is a list that cites the world’s most common health problems like heart disease, diabetes, obesity, high blood pressure, heart attack, high cholesterol, cancer, and depression. The findings were published in the BMJ. Researchers looked at studies that evaluated the impacts of consuming free sugars, which means any food that contains processed or naturally occurring sugars like table sugar, honey, or maple syrup. Sugar found in whole fruits and vegetables and in milk is not free sugar.

U.S. dietary guidelines recommend getting no more than 10% of daily calories from added sugars. For a typical 2,000-calorie-per-day diet, that equals no more than 200 calories, or about 12 teaspoons. The CDC reports that the average person consumes 17 teaspoons per day, with the largest sources being sugar-sweetened beverages, desserts, and snacks. (For context: one 12-ounce can of soda contains the equivalent of 9 teaspoons of sugar, according to beverage maker Coca-Cola.)

The new analysis also found links between sugary beverage consumption and other diet and lifestyle characteristics that may contribute to health problems.

“People who consumed sugar-sweetened beverages more frequently were likely to ingest more total and saturated fat, carbohydrate, and sodium, and less fruit, fiber, dairy products, and whole grain foods,” the authors wrote. “This dietary pattern was also associated with more frequent smoking and drinking, lower physical activity levels, and more time spent watching television. Therefore, the role of these confounding factors should be taken into consideration when explaining the association between sugar consumption and burden of disease.”

Recommendations for limiting sugar consumption are in place worldwide, the authors noted. They concluded that more needs to be done given the known health dangers of sugar.

“To change sugar consumption patterns, especially for children and adolescents, a combination of widespread public health education and policies worldwide is urgently needed,” they said.

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

A new compilation of nearly all research to date on the health impacts of sugar offers dozens of reasons to cut back.

Researchers from China and the United States rounded up 8,601 scientific studies on sugar and combined them to evaluate its impact on 83 health outcomes. The studies accounted for decades of research on the topic, stretching back to the beginning of the largest electronic databases for scientific papers.

The result is a list that cites the world’s most common health problems like heart disease, diabetes, obesity, high blood pressure, heart attack, high cholesterol, cancer, and depression. The findings were published in the BMJ. Researchers looked at studies that evaluated the impacts of consuming free sugars, which means any food that contains processed or naturally occurring sugars like table sugar, honey, or maple syrup. Sugar found in whole fruits and vegetables and in milk is not free sugar.

U.S. dietary guidelines recommend getting no more than 10% of daily calories from added sugars. For a typical 2,000-calorie-per-day diet, that equals no more than 200 calories, or about 12 teaspoons. The CDC reports that the average person consumes 17 teaspoons per day, with the largest sources being sugar-sweetened beverages, desserts, and snacks. (For context: one 12-ounce can of soda contains the equivalent of 9 teaspoons of sugar, according to beverage maker Coca-Cola.)

The new analysis also found links between sugary beverage consumption and other diet and lifestyle characteristics that may contribute to health problems.

“People who consumed sugar-sweetened beverages more frequently were likely to ingest more total and saturated fat, carbohydrate, and sodium, and less fruit, fiber, dairy products, and whole grain foods,” the authors wrote. “This dietary pattern was also associated with more frequent smoking and drinking, lower physical activity levels, and more time spent watching television. Therefore, the role of these confounding factors should be taken into consideration when explaining the association between sugar consumption and burden of disease.”

Recommendations for limiting sugar consumption are in place worldwide, the authors noted. They concluded that more needs to be done given the known health dangers of sugar.

“To change sugar consumption patterns, especially for children and adolescents, a combination of widespread public health education and policies worldwide is urgently needed,” they said.

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

A new compilation of nearly all research to date on the health impacts of sugar offers dozens of reasons to cut back.

Researchers from China and the United States rounded up 8,601 scientific studies on sugar and combined them to evaluate its impact on 83 health outcomes. The studies accounted for decades of research on the topic, stretching back to the beginning of the largest electronic databases for scientific papers.

The result is a list that cites the world’s most common health problems like heart disease, diabetes, obesity, high blood pressure, heart attack, high cholesterol, cancer, and depression. The findings were published in the BMJ. Researchers looked at studies that evaluated the impacts of consuming free sugars, which means any food that contains processed or naturally occurring sugars like table sugar, honey, or maple syrup. Sugar found in whole fruits and vegetables and in milk is not free sugar.

U.S. dietary guidelines recommend getting no more than 10% of daily calories from added sugars. For a typical 2,000-calorie-per-day diet, that equals no more than 200 calories, or about 12 teaspoons. The CDC reports that the average person consumes 17 teaspoons per day, with the largest sources being sugar-sweetened beverages, desserts, and snacks. (For context: one 12-ounce can of soda contains the equivalent of 9 teaspoons of sugar, according to beverage maker Coca-Cola.)

The new analysis also found links between sugary beverage consumption and other diet and lifestyle characteristics that may contribute to health problems.

“People who consumed sugar-sweetened beverages more frequently were likely to ingest more total and saturated fat, carbohydrate, and sodium, and less fruit, fiber, dairy products, and whole grain foods,” the authors wrote. “This dietary pattern was also associated with more frequent smoking and drinking, lower physical activity levels, and more time spent watching television. Therefore, the role of these confounding factors should be taken into consideration when explaining the association between sugar consumption and burden of disease.”

Recommendations for limiting sugar consumption are in place worldwide, the authors noted. They concluded that more needs to be done given the known health dangers of sugar.

“To change sugar consumption patterns, especially for children and adolescents, a combination of widespread public health education and policies worldwide is urgently needed,” they said.

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

A few months ago, after several months of considerable foot dragging, I wrote that I have accepted the American Academy of Pediatrics’ proclamation that we should begin to treat obesity as a disease.

While it may feel like we are just throwing in the towel, it sounds better if we admit that we may have reached the threshold beyond which total focus on prevention is not going to work.

I continue to be troubled by the lingering fear that, in declaring that obesity is a disease, we will suspend our current efforts at preventing the condition. Granted, most of these efforts at prevention have been woefully ineffective. However, I still believe that, much like ADHD, the rise in obesity in this country is a reflection of some serious flaws in our society. On the other hand, as an inveterate optimist I have not given up on the belief that we will find some yet-to-be-discovered changes in our societal fabric that will eventually turn the ship around.

With this somewhat contradictory combination of resignation and optimism in mind, I continue to seek out studies that hold some promise for prevention while we begin tinkering with the let’s-treat-it-like-a-disease approach.

I recently discovered a story about one such study from the Center for Economic and Social Research at the University of Southern California. Using data collected about adolescent dependents of military personnel, the researchers found that “exposure to a more advantageous built environment for more than 2 years was associated with lower probabilities of obesity.” Because more than half of these teenagers were living in housing that had been assigned by the military, the researchers could more easily control for a variety of factors some related to self-selection.

Interestingly, the data did not support associations between the adolescents’ diet, physical activity, or socioeconomic environments. The investigators noted that “more advantageous built environments were associated with lower consumption of unhealthy foods.” However, the study lacked the granularity to determine what segments of the built environment were most associated with the effect they were observing.

Like me, you may not be familiar with the term “built environment.” Turns out it is just exactly what we might expect – anything about the environment that is the result of human action – buildings, roadways, dams, neighborhoods – and what they do and don’t contain. For example, is the adolescent living in an environment that encourages walking or one that is overly motor vehicle–centric? Does his or her neighborhood have easily reachable grocery stores that offer a range of healthy foods or does the teenager live in a nutritional desert populated only by convenience stores? Is there ample space for outdoor physical activity?

The authors’ observation that the adolescents who benefited from living in advantageous environments had a lower consumption of unhealthy foods might suggest that access to a healthy diet might be a significant factor. For me, the take-home message is that in our search for preventive strategies we have barely scratched the surface. The observation that the associations these researchers were making was over a relatively short time span of 2 years should give us hope that if we think more broadly and creatively we may be to find solutions on a grand scale.

Over the last century we have built an environment that is clearly obesogenic. This paper offers a starting point from which we can learn which components of that environment are the most potent contributors to the obesity epidemic. Once we have that information the question remains: Can we find the political will to tear down and rebuilt?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

A few months ago, after several months of considerable foot dragging, I wrote that I have accepted the American Academy of Pediatrics’ proclamation that we should begin to treat obesity as a disease.

While it may feel like we are just throwing in the towel, it sounds better if we admit that we may have reached the threshold beyond which total focus on prevention is not going to work.

I continue to be troubled by the lingering fear that, in declaring that obesity is a disease, we will suspend our current efforts at preventing the condition. Granted, most of these efforts at prevention have been woefully ineffective. However, I still believe that, much like ADHD, the rise in obesity in this country is a reflection of some serious flaws in our society. On the other hand, as an inveterate optimist I have not given up on the belief that we will find some yet-to-be-discovered changes in our societal fabric that will eventually turn the ship around.

With this somewhat contradictory combination of resignation and optimism in mind, I continue to seek out studies that hold some promise for prevention while we begin tinkering with the let’s-treat-it-like-a-disease approach.

I recently discovered a story about one such study from the Center for Economic and Social Research at the University of Southern California. Using data collected about adolescent dependents of military personnel, the researchers found that “exposure to a more advantageous built environment for more than 2 years was associated with lower probabilities of obesity.” Because more than half of these teenagers were living in housing that had been assigned by the military, the researchers could more easily control for a variety of factors some related to self-selection.

Interestingly, the data did not support associations between the adolescents’ diet, physical activity, or socioeconomic environments. The investigators noted that “more advantageous built environments were associated with lower consumption of unhealthy foods.” However, the study lacked the granularity to determine what segments of the built environment were most associated with the effect they were observing.

Like me, you may not be familiar with the term “built environment.” Turns out it is just exactly what we might expect – anything about the environment that is the result of human action – buildings, roadways, dams, neighborhoods – and what they do and don’t contain. For example, is the adolescent living in an environment that encourages walking or one that is overly motor vehicle–centric? Does his or her neighborhood have easily reachable grocery stores that offer a range of healthy foods or does the teenager live in a nutritional desert populated only by convenience stores? Is there ample space for outdoor physical activity?

The authors’ observation that the adolescents who benefited from living in advantageous environments had a lower consumption of unhealthy foods might suggest that access to a healthy diet might be a significant factor. For me, the take-home message is that in our search for preventive strategies we have barely scratched the surface. The observation that the associations these researchers were making was over a relatively short time span of 2 years should give us hope that if we think more broadly and creatively we may be to find solutions on a grand scale.

Over the last century we have built an environment that is clearly obesogenic. This paper offers a starting point from which we can learn which components of that environment are the most potent contributors to the obesity epidemic. Once we have that information the question remains: Can we find the political will to tear down and rebuilt?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

A few months ago, after several months of considerable foot dragging, I wrote that I have accepted the American Academy of Pediatrics’ proclamation that we should begin to treat obesity as a disease.

While it may feel like we are just throwing in the towel, it sounds better if we admit that we may have reached the threshold beyond which total focus on prevention is not going to work.

I continue to be troubled by the lingering fear that, in declaring that obesity is a disease, we will suspend our current efforts at preventing the condition. Granted, most of these efforts at prevention have been woefully ineffective. However, I still believe that, much like ADHD, the rise in obesity in this country is a reflection of some serious flaws in our society. On the other hand, as an inveterate optimist I have not given up on the belief that we will find some yet-to-be-discovered changes in our societal fabric that will eventually turn the ship around.

With this somewhat contradictory combination of resignation and optimism in mind, I continue to seek out studies that hold some promise for prevention while we begin tinkering with the let’s-treat-it-like-a-disease approach.

I recently discovered a story about one such study from the Center for Economic and Social Research at the University of Southern California. Using data collected about adolescent dependents of military personnel, the researchers found that “exposure to a more advantageous built environment for more than 2 years was associated with lower probabilities of obesity.” Because more than half of these teenagers were living in housing that had been assigned by the military, the researchers could more easily control for a variety of factors some related to self-selection.

Interestingly, the data did not support associations between the adolescents’ diet, physical activity, or socioeconomic environments. The investigators noted that “more advantageous built environments were associated with lower consumption of unhealthy foods.” However, the study lacked the granularity to determine what segments of the built environment were most associated with the effect they were observing.

Like me, you may not be familiar with the term “built environment.” Turns out it is just exactly what we might expect – anything about the environment that is the result of human action – buildings, roadways, dams, neighborhoods – and what they do and don’t contain. For example, is the adolescent living in an environment that encourages walking or one that is overly motor vehicle–centric? Does his or her neighborhood have easily reachable grocery stores that offer a range of healthy foods or does the teenager live in a nutritional desert populated only by convenience stores? Is there ample space for outdoor physical activity?

The authors’ observation that the adolescents who benefited from living in advantageous environments had a lower consumption of unhealthy foods might suggest that access to a healthy diet might be a significant factor. For me, the take-home message is that in our search for preventive strategies we have barely scratched the surface. The observation that the associations these researchers were making was over a relatively short time span of 2 years should give us hope that if we think more broadly and creatively we may be to find solutions on a grand scale.

Over the last century we have built an environment that is clearly obesogenic. This paper offers a starting point from which we can learn which components of that environment are the most potent contributors to the obesity epidemic. Once we have that information the question remains: Can we find the political will to tear down and rebuilt?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

Rapid weight gain (RWG) in infants and the mother’s prepregnancy overweight have a synergistic effect in increasing the odds that a child will develop overweight or obesity, new research suggests.

Findings were published online in Pediatrics.

Each factor has independently been associated with higher risk of childhood obesity but whether the two factors together exacerbate the risk has not been well studied, according to the authors led by Stephanie Gilley, MD, PhD, department of pediatrics, section of nutrition, University of Colorado at Denver, Aurora.

“Pediatric providers should monitor infants for RWG, especially in the context of maternal obesity, to reduce future risk of obesity,” the authors conclude.

Dr. Gilley’s team studied mother-infant dyads (n = 414) from the Healthy Start Study, an observational prebirth cohort. RWG was defined as a weight-for-age z score increase of at least 0.67 from birth to 3-7 months.

They found that RWG boosted the link between prepregnancy body mass index (ppBMI) and BMI z score, especially in female infants. Females exposed to both maternal obesity with RWG had an average BMI at the 94th percentile (1.50 increase in childhood BMI z score) “nearly at the cutoff for classification of obesity,” compared with those exposed to normal ppBMI with no RWG, who had an average childhood BMI at the 51st percentile.

“Currently, our nutrition recommendations as pediatricians are that all children are fed the same, essentially, after they’re born. We don’t have different growth parameters or different trajectories or targets for children who may have had different in utero exposures,” Dr. Gilley said.

Do some children need more monitoring for RWG?

Though we can’t necessarily draw conclusions from this one study, she says, the findings raise the question of whether children who were exposed in utero to obesity should be monitored for RWG more closely.

Lydia Shook, MD, Mass General Brigham maternal-fetal specialist and codirector of the Diabetes in Pregnancy Program at Massachusetts General Hospital in Boston, said she was struck by the finding in this study that with female infants, but not males, RWG significantly modified the association between ppBMI and early childhood BMI z scores.

“It’s an interesting finding and should be followed up with larger cohorts,” she said, noting that some previous studies have shown males are more vulnerable to maternal obesity and RWG.

“[Often] when we stratify by sex, you really need larger groups to be able to see the differences well,” Dr. Shook said.

She said she also found it interesting that when the researchers adjusted for breastfeeding status or caloric intake in childhood, the findings did not substantially change.

“That’s something that would warrant further investigation in an observational study or controlled trial,” Dr. Shook said.

Preventing rapid weight gain

The authors note that they did not consider possible interventions for preventing RGW in the study, although there are many, Dr. Gilley said.

Dr. Gilley also noted that a limitation of this study is that the population studied was primarily White.

Recent studies have shown the benefits of responsive parenting (RP) interventions, including a large study in 2022 geared toward Black families to teach better infant sleep practices as a way to prevent rapid weight gain.

That study, which tested the SAAF intervention, (Strong African American Families) found that “RP infants were nearly half as likely to experience upward crossing of two major weight-for-age percentile lines (14.1%), compared with control infants (24.2%); P = .09; odds ratio, 0.52; 95% confidence interval, 0.24-1.12.”

Along with sleep interventions, Dr. Gilley said, some researchers are studying the effects on RWG of better paternal engagement, or more involvement with the Women, Infants, and Children program, particularly with lower-income families.

Other studies have looked at breastfeeding vs. formula feeding – “but there have been mixed results there” – and responsive feeding practices, such as teaching families to recognize when a baby is full.

Dr. Gilley said she hopes this work will help broaden the thinking when it comes to infant weight gain.

“We spend a lot of time thinking about babies who are not growing fast enough and very little time thinking about babies who are growing too fast,” she said, “especially in those first 4-6 months of life.”

Dr. Gilley points to a study that illustrates that point. Pesch et al. concluded in a 2021 study based on interviews that pediatricians “are uncertain about the concept, definition, management, and long-term risks of rapid infant weight gain.”

Authors and Dr. Gilley declare no relevant financial relationships.

Rapid weight gain (RWG) in infants and the mother’s prepregnancy overweight have a synergistic effect in increasing the odds that a child will develop overweight or obesity, new research suggests.

Findings were published online in Pediatrics.

Each factor has independently been associated with higher risk of childhood obesity but whether the two factors together exacerbate the risk has not been well studied, according to the authors led by Stephanie Gilley, MD, PhD, department of pediatrics, section of nutrition, University of Colorado at Denver, Aurora.

“Pediatric providers should monitor infants for RWG, especially in the context of maternal obesity, to reduce future risk of obesity,” the authors conclude.

Dr. Gilley’s team studied mother-infant dyads (n = 414) from the Healthy Start Study, an observational prebirth cohort. RWG was defined as a weight-for-age z score increase of at least 0.67 from birth to 3-7 months.

They found that RWG boosted the link between prepregnancy body mass index (ppBMI) and BMI z score, especially in female infants. Females exposed to both maternal obesity with RWG had an average BMI at the 94th percentile (1.50 increase in childhood BMI z score) “nearly at the cutoff for classification of obesity,” compared with those exposed to normal ppBMI with no RWG, who had an average childhood BMI at the 51st percentile.

“Currently, our nutrition recommendations as pediatricians are that all children are fed the same, essentially, after they’re born. We don’t have different growth parameters or different trajectories or targets for children who may have had different in utero exposures,” Dr. Gilley said.

Do some children need more monitoring for RWG?

Though we can’t necessarily draw conclusions from this one study, she says, the findings raise the question of whether children who were exposed in utero to obesity should be monitored for RWG more closely.

Lydia Shook, MD, Mass General Brigham maternal-fetal specialist and codirector of the Diabetes in Pregnancy Program at Massachusetts General Hospital in Boston, said she was struck by the finding in this study that with female infants, but not males, RWG significantly modified the association between ppBMI and early childhood BMI z scores.

“It’s an interesting finding and should be followed up with larger cohorts,” she said, noting that some previous studies have shown males are more vulnerable to maternal obesity and RWG.

“[Often] when we stratify by sex, you really need larger groups to be able to see the differences well,” Dr. Shook said.

She said she also found it interesting that when the researchers adjusted for breastfeeding status or caloric intake in childhood, the findings did not substantially change.

“That’s something that would warrant further investigation in an observational study or controlled trial,” Dr. Shook said.

Preventing rapid weight gain

The authors note that they did not consider possible interventions for preventing RGW in the study, although there are many, Dr. Gilley said.

Dr. Gilley also noted that a limitation of this study is that the population studied was primarily White.

Recent studies have shown the benefits of responsive parenting (RP) interventions, including a large study in 2022 geared toward Black families to teach better infant sleep practices as a way to prevent rapid weight gain.

That study, which tested the SAAF intervention, (Strong African American Families) found that “RP infants were nearly half as likely to experience upward crossing of two major weight-for-age percentile lines (14.1%), compared with control infants (24.2%); P = .09; odds ratio, 0.52; 95% confidence interval, 0.24-1.12.”

Along with sleep interventions, Dr. Gilley said, some researchers are studying the effects on RWG of better paternal engagement, or more involvement with the Women, Infants, and Children program, particularly with lower-income families.

Other studies have looked at breastfeeding vs. formula feeding – “but there have been mixed results there” – and responsive feeding practices, such as teaching families to recognize when a baby is full.

Dr. Gilley said she hopes this work will help broaden the thinking when it comes to infant weight gain.

“We spend a lot of time thinking about babies who are not growing fast enough and very little time thinking about babies who are growing too fast,” she said, “especially in those first 4-6 months of life.”

Dr. Gilley points to a study that illustrates that point. Pesch et al. concluded in a 2021 study based on interviews that pediatricians “are uncertain about the concept, definition, management, and long-term risks of rapid infant weight gain.”

Authors and Dr. Gilley declare no relevant financial relationships.

Rapid weight gain (RWG) in infants and the mother’s prepregnancy overweight have a synergistic effect in increasing the odds that a child will develop overweight or obesity, new research suggests.

Findings were published online in Pediatrics.

Each factor has independently been associated with higher risk of childhood obesity but whether the two factors together exacerbate the risk has not been well studied, according to the authors led by Stephanie Gilley, MD, PhD, department of pediatrics, section of nutrition, University of Colorado at Denver, Aurora.

“Pediatric providers should monitor infants for RWG, especially in the context of maternal obesity, to reduce future risk of obesity,” the authors conclude.

Dr. Gilley’s team studied mother-infant dyads (n = 414) from the Healthy Start Study, an observational prebirth cohort. RWG was defined as a weight-for-age z score increase of at least 0.67 from birth to 3-7 months.

They found that RWG boosted the link between prepregnancy body mass index (ppBMI) and BMI z score, especially in female infants. Females exposed to both maternal obesity with RWG had an average BMI at the 94th percentile (1.50 increase in childhood BMI z score) “nearly at the cutoff for classification of obesity,” compared with those exposed to normal ppBMI with no RWG, who had an average childhood BMI at the 51st percentile.

“Currently, our nutrition recommendations as pediatricians are that all children are fed the same, essentially, after they’re born. We don’t have different growth parameters or different trajectories or targets for children who may have had different in utero exposures,” Dr. Gilley said.

Do some children need more monitoring for RWG?

Though we can’t necessarily draw conclusions from this one study, she says, the findings raise the question of whether children who were exposed in utero to obesity should be monitored for RWG more closely.

Lydia Shook, MD, Mass General Brigham maternal-fetal specialist and codirector of the Diabetes in Pregnancy Program at Massachusetts General Hospital in Boston, said she was struck by the finding in this study that with female infants, but not males, RWG significantly modified the association between ppBMI and early childhood BMI z scores.

“It’s an interesting finding and should be followed up with larger cohorts,” she said, noting that some previous studies have shown males are more vulnerable to maternal obesity and RWG.

“[Often] when we stratify by sex, you really need larger groups to be able to see the differences well,” Dr. Shook said.

She said she also found it interesting that when the researchers adjusted for breastfeeding status or caloric intake in childhood, the findings did not substantially change.

“That’s something that would warrant further investigation in an observational study or controlled trial,” Dr. Shook said.

Preventing rapid weight gain

The authors note that they did not consider possible interventions for preventing RGW in the study, although there are many, Dr. Gilley said.

Dr. Gilley also noted that a limitation of this study is that the population studied was primarily White.

Recent studies have shown the benefits of responsive parenting (RP) interventions, including a large study in 2022 geared toward Black families to teach better infant sleep practices as a way to prevent rapid weight gain.

That study, which tested the SAAF intervention, (Strong African American Families) found that “RP infants were nearly half as likely to experience upward crossing of two major weight-for-age percentile lines (14.1%), compared with control infants (24.2%); P = .09; odds ratio, 0.52; 95% confidence interval, 0.24-1.12.”

Along with sleep interventions, Dr. Gilley said, some researchers are studying the effects on RWG of better paternal engagement, or more involvement with the Women, Infants, and Children program, particularly with lower-income families.

Other studies have looked at breastfeeding vs. formula feeding – “but there have been mixed results there” – and responsive feeding practices, such as teaching families to recognize when a baby is full.

Dr. Gilley said she hopes this work will help broaden the thinking when it comes to infant weight gain.

“We spend a lot of time thinking about babies who are not growing fast enough and very little time thinking about babies who are growing too fast,” she said, “especially in those first 4-6 months of life.”

Dr. Gilley points to a study that illustrates that point. Pesch et al. concluded in a 2021 study based on interviews that pediatricians “are uncertain about the concept, definition, management, and long-term risks of rapid infant weight gain.”

Authors and Dr. Gilley declare no relevant financial relationships.

Adding 10 minutes to family mealtimes increased children’s consumption of fruits and vegetables by approximately one portion, based on data from 50 parent-child dyads.

Family meals are known to affect children’s food choices and preferences and can be an effective setting for improving children’s nutrition, wrote Mattea Dallacker, PhD, of the University of Mannheim, Germany, and colleagues.

However, the effect of extending meal duration on increasing fruit and vegetable intake in particular has not been examined, they said.

In a study published in JAMA Network Open, the researchers provided two free evening meals to 50 parent-child dyads under each of two different conditions. The control condition was defined by the families as a regular family mealtime duration (an average meal was 20.83 minutes), while the intervention was an average meal time 10 minutes (50%) longer. The age of the parents ranged from 22 to 55 years, with a mean of 43 years; 72% of the parent participants were mothers. The children’s ages ranged from 6 to 11 years, with a mean of 8 years, with approximately equal numbers of boys and girls.

The study was conducted in a family meal laboratory setting in Berlin, and groups were randomized to the longer or shorter meal setting first. The primary outcome was the total number of pieces of fruit and vegetables eaten by the child as part of each of the two meals.

Both meals were the “typical German evening meal of sliced bread, cold cuts of cheese and meat, and bite-sized pieces of fruits and vegetables,” followed by a dessert course of chocolate pudding or fruit yogurt and cookies, the researchers wrote. Beverages were water and one sugar-sweetened beverage; the specific foods and beverages were based on the child’s preferences, reported in an online preassessment, and the foods were consistent for the longer and shorter meals. All participants were asked not to eat for 2 hours prior to arriving for their meals at the laboratory.

During longer meals, children ate an average of seven additional bite-sized pieces of fruits and vegetables, which translates to approximately a full portion (defined as 100 g, such as a medium apple), the researchers wrote. The difference was significant compared with the shorter meals for fruits (P = .01) and vegetables (P < .001).

A piece of fruit was approximately 10 grams (6-10 g for grapes and tangerine segments; 10-14 g for cherry tomatoes; and 9-11 g for apple, banana, carrot, or cucumber). Other foods served with the meals included cheese, meats, butter, and sweet spreads.

Children also ate more slowly (defined as fewer bites per minute) during the longer meals, and they reported significantly greater satiety after the longer meals (P < .001 for both). The consumption of bread and cold cuts was similar for the two meal settings.

“Higher intake of fruits and vegetables during longer meals cannot be explained by longer exposure to food alone; otherwise, an increased intake of bread and cold cuts would have occurred,” the researchers wrote in their discussion. “One possible explanation is that the fruits and vegetables were cut into bite-sized pieces, making them convenient to eat.”

Further analysis showed that during the longer meals, more fruits and vegetables were consumed overall, but more vegetables were eaten from the start of the meal, while the additional fruit was eaten during the additional time at the end.

The findings were limited by several factors, primarily use of a laboratory setting that does not generalize to natural eating environments, the researchers noted. Other potential limitations included the effect of a video cameras on desirable behaviors and the limited ethnic and socioeconomic diversity of the study population, they said. The results were strengthened by the within-dyad study design that allowed for control of factors such as video observation, but more research is needed with more diverse groups and across longer time frames, the researchers said.

However, the results suggest that adding 10 minutes to a family mealtime can yield significant improvements in children’s diets, they said. They suggested strategies including playing music chosen by the child/children and setting rules that everyone must remain at the table for a certain length of time, with fruits and vegetables available on the table.

“If the effects of this simple, inexpensive, and low-threshold intervention prove stable over time, it could contribute to addressing a major public health problem,” the researchers concluded.
 

Findings intriguing, more data needed

The current study is important because food and vegetable intake in the majority of children falls below the recommended daily allowance, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

The key take-home message for clinicians is the continued need to stress the importance of family meals, said Dr. Kinsella. “Many children continue to be overbooked with activities, and it may be rare for many families to sit down together for a meal for any length of time.”

Don’t discount the potential effect of a longer school lunch on children’s fruit and vegetable consumption as well, she added. “Advocating for longer lunch time is important, as many kids report not being able to finish their lunch at school.”

The current study was limited by being conducted in a lab setting, which may have influenced children’s desire for different foods, “also they had fewer distractions, and were being offered favorite foods,” said Dr. Kinsella.

Looking ahead, “it would be interesting to see if this result carried over to nonpreferred fruits and veggies and made any difference for picky eaters,” she said. 

The study received no outside funding. The open-access publication of the study (but not the study itself) was supported by the Max Planck Institute for Human Development Library Open Access Fund. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose and serves on the editorial advisory board of Pediatric News.

Adding 10 minutes to family mealtimes increased children’s consumption of fruits and vegetables by approximately one portion, based on data from 50 parent-child dyads.

Family meals are known to affect children’s food choices and preferences and can be an effective setting for improving children’s nutrition, wrote Mattea Dallacker, PhD, of the University of Mannheim, Germany, and colleagues.

However, the effect of extending meal duration on increasing fruit and vegetable intake in particular has not been examined, they said.

In a study published in JAMA Network Open, the researchers provided two free evening meals to 50 parent-child dyads under each of two different conditions. The control condition was defined by the families as a regular family mealtime duration (an average meal was 20.83 minutes), while the intervention was an average meal time 10 minutes (50%) longer. The age of the parents ranged from 22 to 55 years, with a mean of 43 years; 72% of the parent participants were mothers. The children’s ages ranged from 6 to 11 years, with a mean of 8 years, with approximately equal numbers of boys and girls.

The study was conducted in a family meal laboratory setting in Berlin, and groups were randomized to the longer or shorter meal setting first. The primary outcome was the total number of pieces of fruit and vegetables eaten by the child as part of each of the two meals.

Both meals were the “typical German evening meal of sliced bread, cold cuts of cheese and meat, and bite-sized pieces of fruits and vegetables,” followed by a dessert course of chocolate pudding or fruit yogurt and cookies, the researchers wrote. Beverages were water and one sugar-sweetened beverage; the specific foods and beverages were based on the child’s preferences, reported in an online preassessment, and the foods were consistent for the longer and shorter meals. All participants were asked not to eat for 2 hours prior to arriving for their meals at the laboratory.

During longer meals, children ate an average of seven additional bite-sized pieces of fruits and vegetables, which translates to approximately a full portion (defined as 100 g, such as a medium apple), the researchers wrote. The difference was significant compared with the shorter meals for fruits (P = .01) and vegetables (P < .001).

A piece of fruit was approximately 10 grams (6-10 g for grapes and tangerine segments; 10-14 g for cherry tomatoes; and 9-11 g for apple, banana, carrot, or cucumber). Other foods served with the meals included cheese, meats, butter, and sweet spreads.

Children also ate more slowly (defined as fewer bites per minute) during the longer meals, and they reported significantly greater satiety after the longer meals (P < .001 for both). The consumption of bread and cold cuts was similar for the two meal settings.

“Higher intake of fruits and vegetables during longer meals cannot be explained by longer exposure to food alone; otherwise, an increased intake of bread and cold cuts would have occurred,” the researchers wrote in their discussion. “One possible explanation is that the fruits and vegetables were cut into bite-sized pieces, making them convenient to eat.”

Further analysis showed that during the longer meals, more fruits and vegetables were consumed overall, but more vegetables were eaten from the start of the meal, while the additional fruit was eaten during the additional time at the end.

The findings were limited by several factors, primarily use of a laboratory setting that does not generalize to natural eating environments, the researchers noted. Other potential limitations included the effect of a video cameras on desirable behaviors and the limited ethnic and socioeconomic diversity of the study population, they said. The results were strengthened by the within-dyad study design that allowed for control of factors such as video observation, but more research is needed with more diverse groups and across longer time frames, the researchers said.

However, the results suggest that adding 10 minutes to a family mealtime can yield significant improvements in children’s diets, they said. They suggested strategies including playing music chosen by the child/children and setting rules that everyone must remain at the table for a certain length of time, with fruits and vegetables available on the table.

“If the effects of this simple, inexpensive, and low-threshold intervention prove stable over time, it could contribute to addressing a major public health problem,” the researchers concluded.
 

Findings intriguing, more data needed

The current study is important because food and vegetable intake in the majority of children falls below the recommended daily allowance, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

The key take-home message for clinicians is the continued need to stress the importance of family meals, said Dr. Kinsella. “Many children continue to be overbooked with activities, and it may be rare for many families to sit down together for a meal for any length of time.”

Don’t discount the potential effect of a longer school lunch on children’s fruit and vegetable consumption as well, she added. “Advocating for longer lunch time is important, as many kids report not being able to finish their lunch at school.”

The current study was limited by being conducted in a lab setting, which may have influenced children’s desire for different foods, “also they had fewer distractions, and were being offered favorite foods,” said Dr. Kinsella.

Looking ahead, “it would be interesting to see if this result carried over to nonpreferred fruits and veggies and made any difference for picky eaters,” she said. 

The study received no outside funding. The open-access publication of the study (but not the study itself) was supported by the Max Planck Institute for Human Development Library Open Access Fund. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose and serves on the editorial advisory board of Pediatric News.

Adding 10 minutes to family mealtimes increased children’s consumption of fruits and vegetables by approximately one portion, based on data from 50 parent-child dyads.

Family meals are known to affect children’s food choices and preferences and can be an effective setting for improving children’s nutrition, wrote Mattea Dallacker, PhD, of the University of Mannheim, Germany, and colleagues.

However, the effect of extending meal duration on increasing fruit and vegetable intake in particular has not been examined, they said.

In a study published in JAMA Network Open, the researchers provided two free evening meals to 50 parent-child dyads under each of two different conditions. The control condition was defined by the families as a regular family mealtime duration (an average meal was 20.83 minutes), while the intervention was an average meal time 10 minutes (50%) longer. The age of the parents ranged from 22 to 55 years, with a mean of 43 years; 72% of the parent participants were mothers. The children’s ages ranged from 6 to 11 years, with a mean of 8 years, with approximately equal numbers of boys and girls.

The study was conducted in a family meal laboratory setting in Berlin, and groups were randomized to the longer or shorter meal setting first. The primary outcome was the total number of pieces of fruit and vegetables eaten by the child as part of each of the two meals.

Both meals were the “typical German evening meal of sliced bread, cold cuts of cheese and meat, and bite-sized pieces of fruits and vegetables,” followed by a dessert course of chocolate pudding or fruit yogurt and cookies, the researchers wrote. Beverages were water and one sugar-sweetened beverage; the specific foods and beverages were based on the child’s preferences, reported in an online preassessment, and the foods were consistent for the longer and shorter meals. All participants were asked not to eat for 2 hours prior to arriving for their meals at the laboratory.

During longer meals, children ate an average of seven additional bite-sized pieces of fruits and vegetables, which translates to approximately a full portion (defined as 100 g, such as a medium apple), the researchers wrote. The difference was significant compared with the shorter meals for fruits (P = .01) and vegetables (P < .001).

A piece of fruit was approximately 10 grams (6-10 g for grapes and tangerine segments; 10-14 g for cherry tomatoes; and 9-11 g for apple, banana, carrot, or cucumber). Other foods served with the meals included cheese, meats, butter, and sweet spreads.

Children also ate more slowly (defined as fewer bites per minute) during the longer meals, and they reported significantly greater satiety after the longer meals (P < .001 for both). The consumption of bread and cold cuts was similar for the two meal settings.

“Higher intake of fruits and vegetables during longer meals cannot be explained by longer exposure to food alone; otherwise, an increased intake of bread and cold cuts would have occurred,” the researchers wrote in their discussion. “One possible explanation is that the fruits and vegetables were cut into bite-sized pieces, making them convenient to eat.”

Further analysis showed that during the longer meals, more fruits and vegetables were consumed overall, but more vegetables were eaten from the start of the meal, while the additional fruit was eaten during the additional time at the end.

The findings were limited by several factors, primarily use of a laboratory setting that does not generalize to natural eating environments, the researchers noted. Other potential limitations included the effect of a video cameras on desirable behaviors and the limited ethnic and socioeconomic diversity of the study population, they said. The results were strengthened by the within-dyad study design that allowed for control of factors such as video observation, but more research is needed with more diverse groups and across longer time frames, the researchers said.

However, the results suggest that adding 10 minutes to a family mealtime can yield significant improvements in children’s diets, they said. They suggested strategies including playing music chosen by the child/children and setting rules that everyone must remain at the table for a certain length of time, with fruits and vegetables available on the table.

“If the effects of this simple, inexpensive, and low-threshold intervention prove stable over time, it could contribute to addressing a major public health problem,” the researchers concluded.
 

Findings intriguing, more data needed

The current study is important because food and vegetable intake in the majority of children falls below the recommended daily allowance, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

The key take-home message for clinicians is the continued need to stress the importance of family meals, said Dr. Kinsella. “Many children continue to be overbooked with activities, and it may be rare for many families to sit down together for a meal for any length of time.”

Don’t discount the potential effect of a longer school lunch on children’s fruit and vegetable consumption as well, she added. “Advocating for longer lunch time is important, as many kids report not being able to finish their lunch at school.”

The current study was limited by being conducted in a lab setting, which may have influenced children’s desire for different foods, “also they had fewer distractions, and were being offered favorite foods,” said Dr. Kinsella.

Looking ahead, “it would be interesting to see if this result carried over to nonpreferred fruits and veggies and made any difference for picky eaters,” she said. 

The study received no outside funding. The open-access publication of the study (but not the study itself) was supported by the Max Planck Institute for Human Development Library Open Access Fund. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose and serves on the editorial advisory board of Pediatric News.

The biased discourse and double standards around antiobesity glucagon-like peptide 1 (GLP-1) receptor agonists continue apace, most recently in The New England Journal of Medicine (NEJM) where some economists opined that their coverage would be disastrous for Medicare.

Among their concerns? The drugs need to be taken long term (just like drugs for any other chronic condition). The new drugs are more expensive than the old drugs (just like new drugs for any other chronic condition). Lots of people will want to take them (just like highly effective drugs for any other chronic condition that has a significant quality-of-life or clinical impact). The U.K. recommended that they be covered only for 2 years (unlike drugs for any other chronic condition). And the Institute for Clinical and Economic Review (ICER) on which they lean heavily decided that $13,618 annually was too expensive for a medication that leads to sustained 15%-20% weight losses and those losses’ consequential benefits.

As a clinician working with patients who sustain those levels of weight loss, I find that conclusion confusing. Whether by way of lifestyle alone, or more often by way of lifestyle efforts plus medication or lifestyle efforts plus surgery, the benefits reported and seen with 15%-20% weight losses are almost uniformly huge. Patients are regularly seen discontinuing or reducing the dosage of multiple medications as a result of improvements to multiple weight-responsive comorbidities, and they also report objective benefits to mood, sleep, mobility, pain, and energy. Losing that much weight changes lives. Not to mention the impact that that degree of loss has on the primary prevention of so many diseases, including plausible reductions in many common cancers – reductions that have been shown to occur after surgery-related weight losses and for which there’s no plausible reason to imagine that they wouldn’t occur with pharmaceutical-related losses.

Are those discussions found in the NEJM op-ed or in the ICER report? Well, yes, sort of. However, in the NEJM op-ed, the word “prevention” isn’t used once, and unlike with oral hypoglycemics or antihypertensives, the authors state that with antiobesity medications, additional research is needed to determine whether medication-induced changes to A1c, blood pressure, and waist circumference would have clinical benefits: “Antiobesity medications have been shown to improve the surrogate end points of weight, glycated hemoglobin levels, systolic blood pressure, and waist circumference. Long-term studies are needed, however, to clarify how medication-induced changes in these surrogate markers translate to health outcomes.”

Primary prevention is mentioned in the ICER review, but in the “limitations” section where the authors explain that they didn’t include it in their modeling: “The long-term benefits of preventing other comorbidities including cancer, chronic kidney disease, osteoarthritis, and sleep apnea were not explicitly modeled in the base case.”

And they pretended that the impact on existing weight-responsive comorbidities mostly didn’t exist, too: “To limit the complexity of the cost-effectiveness model and to prevent double-counting of treatment benefits, we limited the long-term effects of treatments for weight management to cardiovascular risk and delays in the onset and/or diagnosis of diabetes mellitus.”

As far as cardiovascular disease (CVD) benefits go, you might have thought that it would be a slam dunk on that basis alone, at least according to a recent simple back-of-the-envelope math exercise presented at a recent American College of Cardiology conference, which applied the semaglutide treatment group weight changes in the STEP 1 trial to estimate the population impact on weight and obesity in 30- to 74-year-olds without prior CVD, and estimated 10-year CVD risks utilizing the BMI-based Framingham CVD risk scores. By their accounting, semaglutide treatment in eligible American patients has the potential to prevent over 1.6 million CVD events over 10 years.

Finally, even putting aside ICER’s admittedly and exceedingly narrow base case, what lifestyle-alone studies could ICER possibly be comparing with drug efficacy? And what does “alone” mean? Does “alone” mean with a months- or years long interprofessional behavioral program? Does “alone” mean by way of diet books? Does “alone” mean by way of simply “moving more and eating less”? I’m not aware of robust studies demonstrating any long-term meaningful, predictable, reproducible, durable weight loss outcomes for any lifestyle-only approach, intensive or otherwise.

It’s difficult for me to imagine a situation in which a drug other than an antiobesity drug would be found to have too many benefits to include in your cost-effectiveness analysis but where you’d be comfortable to run that analysis anyhow, and then come out against the drug’s recommendation and fearmonger about its use.

But then again, systemic weight bias is a hell of a drug.
 

Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa. He disclosed ties with Constant Health and Novo Nordisk, and has shared opinions via Weighty Matters and social media.

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

The biased discourse and double standards around antiobesity glucagon-like peptide 1 (GLP-1) receptor agonists continue apace, most recently in The New England Journal of Medicine (NEJM) where some economists opined that their coverage would be disastrous for Medicare.

Among their concerns? The drugs need to be taken long term (just like drugs for any other chronic condition). The new drugs are more expensive than the old drugs (just like new drugs for any other chronic condition). Lots of people will want to take them (just like highly effective drugs for any other chronic condition that has a significant quality-of-life or clinical impact). The U.K. recommended that they be covered only for 2 years (unlike drugs for any other chronic condition). And the Institute for Clinical and Economic Review (ICER) on which they lean heavily decided that $13,618 annually was too expensive for a medication that leads to sustained 15%-20% weight losses and those losses’ consequential benefits.

As a clinician working with patients who sustain those levels of weight loss, I find that conclusion confusing. Whether by way of lifestyle alone, or more often by way of lifestyle efforts plus medication or lifestyle efforts plus surgery, the benefits reported and seen with 15%-20% weight losses are almost uniformly huge. Patients are regularly seen discontinuing or reducing the dosage of multiple medications as a result of improvements to multiple weight-responsive comorbidities, and they also report objective benefits to mood, sleep, mobility, pain, and energy. Losing that much weight changes lives. Not to mention the impact that that degree of loss has on the primary prevention of so many diseases, including plausible reductions in many common cancers – reductions that have been shown to occur after surgery-related weight losses and for which there’s no plausible reason to imagine that they wouldn’t occur with pharmaceutical-related losses.

Are those discussions found in the NEJM op-ed or in the ICER report? Well, yes, sort of. However, in the NEJM op-ed, the word “prevention” isn’t used once, and unlike with oral hypoglycemics or antihypertensives, the authors state that with antiobesity medications, additional research is needed to determine whether medication-induced changes to A1c, blood pressure, and waist circumference would have clinical benefits: “Antiobesity medications have been shown to improve the surrogate end points of weight, glycated hemoglobin levels, systolic blood pressure, and waist circumference. Long-term studies are needed, however, to clarify how medication-induced changes in these surrogate markers translate to health outcomes.”

Primary prevention is mentioned in the ICER review, but in the “limitations” section where the authors explain that they didn’t include it in their modeling: “The long-term benefits of preventing other comorbidities including cancer, chronic kidney disease, osteoarthritis, and sleep apnea were not explicitly modeled in the base case.”

And they pretended that the impact on existing weight-responsive comorbidities mostly didn’t exist, too: “To limit the complexity of the cost-effectiveness model and to prevent double-counting of treatment benefits, we limited the long-term effects of treatments for weight management to cardiovascular risk and delays in the onset and/or diagnosis of diabetes mellitus.”

As far as cardiovascular disease (CVD) benefits go, you might have thought that it would be a slam dunk on that basis alone, at least according to a recent simple back-of-the-envelope math exercise presented at a recent American College of Cardiology conference, which applied the semaglutide treatment group weight changes in the STEP 1 trial to estimate the population impact on weight and obesity in 30- to 74-year-olds without prior CVD, and estimated 10-year CVD risks utilizing the BMI-based Framingham CVD risk scores. By their accounting, semaglutide treatment in eligible American patients has the potential to prevent over 1.6 million CVD events over 10 years.

Finally, even putting aside ICER’s admittedly and exceedingly narrow base case, what lifestyle-alone studies could ICER possibly be comparing with drug efficacy? And what does “alone” mean? Does “alone” mean with a months- or years long interprofessional behavioral program? Does “alone” mean by way of diet books? Does “alone” mean by way of simply “moving more and eating less”? I’m not aware of robust studies demonstrating any long-term meaningful, predictable, reproducible, durable weight loss outcomes for any lifestyle-only approach, intensive or otherwise.

It’s difficult for me to imagine a situation in which a drug other than an antiobesity drug would be found to have too many benefits to include in your cost-effectiveness analysis but where you’d be comfortable to run that analysis anyhow, and then come out against the drug’s recommendation and fearmonger about its use.

But then again, systemic weight bias is a hell of a drug.
 

Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa. He disclosed ties with Constant Health and Novo Nordisk, and has shared opinions via Weighty Matters and social media.

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

The biased discourse and double standards around antiobesity glucagon-like peptide 1 (GLP-1) receptor agonists continue apace, most recently in The New England Journal of Medicine (NEJM) where some economists opined that their coverage would be disastrous for Medicare.

Among their concerns? The drugs need to be taken long term (just like drugs for any other chronic condition). The new drugs are more expensive than the old drugs (just like new drugs for any other chronic condition). Lots of people will want to take them (just like highly effective drugs for any other chronic condition that has a significant quality-of-life or clinical impact). The U.K. recommended that they be covered only for 2 years (unlike drugs for any other chronic condition). And the Institute for Clinical and Economic Review (ICER) on which they lean heavily decided that $13,618 annually was too expensive for a medication that leads to sustained 15%-20% weight losses and those losses’ consequential benefits.

As a clinician working with patients who sustain those levels of weight loss, I find that conclusion confusing. Whether by way of lifestyle alone, or more often by way of lifestyle efforts plus medication or lifestyle efforts plus surgery, the benefits reported and seen with 15%-20% weight losses are almost uniformly huge. Patients are regularly seen discontinuing or reducing the dosage of multiple medications as a result of improvements to multiple weight-responsive comorbidities, and they also report objective benefits to mood, sleep, mobility, pain, and energy. Losing that much weight changes lives. Not to mention the impact that that degree of loss has on the primary prevention of so many diseases, including plausible reductions in many common cancers – reductions that have been shown to occur after surgery-related weight losses and for which there’s no plausible reason to imagine that they wouldn’t occur with pharmaceutical-related losses.

Are those discussions found in the NEJM op-ed or in the ICER report? Well, yes, sort of. However, in the NEJM op-ed, the word “prevention” isn’t used once, and unlike with oral hypoglycemics or antihypertensives, the authors state that with antiobesity medications, additional research is needed to determine whether medication-induced changes to A1c, blood pressure, and waist circumference would have clinical benefits: “Antiobesity medications have been shown to improve the surrogate end points of weight, glycated hemoglobin levels, systolic blood pressure, and waist circumference. Long-term studies are needed, however, to clarify how medication-induced changes in these surrogate markers translate to health outcomes.”

Primary prevention is mentioned in the ICER review, but in the “limitations” section where the authors explain that they didn’t include it in their modeling: “The long-term benefits of preventing other comorbidities including cancer, chronic kidney disease, osteoarthritis, and sleep apnea were not explicitly modeled in the base case.”

And they pretended that the impact on existing weight-responsive comorbidities mostly didn’t exist, too: “To limit the complexity of the cost-effectiveness model and to prevent double-counting of treatment benefits, we limited the long-term effects of treatments for weight management to cardiovascular risk and delays in the onset and/or diagnosis of diabetes mellitus.”

As far as cardiovascular disease (CVD) benefits go, you might have thought that it would be a slam dunk on that basis alone, at least according to a recent simple back-of-the-envelope math exercise presented at a recent American College of Cardiology conference, which applied the semaglutide treatment group weight changes in the STEP 1 trial to estimate the population impact on weight and obesity in 30- to 74-year-olds without prior CVD, and estimated 10-year CVD risks utilizing the BMI-based Framingham CVD risk scores. By their accounting, semaglutide treatment in eligible American patients has the potential to prevent over 1.6 million CVD events over 10 years.

Finally, even putting aside ICER’s admittedly and exceedingly narrow base case, what lifestyle-alone studies could ICER possibly be comparing with drug efficacy? And what does “alone” mean? Does “alone” mean with a months- or years long interprofessional behavioral program? Does “alone” mean by way of diet books? Does “alone” mean by way of simply “moving more and eating less”? I’m not aware of robust studies demonstrating any long-term meaningful, predictable, reproducible, durable weight loss outcomes for any lifestyle-only approach, intensive or otherwise.

It’s difficult for me to imagine a situation in which a drug other than an antiobesity drug would be found to have too many benefits to include in your cost-effectiveness analysis but where you’d be comfortable to run that analysis anyhow, and then come out against the drug’s recommendation and fearmonger about its use.

But then again, systemic weight bias is a hell of a drug.
 

Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa. He disclosed ties with Constant Health and Novo Nordisk, and has shared opinions via Weighty Matters and social media.

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

Among patients who undergo forceps-assisted vaginal delivery, obesity does not appear to be associated with increased risk for complications such as injuries to the anal sphincter or the need for their babies to be admitted to the neonatal intensive care unit, researchers have found.

But obesity does appear to increase the chances that when physicians attempt operative vaginal delivery with either forceps or a vacuum, patients will wind up undergoing cesarean delivery, another study found.

Taken together, the new data may help inform physicians’ decisions about when to consider operative vaginal delivery as an alternative to emergency cesarean births.

A prospective study showed that failed operative vaginal delivery – that is, a cesarean delivery after an attempted operative vaginal delivery – occurred for 10.1% of patients with obesity and 4.2% of those without obesity.

Researchers presented the findings at the meeting sponsored by the Society for Maternal-Fetal Medicine.

“We want to really try to reduce the rate of C-sections and primary cesarean deliveries. One of the ways to do that is to attempt operative vaginal delivery,” said Marissa Platner, MD, assistant professor of maternal-fetal medicine at Emory University School of Medicine, Atlanta, who was not involved in the new research.

Data on how obesity influences risks with operative vaginal delivery have been limited and mixed, the researchers said.

To examine how often attempted operative vaginal delivery fails in patients with obesity, Jennifer Grasch, MD, a maternal-fetal medicine fellow at the Ohio State University Wexner Medical Center, Columbus, and her colleagues conducted a secondary analysis of data from the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be, which included more than 10,000 participants.

“We know that cesarean sections among people with obesity are associated with increased complications, such as higher rates of infection and wound complications, than for people with lower BMI,” Dr. Grasch said. “Operative vaginal delivery can be an alternative to cesarean delivery in some situations, so we were interested in whether attempted operative vaginal delivery was also associated with higher rates of complications in individuals with obesity than those without obesity.”

The researchers focused on 791 patients with an attempted operative vaginal delivery. About 40% had a BMI of 30 or greater. Clinicians used a vacuum in approximately 60% of the attempts.

After an attempted vacuum-assisted delivery, neonatal morbidity was more common for infants whose mothers had obesity than for those whose mothers did not (32.7% vs. 22.3%; adjusted odds ratio, 1.61 [1.07-2.43]). Neonatal morbidity did not differ by obesity status following forceps-attempted delivery. Other adverse outcomes, including measures of maternal morbidity, did not significantly differ by obesity status, according to the researchers.
 

Choice may come down to experience

Several factors influence whether a clinician chooses forceps- or vacuum-assisted delivery or cesarean delivery, “but one of the most important is experience,” Dr. Grasch said. “Complication rates with both forms of operative vaginal delivery are low, yet there has been a trend toward lower rates of both in the last few decades.”

Elizabeth Cochrane, MD, a maternal-fetal medicine fellow at Mount Sinai Hospital, New York, and her colleagues investigated the relationship between obesity and adverse outcomes among patients with forceps-assisted vaginal deliveries.

The researchers analyzed data from 897 patients who underwent a forceps-assisted vaginal delivery between 2017 and 2021; 29% had a BMI of 30 or greater.

Injuries to the anal sphincter – which can lead to fecal incontinence – occurred in 18.7% of patients without obesity and in 17.7% of those with obesity. Admission to the neonatal intensive care unit occurred in 11.5% of patients without obesity and in 12.3% of patients with obesity. The differences were not statistically significant.

The bottom line: For forceps-assisted vaginal delivery, “obesity does not appear to be associated with increased rates” of adverse outcomes for mothers or newborns, the researchers concluded.
 

Reassuring data

The study by Dr. Cochrane’s group “provides helpful information for providers to be reassured when they are performing forceps deliveries” for patients with obesity, Dr. Platner said.

Rates of obesity have risen in the United States, and physicians often wonder whether a patient with obesity could be a candidate for forceps-assisted delivery, Dr. Cochrane said. In 2019, 29% of women had obesity before becoming pregnant.

“It all really comes down to how comfortable the provider is in that skill set and also the overall clinical scenario,” she said. “Sometimes an operative delivery with forceps or a vacuum can be the fastest way to deliver a baby when there is acute concern for maternal decompensation or fetal decompensation.”

The alternative is an emergency cesarean delivery. Given that those operations can be riskier and more difficult for patients with higher BMIs, a forceps-assisted delivery may be “an interesting alternative to emergency caesarean sections, as long as it is in an appropriate clinical setting with providers who feel very confident and comfortable using those devices,” Dr. Cochrane said.

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

Among patients who undergo forceps-assisted vaginal delivery, obesity does not appear to be associated with increased risk for complications such as injuries to the anal sphincter or the need for their babies to be admitted to the neonatal intensive care unit, researchers have found.

But obesity does appear to increase the chances that when physicians attempt operative vaginal delivery with either forceps or a vacuum, patients will wind up undergoing cesarean delivery, another study found.

Taken together, the new data may help inform physicians’ decisions about when to consider operative vaginal delivery as an alternative to emergency cesarean births.

A prospective study showed that failed operative vaginal delivery – that is, a cesarean delivery after an attempted operative vaginal delivery – occurred for 10.1% of patients with obesity and 4.2% of those without obesity.

Researchers presented the findings at the meeting sponsored by the Society for Maternal-Fetal Medicine.

“We want to really try to reduce the rate of C-sections and primary cesarean deliveries. One of the ways to do that is to attempt operative vaginal delivery,” said Marissa Platner, MD, assistant professor of maternal-fetal medicine at Emory University School of Medicine, Atlanta, who was not involved in the new research.

Data on how obesity influences risks with operative vaginal delivery have been limited and mixed, the researchers said.

To examine how often attempted operative vaginal delivery fails in patients with obesity, Jennifer Grasch, MD, a maternal-fetal medicine fellow at the Ohio State University Wexner Medical Center, Columbus, and her colleagues conducted a secondary analysis of data from the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be, which included more than 10,000 participants.

“We know that cesarean sections among people with obesity are associated with increased complications, such as higher rates of infection and wound complications, than for people with lower BMI,” Dr. Grasch said. “Operative vaginal delivery can be an alternative to cesarean delivery in some situations, so we were interested in whether attempted operative vaginal delivery was also associated with higher rates of complications in individuals with obesity than those without obesity.”

The researchers focused on 791 patients with an attempted operative vaginal delivery. About 40% had a BMI of 30 or greater. Clinicians used a vacuum in approximately 60% of the attempts.

After an attempted vacuum-assisted delivery, neonatal morbidity was more common for infants whose mothers had obesity than for those whose mothers did not (32.7% vs. 22.3%; adjusted odds ratio, 1.61 [1.07-2.43]). Neonatal morbidity did not differ by obesity status following forceps-attempted delivery. Other adverse outcomes, including measures of maternal morbidity, did not significantly differ by obesity status, according to the researchers.
 

Choice may come down to experience

Several factors influence whether a clinician chooses forceps- or vacuum-assisted delivery or cesarean delivery, “but one of the most important is experience,” Dr. Grasch said. “Complication rates with both forms of operative vaginal delivery are low, yet there has been a trend toward lower rates of both in the last few decades.”

Elizabeth Cochrane, MD, a maternal-fetal medicine fellow at Mount Sinai Hospital, New York, and her colleagues investigated the relationship between obesity and adverse outcomes among patients with forceps-assisted vaginal deliveries.

The researchers analyzed data from 897 patients who underwent a forceps-assisted vaginal delivery between 2017 and 2021; 29% had a BMI of 30 or greater.

Injuries to the anal sphincter – which can lead to fecal incontinence – occurred in 18.7% of patients without obesity and in 17.7% of those with obesity. Admission to the neonatal intensive care unit occurred in 11.5% of patients without obesity and in 12.3% of patients with obesity. The differences were not statistically significant.

The bottom line: For forceps-assisted vaginal delivery, “obesity does not appear to be associated with increased rates” of adverse outcomes for mothers or newborns, the researchers concluded.
 

Reassuring data

The study by Dr. Cochrane’s group “provides helpful information for providers to be reassured when they are performing forceps deliveries” for patients with obesity, Dr. Platner said.

Rates of obesity have risen in the United States, and physicians often wonder whether a patient with obesity could be a candidate for forceps-assisted delivery, Dr. Cochrane said. In 2019, 29% of women had obesity before becoming pregnant.

“It all really comes down to how comfortable the provider is in that skill set and also the overall clinical scenario,” she said. “Sometimes an operative delivery with forceps or a vacuum can be the fastest way to deliver a baby when there is acute concern for maternal decompensation or fetal decompensation.”

The alternative is an emergency cesarean delivery. Given that those operations can be riskier and more difficult for patients with higher BMIs, a forceps-assisted delivery may be “an interesting alternative to emergency caesarean sections, as long as it is in an appropriate clinical setting with providers who feel very confident and comfortable using those devices,” Dr. Cochrane said.

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

Among patients who undergo forceps-assisted vaginal delivery, obesity does not appear to be associated with increased risk for complications such as injuries to the anal sphincter or the need for their babies to be admitted to the neonatal intensive care unit, researchers have found.

But obesity does appear to increase the chances that when physicians attempt operative vaginal delivery with either forceps or a vacuum, patients will wind up undergoing cesarean delivery, another study found.

Taken together, the new data may help inform physicians’ decisions about when to consider operative vaginal delivery as an alternative to emergency cesarean births.

A prospective study showed that failed operative vaginal delivery – that is, a cesarean delivery after an attempted operative vaginal delivery – occurred for 10.1% of patients with obesity and 4.2% of those without obesity.

Researchers presented the findings at the meeting sponsored by the Society for Maternal-Fetal Medicine.

“We want to really try to reduce the rate of C-sections and primary cesarean deliveries. One of the ways to do that is to attempt operative vaginal delivery,” said Marissa Platner, MD, assistant professor of maternal-fetal medicine at Emory University School of Medicine, Atlanta, who was not involved in the new research.

Data on how obesity influences risks with operative vaginal delivery have been limited and mixed, the researchers said.

To examine how often attempted operative vaginal delivery fails in patients with obesity, Jennifer Grasch, MD, a maternal-fetal medicine fellow at the Ohio State University Wexner Medical Center, Columbus, and her colleagues conducted a secondary analysis of data from the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be, which included more than 10,000 participants.

“We know that cesarean sections among people with obesity are associated with increased complications, such as higher rates of infection and wound complications, than for people with lower BMI,” Dr. Grasch said. “Operative vaginal delivery can be an alternative to cesarean delivery in some situations, so we were interested in whether attempted operative vaginal delivery was also associated with higher rates of complications in individuals with obesity than those without obesity.”

The researchers focused on 791 patients with an attempted operative vaginal delivery. About 40% had a BMI of 30 or greater. Clinicians used a vacuum in approximately 60% of the attempts.

After an attempted vacuum-assisted delivery, neonatal morbidity was more common for infants whose mothers had obesity than for those whose mothers did not (32.7% vs. 22.3%; adjusted odds ratio, 1.61 [1.07-2.43]). Neonatal morbidity did not differ by obesity status following forceps-attempted delivery. Other adverse outcomes, including measures of maternal morbidity, did not significantly differ by obesity status, according to the researchers.
 

Choice may come down to experience

Several factors influence whether a clinician chooses forceps- or vacuum-assisted delivery or cesarean delivery, “but one of the most important is experience,” Dr. Grasch said. “Complication rates with both forms of operative vaginal delivery are low, yet there has been a trend toward lower rates of both in the last few decades.”

Elizabeth Cochrane, MD, a maternal-fetal medicine fellow at Mount Sinai Hospital, New York, and her colleagues investigated the relationship between obesity and adverse outcomes among patients with forceps-assisted vaginal deliveries.

The researchers analyzed data from 897 patients who underwent a forceps-assisted vaginal delivery between 2017 and 2021; 29% had a BMI of 30 or greater.

Injuries to the anal sphincter – which can lead to fecal incontinence – occurred in 18.7% of patients without obesity and in 17.7% of those with obesity. Admission to the neonatal intensive care unit occurred in 11.5% of patients without obesity and in 12.3% of patients with obesity. The differences were not statistically significant.

The bottom line: For forceps-assisted vaginal delivery, “obesity does not appear to be associated with increased rates” of adverse outcomes for mothers or newborns, the researchers concluded.
 

Reassuring data

The study by Dr. Cochrane’s group “provides helpful information for providers to be reassured when they are performing forceps deliveries” for patients with obesity, Dr. Platner said.

Rates of obesity have risen in the United States, and physicians often wonder whether a patient with obesity could be a candidate for forceps-assisted delivery, Dr. Cochrane said. In 2019, 29% of women had obesity before becoming pregnant.

“It all really comes down to how comfortable the provider is in that skill set and also the overall clinical scenario,” she said. “Sometimes an operative delivery with forceps or a vacuum can be the fastest way to deliver a baby when there is acute concern for maternal decompensation or fetal decompensation.”

The alternative is an emergency cesarean delivery. Given that those operations can be riskier and more difficult for patients with higher BMIs, a forceps-assisted delivery may be “an interesting alternative to emergency caesarean sections, as long as it is in an appropriate clinical setting with providers who feel very confident and comfortable using those devices,” Dr. Cochrane said.

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

Social media outlets are full of stories about celebrities who have lost weight with the new generation of incretin medications like semaglutide (Ozempic and Wegovy) and tirzepatide (Mounjaro).

Some of these medicines are approved for treating obesity (Wegovy), whereas others are approved for type 2 diabetes (Ozempic and Mounjaro). Tirzepatide (Mounjaro) has been fast-tracked for approval for weight loss by the U.S. Food and Drug Administration this year, and in the first of the series of studies looking at its effect on obesity, the SURMOUNT-1 trial, tirzepatide demonstrated a mean weight loss of around 22% in people without diabetes, spurring significant off-label use.

Our offices are full of patients who have taken these medications, with unprecedented improvements in their weight, cardiometabolic health, and quality of life. What happens when patients stop taking these medications? Or more importantly, why stop them?

Although these drugs are very effective for weight loss and treating diabetes, there can be adverse effects, primarily gastrointestinal, that limit treatment continuation. Nausea is the most common side effect and usually diminishes over time. Slow dose titration and dietary modification can minimize unwanted gastrointestinal side effects.

Drug-induced acute pancreatitis, a rare adverse event requiring patients to stop therapy, was seen in approximately 0.2% of people in clinical trials.
 

Medications effective but cost prohibitive?

Beyond adverse effects, patients may be forced to stop treatment because of medication cost, changes in insurance coverage, or issues with drug availability.

Two incretin therapies currently approved for treating obesity – liraglutide (Saxenda) and semaglutide (Wegovy) – cost around $1,400 per month. Insurance coverage and manufacturer discounts can make treatment affordable, but anti-obesity medicines aren’t covered by Medicare or by many employer-sponsored commercial plans.

Changes in employment or insurance coverage, or expiration of manufacturer copay cards, may require patients to stop or change therapies. The increased prescribing and overall expense of these drugs have prompted insurance plans and self-insured groups to consider whether providing coverage for these medications is sustainable.

Limited coverage has led to significant off-label prescribing of incretin therapies that aren’t approved for treating obesity (for instance, Ozempic and Mounjaro) and compounding pharmacies selling peptides that allegedly contain the active pharmaceutical ingredients. High demand for these medications has created significant supply shortages over the past year, causing many people to be without treatment for significant periods of time, as reported by this news organization.

Recently, I saw a patient who lost more than 30 pounds with semaglutide (Wegovy). She then changed employers and the medication was no longer covered. She gained back almost 10 pounds over 3 months and was prescribed tirzepatide (Mounjaro) off-label for weight loss by another provider, using a manufacturer discount card to make the medication affordable. The patient did well with the new regimen and lost about 20 pounds, but the pharmacy stopped filling the prescription when changes were made to the discount card. Afraid of regaining the weight, she came to see us as a new patient to discuss her options with her lack of coverage for anti-obesity medications.
 

Stopping equals weight regain

Obesity is a chronic disease like hypertension. It responds to treatment and when people stop taking these anti-obesity medications, this is generally associated with increased appetite and less satiety, and there is subsequent weight regain and a recurrence in excess weight-related complications.

The STEP-1 trial extension showed an initial mean body weight reduction of 17.3% with weekly semaglutide 2.4 mg over 1 year. On average, two-thirds of the weight lost was regained by participants within 1 year of stopping semaglutide and the study’s lifestyle intervention. Many of the improvements seen in cardiometabolic variables, like blood glucose and blood pressure, similarly reverted to baseline.

There are also 2-year data from the STEP-5 trial with semaglutide; 3-year data from the SCALE trial with liraglutide; and 5-year nonrandomized data with multiple agents that show durable, clinically significant weight loss from medical therapies for obesity.

These data together demonstrate that medications are effective for durable weight loss if they are continued. However, this is not how obesity is currently treated. Anti-obesity medications are prescribed to less than 3% of eligible people in the United States, and the average duration of therapy is less than 90 days. This treatment length isn’t sufficient to see the full benefits most medications offer and certainly doesn’t support long-term weight maintenance.

A recent study showed that, in addition to maintaining weight loss from medical therapies, incretin-containing anti-obesity medication regimens were effective for treating weight regain and facilitating healthier weight after bariatric surgery.

Chronic therapy is needed for weight maintenance because several neurohormonal changes occur owing to weight loss. Metabolic adaptation is the relative reduction in energy expenditure, below what would be expected, in people after weight loss. When this is combined with physiologic changes that increase appetite and decrease satiety, many people create a positive energy balance that results in weight regain. This has been observed in reality TV shows such as “The Biggest Loser”: It’s biology, not willpower.

Unfortunately, many people – including health care providers – don’t understand how these changes promote weight regain and patients are too often blamed when their weight goes back up after medications are stopped. This blame is greatly misinformed by weight-biased beliefs that people with obesity are lazy and lack self-control for weight loss or maintenance. Nobody would be surprised if someone’s blood pressure went up if their antihypertensive medications were stopped. Why do we think so differently when treating obesity?

The prevalence of obesity in the United States is over 40% and growing. We are fortunate to have new medications that on average lead to 15% or greater weight loss when combined with lifestyle modification.

However, these medications are expensive and the limited insurance coverage currently available may not improve. From a patient experience perspective, it’s distressing to have to discontinue treatments that have helped to achieve a healthier weight and then experience regain.

People need better access to evidence-based treatments for obesity, which include lifestyle interventions, anti-obesity medications, and bariatric procedures. Successful treatment of obesity should include a personalized, patient-centered approach that may require a combination of therapies, such as medications and surgery, for lasting weight control.

Dr. Almandoz is associate professor, department of internal medicine, division of endocrinology; medical director, weight wellness program, University of Texas Southwestern, Dallas. He disclosed ties with Novo Nordisk and Eli Lilly. Follow Dr. Almandoz on Twitter: @JaimeAlmandoz.

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

Social media outlets are full of stories about celebrities who have lost weight with the new generation of incretin medications like semaglutide (Ozempic and Wegovy) and tirzepatide (Mounjaro).

Some of these medicines are approved for treating obesity (Wegovy), whereas others are approved for type 2 diabetes (Ozempic and Mounjaro). Tirzepatide (Mounjaro) has been fast-tracked for approval for weight loss by the U.S. Food and Drug Administration this year, and in the first of the series of studies looking at its effect on obesity, the SURMOUNT-1 trial, tirzepatide demonstrated a mean weight loss of around 22% in people without diabetes, spurring significant off-label use.

Our offices are full of patients who have taken these medications, with unprecedented improvements in their weight, cardiometabolic health, and quality of life. What happens when patients stop taking these medications? Or more importantly, why stop them?

Although these drugs are very effective for weight loss and treating diabetes, there can be adverse effects, primarily gastrointestinal, that limit treatment continuation. Nausea is the most common side effect and usually diminishes over time. Slow dose titration and dietary modification can minimize unwanted gastrointestinal side effects.

Drug-induced acute pancreatitis, a rare adverse event requiring patients to stop therapy, was seen in approximately 0.2% of people in clinical trials.
 

Medications effective but cost prohibitive?

Beyond adverse effects, patients may be forced to stop treatment because of medication cost, changes in insurance coverage, or issues with drug availability.

Two incretin therapies currently approved for treating obesity – liraglutide (Saxenda) and semaglutide (Wegovy) – cost around $1,400 per month. Insurance coverage and manufacturer discounts can make treatment affordable, but anti-obesity medicines aren’t covered by Medicare or by many employer-sponsored commercial plans.

Changes in employment or insurance coverage, or expiration of manufacturer copay cards, may require patients to stop or change therapies. The increased prescribing and overall expense of these drugs have prompted insurance plans and self-insured groups to consider whether providing coverage for these medications is sustainable.

Limited coverage has led to significant off-label prescribing of incretin therapies that aren’t approved for treating obesity (for instance, Ozempic and Mounjaro) and compounding pharmacies selling peptides that allegedly contain the active pharmaceutical ingredients. High demand for these medications has created significant supply shortages over the past year, causing many people to be without treatment for significant periods of time, as reported by this news organization.

Recently, I saw a patient who lost more than 30 pounds with semaglutide (Wegovy). She then changed employers and the medication was no longer covered. She gained back almost 10 pounds over 3 months and was prescribed tirzepatide (Mounjaro) off-label for weight loss by another provider, using a manufacturer discount card to make the medication affordable. The patient did well with the new regimen and lost about 20 pounds, but the pharmacy stopped filling the prescription when changes were made to the discount card. Afraid of regaining the weight, she came to see us as a new patient to discuss her options with her lack of coverage for anti-obesity medications.
 

Stopping equals weight regain

Obesity is a chronic disease like hypertension. It responds to treatment and when people stop taking these anti-obesity medications, this is generally associated with increased appetite and less satiety, and there is subsequent weight regain and a recurrence in excess weight-related complications.

The STEP-1 trial extension showed an initial mean body weight reduction of 17.3% with weekly semaglutide 2.4 mg over 1 year. On average, two-thirds of the weight lost was regained by participants within 1 year of stopping semaglutide and the study’s lifestyle intervention. Many of the improvements seen in cardiometabolic variables, like blood glucose and blood pressure, similarly reverted to baseline.

There are also 2-year data from the STEP-5 trial with semaglutide; 3-year data from the SCALE trial with liraglutide; and 5-year nonrandomized data with multiple agents that show durable, clinically significant weight loss from medical therapies for obesity.

These data together demonstrate that medications are effective for durable weight loss if they are continued. However, this is not how obesity is currently treated. Anti-obesity medications are prescribed to less than 3% of eligible people in the United States, and the average duration of therapy is less than 90 days. This treatment length isn’t sufficient to see the full benefits most medications offer and certainly doesn’t support long-term weight maintenance.

A recent study showed that, in addition to maintaining weight loss from medical therapies, incretin-containing anti-obesity medication regimens were effective for treating weight regain and facilitating healthier weight after bariatric surgery.

Chronic therapy is needed for weight maintenance because several neurohormonal changes occur owing to weight loss. Metabolic adaptation is the relative reduction in energy expenditure, below what would be expected, in people after weight loss. When this is combined with physiologic changes that increase appetite and decrease satiety, many people create a positive energy balance that results in weight regain. This has been observed in reality TV shows such as “The Biggest Loser”: It’s biology, not willpower.

Unfortunately, many people – including health care providers – don’t understand how these changes promote weight regain and patients are too often blamed when their weight goes back up after medications are stopped. This blame is greatly misinformed by weight-biased beliefs that people with obesity are lazy and lack self-control for weight loss or maintenance. Nobody would be surprised if someone’s blood pressure went up if their antihypertensive medications were stopped. Why do we think so differently when treating obesity?

The prevalence of obesity in the United States is over 40% and growing. We are fortunate to have new medications that on average lead to 15% or greater weight loss when combined with lifestyle modification.

However, these medications are expensive and the limited insurance coverage currently available may not improve. From a patient experience perspective, it’s distressing to have to discontinue treatments that have helped to achieve a healthier weight and then experience regain.

People need better access to evidence-based treatments for obesity, which include lifestyle interventions, anti-obesity medications, and bariatric procedures. Successful treatment of obesity should include a personalized, patient-centered approach that may require a combination of therapies, such as medications and surgery, for lasting weight control.

Dr. Almandoz is associate professor, department of internal medicine, division of endocrinology; medical director, weight wellness program, University of Texas Southwestern, Dallas. He disclosed ties with Novo Nordisk and Eli Lilly. Follow Dr. Almandoz on Twitter: @JaimeAlmandoz.

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

Social media outlets are full of stories about celebrities who have lost weight with the new generation of incretin medications like semaglutide (Ozempic and Wegovy) and tirzepatide (Mounjaro).

Some of these medicines are approved for treating obesity (Wegovy), whereas others are approved for type 2 diabetes (Ozempic and Mounjaro). Tirzepatide (Mounjaro) has been fast-tracked for approval for weight loss by the U.S. Food and Drug Administration this year, and in the first of the series of studies looking at its effect on obesity, the SURMOUNT-1 trial, tirzepatide demonstrated a mean weight loss of around 22% in people without diabetes, spurring significant off-label use.

Our offices are full of patients who have taken these medications, with unprecedented improvements in their weight, cardiometabolic health, and quality of life. What happens when patients stop taking these medications? Or more importantly, why stop them?

Although these drugs are very effective for weight loss and treating diabetes, there can be adverse effects, primarily gastrointestinal, that limit treatment continuation. Nausea is the most common side effect and usually diminishes over time. Slow dose titration and dietary modification can minimize unwanted gastrointestinal side effects.

Drug-induced acute pancreatitis, a rare adverse event requiring patients to stop therapy, was seen in approximately 0.2% of people in clinical trials.
 

Medications effective but cost prohibitive?

Beyond adverse effects, patients may be forced to stop treatment because of medication cost, changes in insurance coverage, or issues with drug availability.

Two incretin therapies currently approved for treating obesity – liraglutide (Saxenda) and semaglutide (Wegovy) – cost around $1,400 per month. Insurance coverage and manufacturer discounts can make treatment affordable, but anti-obesity medicines aren’t covered by Medicare or by many employer-sponsored commercial plans.

Changes in employment or insurance coverage, or expiration of manufacturer copay cards, may require patients to stop or change therapies. The increased prescribing and overall expense of these drugs have prompted insurance plans and self-insured groups to consider whether providing coverage for these medications is sustainable.

Limited coverage has led to significant off-label prescribing of incretin therapies that aren’t approved for treating obesity (for instance, Ozempic and Mounjaro) and compounding pharmacies selling peptides that allegedly contain the active pharmaceutical ingredients. High demand for these medications has created significant supply shortages over the past year, causing many people to be without treatment for significant periods of time, as reported by this news organization.

Recently, I saw a patient who lost more than 30 pounds with semaglutide (Wegovy). She then changed employers and the medication was no longer covered. She gained back almost 10 pounds over 3 months and was prescribed tirzepatide (Mounjaro) off-label for weight loss by another provider, using a manufacturer discount card to make the medication affordable. The patient did well with the new regimen and lost about 20 pounds, but the pharmacy stopped filling the prescription when changes were made to the discount card. Afraid of regaining the weight, she came to see us as a new patient to discuss her options with her lack of coverage for anti-obesity medications.
 

Stopping equals weight regain

Obesity is a chronic disease like hypertension. It responds to treatment and when people stop taking these anti-obesity medications, this is generally associated with increased appetite and less satiety, and there is subsequent weight regain and a recurrence in excess weight-related complications.

The STEP-1 trial extension showed an initial mean body weight reduction of 17.3% with weekly semaglutide 2.4 mg over 1 year. On average, two-thirds of the weight lost was regained by participants within 1 year of stopping semaglutide and the study’s lifestyle intervention. Many of the improvements seen in cardiometabolic variables, like blood glucose and blood pressure, similarly reverted to baseline.

There are also 2-year data from the STEP-5 trial with semaglutide; 3-year data from the SCALE trial with liraglutide; and 5-year nonrandomized data with multiple agents that show durable, clinically significant weight loss from medical therapies for obesity.

These data together demonstrate that medications are effective for durable weight loss if they are continued. However, this is not how obesity is currently treated. Anti-obesity medications are prescribed to less than 3% of eligible people in the United States, and the average duration of therapy is less than 90 days. This treatment length isn’t sufficient to see the full benefits most medications offer and certainly doesn’t support long-term weight maintenance.

A recent study showed that, in addition to maintaining weight loss from medical therapies, incretin-containing anti-obesity medication regimens were effective for treating weight regain and facilitating healthier weight after bariatric surgery.

Chronic therapy is needed for weight maintenance because several neurohormonal changes occur owing to weight loss. Metabolic adaptation is the relative reduction in energy expenditure, below what would be expected, in people after weight loss. When this is combined with physiologic changes that increase appetite and decrease satiety, many people create a positive energy balance that results in weight regain. This has been observed in reality TV shows such as “The Biggest Loser”: It’s biology, not willpower.

Unfortunately, many people – including health care providers – don’t understand how these changes promote weight regain and patients are too often blamed when their weight goes back up after medications are stopped. This blame is greatly misinformed by weight-biased beliefs that people with obesity are lazy and lack self-control for weight loss or maintenance. Nobody would be surprised if someone’s blood pressure went up if their antihypertensive medications were stopped. Why do we think so differently when treating obesity?

The prevalence of obesity in the United States is over 40% and growing. We are fortunate to have new medications that on average lead to 15% or greater weight loss when combined with lifestyle modification.

However, these medications are expensive and the limited insurance coverage currently available may not improve. From a patient experience perspective, it’s distressing to have to discontinue treatments that have helped to achieve a healthier weight and then experience regain.

People need better access to evidence-based treatments for obesity, which include lifestyle interventions, anti-obesity medications, and bariatric procedures. Successful treatment of obesity should include a personalized, patient-centered approach that may require a combination of therapies, such as medications and surgery, for lasting weight control.

Dr. Almandoz is associate professor, department of internal medicine, division of endocrinology; medical director, weight wellness program, University of Texas Southwestern, Dallas. He disclosed ties with Novo Nordisk and Eli Lilly. Follow Dr. Almandoz on Twitter: @JaimeAlmandoz.

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