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Guidelines for children with obesity: Family and treatment are key
Douglas Lunsford’s son Samuel has struggled with obesity all his life.
Just before turning 14, Samuel, now 25, took part in a program at Ohio-based Nationwide Children’s Hospital’s Center for Healthy Weight and Nutrition. The program consisted of twice-weekly meetings with a nutritionist, including lessons in food portion size, what food does within the body, what foods can be used to supplement other foods, and similar topics, as well as physical exercise.
Although the program was designed for youngsters with weight problems, Mr. Lunsford also took part.
“They would exercise us and work us out,” he said.
Father and son did the program together for 2 years. Since then, Mr. Lunsford has advocated for youngsters with obesity.
“Samuel’s struggle spurred us into action,” he said.
Eventually, Mr. Lunsford helped create the American Academy of Pediatrics’ recently released Clinical Practice Guideline for the Evaluation and Treatment of Children and Adolescents With Obesity.
Helping create change
According to Sandra Hassink, MD, coauthor of the guideline and vice chair of the Clinical Practice Guideline Subcommittee on Obesity, the goal was to “help patients make changes in lifestyle, behaviors, or environment in a sustainable way and also to involve families in decision-making at every step of the way.”
Ideally, a child would receive intense behavioral and lifestyle treatment, although this approach isn’t always available and might be challenging to deliver. The most effective treatments include at least 26 hours of face-to-face, family-based treatments, consisting of many different components and lasting 3-12 months.
The guideline suggests that doctors offer adolescents 12 and older medication to assist in weight loss, along with health, behavior, and lifestyle treatment, and that teens who have severe obesity should consider metabolic and bariatric surgery as they continue intense health behavior and lifestyle treatment.
“We’re living at a time where we’ve watched obesity affect our children and adult population for 4 decades and, along with the risk of obesity, we’ve watched a rise in obesity; we’re seeing increases in illness that go along with obesity, such as type 2 diabetes, lipid diseases like high cholesterol, and nonalcoholic fatty liver disease,” Dr. Hassink said.
She explained that, as people gain weight, the cells in adipose (fatty) tissues start to malfunction and produce inflammatory chemicals that cause these illnesses.
“So having extra adipose tissue is a risk,” she said. “As pediatricians, we measure body mass index [BMI] – which is calculated based on height and weight – as a way of seeing whether the child could be at risk for developing these dysfunctioning cells. If so, we screen them for prediabetes, lipid disease, or liver disease and other obesity-related comorbidities.”
In addition, “we’re concerned about the mental health of children with obesity because of the weight bias in our culture,” said Dr. Hassink. “A child gets stigmatized, and this takes the form of bullying and teasing, and leads to low self-esteem, depression, and anxiety. So we know we have a host of physical problems we need to look out for, as well as the emotional and psychological effects of how our culture views things.”
Are parents ready for the new approach?
A new report from Harmony Healthcare IT, a data management firm that works with health data, looked at how parents regard their children’s obesity. The company surveyed more than 1,000 parents and found that one-tenth of respondents had children who were overweight or obese and over a quarter (26%) worried about their child’s weight.
Nearly 40% of parents would consider weight loss medication for their child if the child became obese at age 12, and about 16% would consider weight loss surgery. But most parents would not consider this surgery until their child was an average age of 15 rather than the AAP’s recommended age of 13.
Mr. Lunsford said that his son considered surgery and medication but was “never comfortable” with these approaches.
This isn’t unusual, Dr. Hassink said. “Not every parent will think the same way, and their view will be based on their experience and what’s going on with their child.”
The guideline wasn’t designed to encourage every child to try medication or have surgery, she said.
“But parents now know that there are potentially helpful choices here that we didn’t have years ago, and those can be discussed with the child’s pediatrician.”
Challenges to keeping healthy
It’s tough to stay healthy and not develop obesity in our modern environment, Dr. Hassink said.
“There’s a lot of processed food, a lot of sugar in our foods, a lot of sedentary behavior, and a decrease in physical activity. In many communities, it’s hard for people to get healthy foods.”
Mr. Lunsford said that when his son was in his late teens and would go out with friends, they typically went to fast-food restaurants.
“Sam would say ‘yes’ to these foods, although he knew they weren’t good for him, because he wanted to be like everyone else,” he said.
But parents now know that there are potentially helpful choices here that we didn’t have years ago, and those can be discussed with the child’s pediatrician, he said.
Harmony Health IT’s survey found that many parents say it is a struggle to get kids to eat healthy foods and get enough sleep. Although almost all respondents (83%) said they try to prepare healthy, home-cooked meals, 39% eat fast food at least once a week, mostly because parents are too tired to cook.
Dr. Hassink said the COVID-19 pandemic also played a role.
“We knew that COVID would be hard for kids with obesity, and there might be weight gain because of the extra sedentary time and fewer sporting activities, and there was a high cost of food to families who are already economically strapped,” she said.
In general, family support is essential, Dr. Hassink said. “Obesity treatment requires that the family be involved. The family is living in the same nutritional and activity environment as their child. Everyone has to be on board.”
Talking to kids about food and weight
The survey found that many parents struggle to talk about food and weight with their children. The AAP guideline notes that involving a health care professional can help.
“If a parent or caregiver is concerned about a child’s weight, he or she can take the child to their pediatrician,” Dr. Hassink said. “The first thing the pediatrician will do is ask about the child’s overall health, review the family history – because obesity tends to run in families – and see if other conditions, like diabetes, also run in the family.”
The pediatrician will do a physical examination that includes BMI and, if it’s high, other tests looking at blood sugar, lipids, and liver function may be performed.
Ideally, the child will be prescribed intense lifestyle and behavioral treatment that will take the child’s and family’s nutrition into account, as well as physical activity and the amount of sleep the child is getting, which is sometimes tied to weight gain. If the child has disordered eating, such as binge eating disorder, they can be evaluated and treated for that.
Each child is seen as an individual with a particular set of needs. “One size doesn’t fit all,” Dr. Hassink said.
Providing emotional support for children with obesity
Pediatricians can assess the child’s mental, emotional, and social well-being. “Children who are bullied or teased may need help working through that. Children experiencing depression may need treatment,” Dr. Hassink said.
Mr. Lunsford said Samuel was fortunate in that he rarely got taunted.
“Part of the reason is that, although weight was an issue, he never allowed his weight to define him,” he said. “He was always an extroverted kind of kid, athletic, very outgoing and friendly, and being overweight was never part of his identity.”
Mr. Lunsford encourages parents whose children are teased or bullied to create a “no-judgment” zone at home.
“Let your kids know that their parents love them for who they are,” he said. “Emphasize that weight is a ‘number’ and health is a ‘lifestyle.’ Try to highlight the good things in their lives and encourage them to be as active as they can in the things that interest them.”
A version of this article originally appeared on WebMD.com.
Douglas Lunsford’s son Samuel has struggled with obesity all his life.
Just before turning 14, Samuel, now 25, took part in a program at Ohio-based Nationwide Children’s Hospital’s Center for Healthy Weight and Nutrition. The program consisted of twice-weekly meetings with a nutritionist, including lessons in food portion size, what food does within the body, what foods can be used to supplement other foods, and similar topics, as well as physical exercise.
Although the program was designed for youngsters with weight problems, Mr. Lunsford also took part.
“They would exercise us and work us out,” he said.
Father and son did the program together for 2 years. Since then, Mr. Lunsford has advocated for youngsters with obesity.
“Samuel’s struggle spurred us into action,” he said.
Eventually, Mr. Lunsford helped create the American Academy of Pediatrics’ recently released Clinical Practice Guideline for the Evaluation and Treatment of Children and Adolescents With Obesity.
Helping create change
According to Sandra Hassink, MD, coauthor of the guideline and vice chair of the Clinical Practice Guideline Subcommittee on Obesity, the goal was to “help patients make changes in lifestyle, behaviors, or environment in a sustainable way and also to involve families in decision-making at every step of the way.”
Ideally, a child would receive intense behavioral and lifestyle treatment, although this approach isn’t always available and might be challenging to deliver. The most effective treatments include at least 26 hours of face-to-face, family-based treatments, consisting of many different components and lasting 3-12 months.
The guideline suggests that doctors offer adolescents 12 and older medication to assist in weight loss, along with health, behavior, and lifestyle treatment, and that teens who have severe obesity should consider metabolic and bariatric surgery as they continue intense health behavior and lifestyle treatment.
“We’re living at a time where we’ve watched obesity affect our children and adult population for 4 decades and, along with the risk of obesity, we’ve watched a rise in obesity; we’re seeing increases in illness that go along with obesity, such as type 2 diabetes, lipid diseases like high cholesterol, and nonalcoholic fatty liver disease,” Dr. Hassink said.
She explained that, as people gain weight, the cells in adipose (fatty) tissues start to malfunction and produce inflammatory chemicals that cause these illnesses.
“So having extra adipose tissue is a risk,” she said. “As pediatricians, we measure body mass index [BMI] – which is calculated based on height and weight – as a way of seeing whether the child could be at risk for developing these dysfunctioning cells. If so, we screen them for prediabetes, lipid disease, or liver disease and other obesity-related comorbidities.”
In addition, “we’re concerned about the mental health of children with obesity because of the weight bias in our culture,” said Dr. Hassink. “A child gets stigmatized, and this takes the form of bullying and teasing, and leads to low self-esteem, depression, and anxiety. So we know we have a host of physical problems we need to look out for, as well as the emotional and psychological effects of how our culture views things.”
Are parents ready for the new approach?
A new report from Harmony Healthcare IT, a data management firm that works with health data, looked at how parents regard their children’s obesity. The company surveyed more than 1,000 parents and found that one-tenth of respondents had children who were overweight or obese and over a quarter (26%) worried about their child’s weight.
Nearly 40% of parents would consider weight loss medication for their child if the child became obese at age 12, and about 16% would consider weight loss surgery. But most parents would not consider this surgery until their child was an average age of 15 rather than the AAP’s recommended age of 13.
Mr. Lunsford said that his son considered surgery and medication but was “never comfortable” with these approaches.
This isn’t unusual, Dr. Hassink said. “Not every parent will think the same way, and their view will be based on their experience and what’s going on with their child.”
The guideline wasn’t designed to encourage every child to try medication or have surgery, she said.
“But parents now know that there are potentially helpful choices here that we didn’t have years ago, and those can be discussed with the child’s pediatrician.”
Challenges to keeping healthy
It’s tough to stay healthy and not develop obesity in our modern environment, Dr. Hassink said.
“There’s a lot of processed food, a lot of sugar in our foods, a lot of sedentary behavior, and a decrease in physical activity. In many communities, it’s hard for people to get healthy foods.”
Mr. Lunsford said that when his son was in his late teens and would go out with friends, they typically went to fast-food restaurants.
“Sam would say ‘yes’ to these foods, although he knew they weren’t good for him, because he wanted to be like everyone else,” he said.
But parents now know that there are potentially helpful choices here that we didn’t have years ago, and those can be discussed with the child’s pediatrician, he said.
Harmony Health IT’s survey found that many parents say it is a struggle to get kids to eat healthy foods and get enough sleep. Although almost all respondents (83%) said they try to prepare healthy, home-cooked meals, 39% eat fast food at least once a week, mostly because parents are too tired to cook.
Dr. Hassink said the COVID-19 pandemic also played a role.
“We knew that COVID would be hard for kids with obesity, and there might be weight gain because of the extra sedentary time and fewer sporting activities, and there was a high cost of food to families who are already economically strapped,” she said.
In general, family support is essential, Dr. Hassink said. “Obesity treatment requires that the family be involved. The family is living in the same nutritional and activity environment as their child. Everyone has to be on board.”
Talking to kids about food and weight
The survey found that many parents struggle to talk about food and weight with their children. The AAP guideline notes that involving a health care professional can help.
“If a parent or caregiver is concerned about a child’s weight, he or she can take the child to their pediatrician,” Dr. Hassink said. “The first thing the pediatrician will do is ask about the child’s overall health, review the family history – because obesity tends to run in families – and see if other conditions, like diabetes, also run in the family.”
The pediatrician will do a physical examination that includes BMI and, if it’s high, other tests looking at blood sugar, lipids, and liver function may be performed.
Ideally, the child will be prescribed intense lifestyle and behavioral treatment that will take the child’s and family’s nutrition into account, as well as physical activity and the amount of sleep the child is getting, which is sometimes tied to weight gain. If the child has disordered eating, such as binge eating disorder, they can be evaluated and treated for that.
Each child is seen as an individual with a particular set of needs. “One size doesn’t fit all,” Dr. Hassink said.
Providing emotional support for children with obesity
Pediatricians can assess the child’s mental, emotional, and social well-being. “Children who are bullied or teased may need help working through that. Children experiencing depression may need treatment,” Dr. Hassink said.
Mr. Lunsford said Samuel was fortunate in that he rarely got taunted.
“Part of the reason is that, although weight was an issue, he never allowed his weight to define him,” he said. “He was always an extroverted kind of kid, athletic, very outgoing and friendly, and being overweight was never part of his identity.”
Mr. Lunsford encourages parents whose children are teased or bullied to create a “no-judgment” zone at home.
“Let your kids know that their parents love them for who they are,” he said. “Emphasize that weight is a ‘number’ and health is a ‘lifestyle.’ Try to highlight the good things in their lives and encourage them to be as active as they can in the things that interest them.”
A version of this article originally appeared on WebMD.com.
Douglas Lunsford’s son Samuel has struggled with obesity all his life.
Just before turning 14, Samuel, now 25, took part in a program at Ohio-based Nationwide Children’s Hospital’s Center for Healthy Weight and Nutrition. The program consisted of twice-weekly meetings with a nutritionist, including lessons in food portion size, what food does within the body, what foods can be used to supplement other foods, and similar topics, as well as physical exercise.
Although the program was designed for youngsters with weight problems, Mr. Lunsford also took part.
“They would exercise us and work us out,” he said.
Father and son did the program together for 2 years. Since then, Mr. Lunsford has advocated for youngsters with obesity.
“Samuel’s struggle spurred us into action,” he said.
Eventually, Mr. Lunsford helped create the American Academy of Pediatrics’ recently released Clinical Practice Guideline for the Evaluation and Treatment of Children and Adolescents With Obesity.
Helping create change
According to Sandra Hassink, MD, coauthor of the guideline and vice chair of the Clinical Practice Guideline Subcommittee on Obesity, the goal was to “help patients make changes in lifestyle, behaviors, or environment in a sustainable way and also to involve families in decision-making at every step of the way.”
Ideally, a child would receive intense behavioral and lifestyle treatment, although this approach isn’t always available and might be challenging to deliver. The most effective treatments include at least 26 hours of face-to-face, family-based treatments, consisting of many different components and lasting 3-12 months.
The guideline suggests that doctors offer adolescents 12 and older medication to assist in weight loss, along with health, behavior, and lifestyle treatment, and that teens who have severe obesity should consider metabolic and bariatric surgery as they continue intense health behavior and lifestyle treatment.
“We’re living at a time where we’ve watched obesity affect our children and adult population for 4 decades and, along with the risk of obesity, we’ve watched a rise in obesity; we’re seeing increases in illness that go along with obesity, such as type 2 diabetes, lipid diseases like high cholesterol, and nonalcoholic fatty liver disease,” Dr. Hassink said.
She explained that, as people gain weight, the cells in adipose (fatty) tissues start to malfunction and produce inflammatory chemicals that cause these illnesses.
“So having extra adipose tissue is a risk,” she said. “As pediatricians, we measure body mass index [BMI] – which is calculated based on height and weight – as a way of seeing whether the child could be at risk for developing these dysfunctioning cells. If so, we screen them for prediabetes, lipid disease, or liver disease and other obesity-related comorbidities.”
In addition, “we’re concerned about the mental health of children with obesity because of the weight bias in our culture,” said Dr. Hassink. “A child gets stigmatized, and this takes the form of bullying and teasing, and leads to low self-esteem, depression, and anxiety. So we know we have a host of physical problems we need to look out for, as well as the emotional and psychological effects of how our culture views things.”
Are parents ready for the new approach?
A new report from Harmony Healthcare IT, a data management firm that works with health data, looked at how parents regard their children’s obesity. The company surveyed more than 1,000 parents and found that one-tenth of respondents had children who were overweight or obese and over a quarter (26%) worried about their child’s weight.
Nearly 40% of parents would consider weight loss medication for their child if the child became obese at age 12, and about 16% would consider weight loss surgery. But most parents would not consider this surgery until their child was an average age of 15 rather than the AAP’s recommended age of 13.
Mr. Lunsford said that his son considered surgery and medication but was “never comfortable” with these approaches.
This isn’t unusual, Dr. Hassink said. “Not every parent will think the same way, and their view will be based on their experience and what’s going on with their child.”
The guideline wasn’t designed to encourage every child to try medication or have surgery, she said.
“But parents now know that there are potentially helpful choices here that we didn’t have years ago, and those can be discussed with the child’s pediatrician.”
Challenges to keeping healthy
It’s tough to stay healthy and not develop obesity in our modern environment, Dr. Hassink said.
“There’s a lot of processed food, a lot of sugar in our foods, a lot of sedentary behavior, and a decrease in physical activity. In many communities, it’s hard for people to get healthy foods.”
Mr. Lunsford said that when his son was in his late teens and would go out with friends, they typically went to fast-food restaurants.
“Sam would say ‘yes’ to these foods, although he knew they weren’t good for him, because he wanted to be like everyone else,” he said.
But parents now know that there are potentially helpful choices here that we didn’t have years ago, and those can be discussed with the child’s pediatrician, he said.
Harmony Health IT’s survey found that many parents say it is a struggle to get kids to eat healthy foods and get enough sleep. Although almost all respondents (83%) said they try to prepare healthy, home-cooked meals, 39% eat fast food at least once a week, mostly because parents are too tired to cook.
Dr. Hassink said the COVID-19 pandemic also played a role.
“We knew that COVID would be hard for kids with obesity, and there might be weight gain because of the extra sedentary time and fewer sporting activities, and there was a high cost of food to families who are already economically strapped,” she said.
In general, family support is essential, Dr. Hassink said. “Obesity treatment requires that the family be involved. The family is living in the same nutritional and activity environment as their child. Everyone has to be on board.”
Talking to kids about food and weight
The survey found that many parents struggle to talk about food and weight with their children. The AAP guideline notes that involving a health care professional can help.
“If a parent or caregiver is concerned about a child’s weight, he or she can take the child to their pediatrician,” Dr. Hassink said. “The first thing the pediatrician will do is ask about the child’s overall health, review the family history – because obesity tends to run in families – and see if other conditions, like diabetes, also run in the family.”
The pediatrician will do a physical examination that includes BMI and, if it’s high, other tests looking at blood sugar, lipids, and liver function may be performed.
Ideally, the child will be prescribed intense lifestyle and behavioral treatment that will take the child’s and family’s nutrition into account, as well as physical activity and the amount of sleep the child is getting, which is sometimes tied to weight gain. If the child has disordered eating, such as binge eating disorder, they can be evaluated and treated for that.
Each child is seen as an individual with a particular set of needs. “One size doesn’t fit all,” Dr. Hassink said.
Providing emotional support for children with obesity
Pediatricians can assess the child’s mental, emotional, and social well-being. “Children who are bullied or teased may need help working through that. Children experiencing depression may need treatment,” Dr. Hassink said.
Mr. Lunsford said Samuel was fortunate in that he rarely got taunted.
“Part of the reason is that, although weight was an issue, he never allowed his weight to define him,” he said. “He was always an extroverted kind of kid, athletic, very outgoing and friendly, and being overweight was never part of his identity.”
Mr. Lunsford encourages parents whose children are teased or bullied to create a “no-judgment” zone at home.
“Let your kids know that their parents love them for who they are,” he said. “Emphasize that weight is a ‘number’ and health is a ‘lifestyle.’ Try to highlight the good things in their lives and encourage them to be as active as they can in the things that interest them.”
A version of this article originally appeared on WebMD.com.
Emotional eating isn’t all emotional
“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.
Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.
Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
Fact: Emotional eating isn’t all emotional
It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.
Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.
Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.
These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
Feelings: Patterns, personality, places, psychological factors
Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.
For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.
But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
Places and people
Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.
Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.
Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
Putting it together: Addressing the facts and feelings of emotional eating
1. Treat biological causes that impact physiologic hunger and trigger emotional eating.
2. Triggers: Address patterns, places/people, psychological events.
3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.
4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.
5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:
- Psychologist
- Psychiatrist
- coach and/or certified wellness coaches
- Obesity specialist
Back to Ms. S
Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.
Conclusion
Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.
In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.
As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.
*Name/initial changed for privacy.
Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.
A version of this article first appeared on Medscape.com.
“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.
Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.
Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
Fact: Emotional eating isn’t all emotional
It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.
Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.
Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.
These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
Feelings: Patterns, personality, places, psychological factors
Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.
For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.
But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
Places and people
Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.
Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.
Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
Putting it together: Addressing the facts and feelings of emotional eating
1. Treat biological causes that impact physiologic hunger and trigger emotional eating.
2. Triggers: Address patterns, places/people, psychological events.
3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.
4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.
5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:
- Psychologist
- Psychiatrist
- coach and/or certified wellness coaches
- Obesity specialist
Back to Ms. S
Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.
Conclusion
Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.
In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.
As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.
*Name/initial changed for privacy.
Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.
A version of this article first appeared on Medscape.com.
“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.
Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.
Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
Fact: Emotional eating isn’t all emotional
It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.
Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.
Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.
These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
Feelings: Patterns, personality, places, psychological factors
Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.
For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.
But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
Places and people
Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.
Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.
Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
Putting it together: Addressing the facts and feelings of emotional eating
1. Treat biological causes that impact physiologic hunger and trigger emotional eating.
2. Triggers: Address patterns, places/people, psychological events.
3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.
4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.
5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:
- Psychologist
- Psychiatrist
- coach and/or certified wellness coaches
- Obesity specialist
Back to Ms. S
Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.
Conclusion
Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.
In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.
As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.
*Name/initial changed for privacy.
Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.
A version of this article first appeared on Medscape.com.
How BMI over time impacts GI cancer risk
according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.
The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.
Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.
The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.
These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.
The analysis was published online in JAMA Network Open.
A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.
In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.
BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m2 and obese BMI was 30 or higher.
During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).
Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively).
The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.
“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.
Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.
Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).
The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.
Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.
“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.
This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.
A version of this article originally appeared on Medscape.com.
according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.
The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.
Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.
The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.
These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.
The analysis was published online in JAMA Network Open.
A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.
In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.
BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m2 and obese BMI was 30 or higher.
During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).
Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively).
The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.
“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.
Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.
Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).
The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.
Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.
“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.
This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.
A version of this article originally appeared on Medscape.com.
according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.
The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.
Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.
The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.
These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.
The analysis was published online in JAMA Network Open.
A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.
In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.
BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m2 and obese BMI was 30 or higher.
During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).
Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively).
The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.
“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.
Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.
Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).
The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.
Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.
“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.
This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.
A version of this article originally appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Metabolic abnormalities boost obesity-related cancer risk
, and an even higher risk, two- to threefold higher, for specific cancers, such as endometrial, liver, and renal cell cancers, compared with metabolically healthy normal weight.
Even in people with so-called “metabolically healthy” obesity, the risk for overall obesity-related cancer is increased, compared with normal-weight, metabolically healthy individuals; however, the associations here are weaker than in people with metabolically unhealthy obesity.
“The type of metabolic obesity phenotype is important when assessing obesity-related cancer risk,” lead researcher Ming Sun, PhD, from Lund University, Malmö, Sweden, said in an interview. “In general, metabolic aberrations further increased the obesity-induced cancer risk, suggesting that obesity and metabolic aberrations are useful targets for prevention.”
“This synergy means that when obesity and metabolic unhealth occur together, that’s particularly bad,” added Tanja Stocks, PhD, senior author, also of Lund University.
“But the data also highlight that even obesity and overweight alone comprise an increased risk of cancer,” Dr. Stocks noted.
Dr. Sun said the findings have important public health implications, suggesting that “a significant number of cancer cases could potentially be prevented by targeting the coexistence of metabolic problems and obesity, in particular for obesity-related cancers among men.”
The results will be presented as a poster by Dr. Sun at the European Congress on Obesity 2023, being held in Dublin, and have been published in the Journal of the National Cancer Institute.
Metabolically unhealthy obesity worst for cancer risks
Andrew G. Renehan, PhD, FRCS, professor of cancer studies and surgery, University of Manchester, England, welcomed the new work, saying it addresses the issue with very large study numbers. “[It] nicely demonstrates that there are clear examples where metabolically unhealthy overweight and obese phenotypes have increased cancer risk relative to [metabolically] healthy overweight and obese phenotypes,” he said.
“There is a clear need for clinically based research addressing these hypotheses ... but these studies will additionally need to factor in other dimensions such as the selection of treatment for metabolic aberrations, both medical and surgical, and the consequent metabolic control resulting from these interventions,” Dr. Renehan observed.
Vibhu Chittajallu, MD, a gastroenterologist based at University Hospitals Cleveland Medical Center, said it was beneficial to see another study further validating the association of obesity with the development of obesity-associated cancers.
“This is an interesting study [because it focuses] on the role of metabolic syndrome in obesity and how it affects the risk of development of obesity-associated cancers,” he said in an interview.
“I believe that the results of this study further strengthen the need for improved management of obesity and metabolic syndrome to reduce the risk of obesity-associated cancer formation that plays a role in preventable and premature deaths in adult patients with obesity.”
Synergy between metabolic aberrations and obesity, and cancer risk
Dr. Sun and colleagues note that obesity is an established risk factor for several cancers. It is often accompanied by metabolic aberrations, which have been a commonly proposed mechanism to link obesity with cancer. During the last decade, obesity with or without metabolic aberrations – commonly termed “metabolically unhealthy” or “healthy obesity” – has been extensively investigated in the cardiovascular field; however, studies regarding cancer are limited.
According to Dr. Sun, this new study is the first to look at the synergistic effect of unhealthy metabolism and body mass index – the latter was further categorized as normal weight (BMI < 25 kg/m2), overweight (BMI < 30) and obesity (BMI ≤ 30) – and the association with cancer risk, both overall and in relation to site-specific cancers.
Data were drawn from 797,193 European individuals (in Norway, Sweden, and Austria), of whom 23,630 developed an obesity-related cancer during the follow-up period. A metabolic score comprising mid-blood pressure, plasma glucose, and triglycerides was used to provide a measure of healthy or unhealthy metabolic status. Relative risks (hazard ratios) for overall and site-specific cancers were determined. Comparisons were made with metabolically healthy people of normal weight (effectively controls).
When different metabolic scores and BMIs were combined, participants fell into six categories: metabolically unhealthy obesity (6.8% of participants); metabolically healthy obesity (3.4%), metabolically unhealthy overweight (15.4%), metabolically healthy overweight (19.8%), metabolically unhealthy normal weight (12.5%), and metabolically healthy normal weight (42.0%).
Metabolically unhealthy women with obesity had a hazard ratio of 1.43 for overall obesity-related cancers, compared with metabolically healthy women of normal weight. Of particular note were risks of two cancer types in women with metabolically unhealthy obesity: renal cancer, with an HR of 2.43, and endometrial cancer, with an HR of 3.0, compared with controls.
Even in metabolically healthy women with obesity, compared with metabolically healthy women of normal weight, there was an increased risk of endometrial cancer, with an HR of 2.36.
“If you look at individual cancers, in particular endometrial cancer, this seems to be very much driven by obesity and not so much by the metabolic factor,” remarked Dr. Stocks.
In males, compared with metabolically healthy men of normal weight, metabolically unhealthy men with obesity had an overall obesity-related cancer risk HR of 1.91. Specifically, the risk of renal cell cancer was more than doubled, with an HR of 2.59. The HR for colon cancer was 1.85, and that for rectal cancer and pancreatic cancer was similar, both having HRs of 1.32.
Again, risk was lower in metabolically healthy men with obesity, although still higher than for metabolically healthy normal-weight men.
A version of this article first appeared on Medscape.com.
, and an even higher risk, two- to threefold higher, for specific cancers, such as endometrial, liver, and renal cell cancers, compared with metabolically healthy normal weight.
Even in people with so-called “metabolically healthy” obesity, the risk for overall obesity-related cancer is increased, compared with normal-weight, metabolically healthy individuals; however, the associations here are weaker than in people with metabolically unhealthy obesity.
“The type of metabolic obesity phenotype is important when assessing obesity-related cancer risk,” lead researcher Ming Sun, PhD, from Lund University, Malmö, Sweden, said in an interview. “In general, metabolic aberrations further increased the obesity-induced cancer risk, suggesting that obesity and metabolic aberrations are useful targets for prevention.”
“This synergy means that when obesity and metabolic unhealth occur together, that’s particularly bad,” added Tanja Stocks, PhD, senior author, also of Lund University.
“But the data also highlight that even obesity and overweight alone comprise an increased risk of cancer,” Dr. Stocks noted.
Dr. Sun said the findings have important public health implications, suggesting that “a significant number of cancer cases could potentially be prevented by targeting the coexistence of metabolic problems and obesity, in particular for obesity-related cancers among men.”
The results will be presented as a poster by Dr. Sun at the European Congress on Obesity 2023, being held in Dublin, and have been published in the Journal of the National Cancer Institute.
Metabolically unhealthy obesity worst for cancer risks
Andrew G. Renehan, PhD, FRCS, professor of cancer studies and surgery, University of Manchester, England, welcomed the new work, saying it addresses the issue with very large study numbers. “[It] nicely demonstrates that there are clear examples where metabolically unhealthy overweight and obese phenotypes have increased cancer risk relative to [metabolically] healthy overweight and obese phenotypes,” he said.
“There is a clear need for clinically based research addressing these hypotheses ... but these studies will additionally need to factor in other dimensions such as the selection of treatment for metabolic aberrations, both medical and surgical, and the consequent metabolic control resulting from these interventions,” Dr. Renehan observed.
Vibhu Chittajallu, MD, a gastroenterologist based at University Hospitals Cleveland Medical Center, said it was beneficial to see another study further validating the association of obesity with the development of obesity-associated cancers.
“This is an interesting study [because it focuses] on the role of metabolic syndrome in obesity and how it affects the risk of development of obesity-associated cancers,” he said in an interview.
“I believe that the results of this study further strengthen the need for improved management of obesity and metabolic syndrome to reduce the risk of obesity-associated cancer formation that plays a role in preventable and premature deaths in adult patients with obesity.”
Synergy between metabolic aberrations and obesity, and cancer risk
Dr. Sun and colleagues note that obesity is an established risk factor for several cancers. It is often accompanied by metabolic aberrations, which have been a commonly proposed mechanism to link obesity with cancer. During the last decade, obesity with or without metabolic aberrations – commonly termed “metabolically unhealthy” or “healthy obesity” – has been extensively investigated in the cardiovascular field; however, studies regarding cancer are limited.
According to Dr. Sun, this new study is the first to look at the synergistic effect of unhealthy metabolism and body mass index – the latter was further categorized as normal weight (BMI < 25 kg/m2), overweight (BMI < 30) and obesity (BMI ≤ 30) – and the association with cancer risk, both overall and in relation to site-specific cancers.
Data were drawn from 797,193 European individuals (in Norway, Sweden, and Austria), of whom 23,630 developed an obesity-related cancer during the follow-up period. A metabolic score comprising mid-blood pressure, plasma glucose, and triglycerides was used to provide a measure of healthy or unhealthy metabolic status. Relative risks (hazard ratios) for overall and site-specific cancers were determined. Comparisons were made with metabolically healthy people of normal weight (effectively controls).
When different metabolic scores and BMIs were combined, participants fell into six categories: metabolically unhealthy obesity (6.8% of participants); metabolically healthy obesity (3.4%), metabolically unhealthy overweight (15.4%), metabolically healthy overweight (19.8%), metabolically unhealthy normal weight (12.5%), and metabolically healthy normal weight (42.0%).
Metabolically unhealthy women with obesity had a hazard ratio of 1.43 for overall obesity-related cancers, compared with metabolically healthy women of normal weight. Of particular note were risks of two cancer types in women with metabolically unhealthy obesity: renal cancer, with an HR of 2.43, and endometrial cancer, with an HR of 3.0, compared with controls.
Even in metabolically healthy women with obesity, compared with metabolically healthy women of normal weight, there was an increased risk of endometrial cancer, with an HR of 2.36.
“If you look at individual cancers, in particular endometrial cancer, this seems to be very much driven by obesity and not so much by the metabolic factor,” remarked Dr. Stocks.
In males, compared with metabolically healthy men of normal weight, metabolically unhealthy men with obesity had an overall obesity-related cancer risk HR of 1.91. Specifically, the risk of renal cell cancer was more than doubled, with an HR of 2.59. The HR for colon cancer was 1.85, and that for rectal cancer and pancreatic cancer was similar, both having HRs of 1.32.
Again, risk was lower in metabolically healthy men with obesity, although still higher than for metabolically healthy normal-weight men.
A version of this article first appeared on Medscape.com.
, and an even higher risk, two- to threefold higher, for specific cancers, such as endometrial, liver, and renal cell cancers, compared with metabolically healthy normal weight.
Even in people with so-called “metabolically healthy” obesity, the risk for overall obesity-related cancer is increased, compared with normal-weight, metabolically healthy individuals; however, the associations here are weaker than in people with metabolically unhealthy obesity.
“The type of metabolic obesity phenotype is important when assessing obesity-related cancer risk,” lead researcher Ming Sun, PhD, from Lund University, Malmö, Sweden, said in an interview. “In general, metabolic aberrations further increased the obesity-induced cancer risk, suggesting that obesity and metabolic aberrations are useful targets for prevention.”
“This synergy means that when obesity and metabolic unhealth occur together, that’s particularly bad,” added Tanja Stocks, PhD, senior author, also of Lund University.
“But the data also highlight that even obesity and overweight alone comprise an increased risk of cancer,” Dr. Stocks noted.
Dr. Sun said the findings have important public health implications, suggesting that “a significant number of cancer cases could potentially be prevented by targeting the coexistence of metabolic problems and obesity, in particular for obesity-related cancers among men.”
The results will be presented as a poster by Dr. Sun at the European Congress on Obesity 2023, being held in Dublin, and have been published in the Journal of the National Cancer Institute.
Metabolically unhealthy obesity worst for cancer risks
Andrew G. Renehan, PhD, FRCS, professor of cancer studies and surgery, University of Manchester, England, welcomed the new work, saying it addresses the issue with very large study numbers. “[It] nicely demonstrates that there are clear examples where metabolically unhealthy overweight and obese phenotypes have increased cancer risk relative to [metabolically] healthy overweight and obese phenotypes,” he said.
“There is a clear need for clinically based research addressing these hypotheses ... but these studies will additionally need to factor in other dimensions such as the selection of treatment for metabolic aberrations, both medical and surgical, and the consequent metabolic control resulting from these interventions,” Dr. Renehan observed.
Vibhu Chittajallu, MD, a gastroenterologist based at University Hospitals Cleveland Medical Center, said it was beneficial to see another study further validating the association of obesity with the development of obesity-associated cancers.
“This is an interesting study [because it focuses] on the role of metabolic syndrome in obesity and how it affects the risk of development of obesity-associated cancers,” he said in an interview.
“I believe that the results of this study further strengthen the need for improved management of obesity and metabolic syndrome to reduce the risk of obesity-associated cancer formation that plays a role in preventable and premature deaths in adult patients with obesity.”
Synergy between metabolic aberrations and obesity, and cancer risk
Dr. Sun and colleagues note that obesity is an established risk factor for several cancers. It is often accompanied by metabolic aberrations, which have been a commonly proposed mechanism to link obesity with cancer. During the last decade, obesity with or without metabolic aberrations – commonly termed “metabolically unhealthy” or “healthy obesity” – has been extensively investigated in the cardiovascular field; however, studies regarding cancer are limited.
According to Dr. Sun, this new study is the first to look at the synergistic effect of unhealthy metabolism and body mass index – the latter was further categorized as normal weight (BMI < 25 kg/m2), overweight (BMI < 30) and obesity (BMI ≤ 30) – and the association with cancer risk, both overall and in relation to site-specific cancers.
Data were drawn from 797,193 European individuals (in Norway, Sweden, and Austria), of whom 23,630 developed an obesity-related cancer during the follow-up period. A metabolic score comprising mid-blood pressure, plasma glucose, and triglycerides was used to provide a measure of healthy or unhealthy metabolic status. Relative risks (hazard ratios) for overall and site-specific cancers were determined. Comparisons were made with metabolically healthy people of normal weight (effectively controls).
When different metabolic scores and BMIs were combined, participants fell into six categories: metabolically unhealthy obesity (6.8% of participants); metabolically healthy obesity (3.4%), metabolically unhealthy overweight (15.4%), metabolically healthy overweight (19.8%), metabolically unhealthy normal weight (12.5%), and metabolically healthy normal weight (42.0%).
Metabolically unhealthy women with obesity had a hazard ratio of 1.43 for overall obesity-related cancers, compared with metabolically healthy women of normal weight. Of particular note were risks of two cancer types in women with metabolically unhealthy obesity: renal cancer, with an HR of 2.43, and endometrial cancer, with an HR of 3.0, compared with controls.
Even in metabolically healthy women with obesity, compared with metabolically healthy women of normal weight, there was an increased risk of endometrial cancer, with an HR of 2.36.
“If you look at individual cancers, in particular endometrial cancer, this seems to be very much driven by obesity and not so much by the metabolic factor,” remarked Dr. Stocks.
In males, compared with metabolically healthy men of normal weight, metabolically unhealthy men with obesity had an overall obesity-related cancer risk HR of 1.91. Specifically, the risk of renal cell cancer was more than doubled, with an HR of 2.59. The HR for colon cancer was 1.85, and that for rectal cancer and pancreatic cancer was similar, both having HRs of 1.32.
Again, risk was lower in metabolically healthy men with obesity, although still higher than for metabolically healthy normal-weight men.
A version of this article first appeared on Medscape.com.
FROM ECO 2023
Risk for breast cancer reduced after bariatric surgery
In a matched cohort study of more than 69,000 Canadian women, risk for incident breast cancer at 1 year was 40% higher among women who had not undergone bariatric surgery, compared with those who had. The risk remained elevated through 5 years of follow-up.
The findings were “definitely a bit surprising,” study author Aristithes G. Doumouras, MD, MPH, assistant professor of surgery at McMaster University, Hamilton, Ont., said in an interview. “The patients that underwent bariatric surgery had better cancer outcomes than patients who weighed less than they did, so it showed that there was more at play than just weight loss. This effect was durable [and] shows how powerful the surgery is, [as well as] the fact that we haven’t even explored all of its effects.”
The study was published online in JAMA Surgery.
Protective association
To determine whether there is a residual risk for breast cancer following bariatric surgery for obesity, the investigators analyzed clinical and administrative data collected between 2010 and 2016 in Ontario. They retrospectively matched women with obesity who underwent bariatric surgery with women without a history of bariatric surgery. Participants were matched by age and breast cancer screening status. Covariates included diabetes status, neighborhood income quintile, and measures of health care use. The population included 69,260 women (mean age, 45 years).
Among participants who underwent bariatric surgery for obesity, baseline body mass index was greater than 35 for those with related comorbid conditions, and BMI was greater than 40 for those without comorbid conditions. The investigators categorized nonsurgical control patients in accordance with the following four BMI categories: less than 25, 25-29, 30-34, and greater than or equal to 35. Each control group, as well as the surgical group, included 13,852 women.
Participants in the surgical group were followed for 5 years after bariatric surgery. Those in the nonsurgical group were followed for 5 years after the index date (that is, the date of BMI measurement).
In the overall population, 659 cases of breast cancer were diagnosed in the overall population (0.95%) during the study period. This total included 103 (0.74%) cancers in the surgical cohort; 128 (0.92%) in the group with BMI less than 25; 143 (1.03%) among those with BMI 25-29; 150 (1.08%) in the group with BMI 30-34; and 135 (0.97%) among those with BMI greater than or equal to 35.
Most cancers were stage I. There were 65 cases among those with BMI less than 25; 76 for those with BMI of 25-29; 65 for BMI of 30-34; 67 for BMI greater than or equal to 35, and 60 for the surgery group.
Most tumors were of medium grade and were estrogen receptor positive, progesterone receptor positive, and ERBB2 negative. No significant differences were observed across the groups for stage, grade, or hormone status.
There was an increased hazard for incident breast cancer in the nonsurgical group, compared with the postsurgical group after washout periods of 1 year (hazard ratio, 1.40), 2 years (HR, 1.31), and 5 years (HR, 1.38).
In a comparison of the postsurgical cohort with the nonsurgical cohort with BMI less than 25, the hazard of incident breast cancer was not significantly different for any of the washout periods, but there was a reduced hazard for incident breast cancer among postsurgical patients than among nonsurgical patients in all high BMI categories (BMI ≥ 25).
“Taken together, these results demonstrate that the protective association between substantial weight loss via bariatric surgery and breast cancer risk is sustained after 5 years following surgery and that it is associated with a baseline risk similar to that of women with BMI less than 25,” the investigators write.
Nevertheless, Dr. Doumouras said “the interaction between the surgery and individuals is poorly studied, and this level of personalized medicine is simply not there yet. We are working on developing a prospective cohort that has genetic, protein, and microbiome [data] to help answer these questions.”
There are not enough women in subpopulations such as BRCA carriers to study at this point, he added. “This is where more patients and time will really help the research process.”
A universal benefit?
“Although these findings are important overall for the general population at risk for breast cancer, we raise an important caveat: The benefit of surgical weight loss may not be universal,” write Justin B. Dimick, MD, MPH, surgical innovation editor for JAMA Surgery, and Melissa L. Pilewskie, MD, both of the University of Michigan, Ann Arbor, in an accompanying commentary.
“In addition to lifestyle factors, several nonmodifiable risk factors, such as a genetic predisposition, strong family history, personal history of a high-risk breast lesion, or history of chest wall radiation, impart significant elevation in risk, and the data remain mixed on the impact of weight loss for individuals in these high-risk cohorts,” they add.
“Further study to elucidate the underlying mechanism associated with obesity, weight loss, and breast cancer risk should help guide strategies for risk reduction that are specific to unique high-risk cohorts, because modifiable risk factors may not portend the same benefit among all groups.”
Commenting on the findings, Stephen Edge, MD, breast surgeon and vice president for system quality and outcomes at Roswell Park Comprehensive Cancer Center, Buffalo, N.Y., said, “The importance of this study is that it shows that weight loss in midlife can reduce breast cancer risk back to or even below the risk of similar people who were not obese. This has major implications for counseling women.”
The investigators did not have information on the extent of weight loss with surgery or on which participants maintained the lower weight, Dr. Edge noted; “However, overall, most people who have weight reduction surgery have major weight loss.”
At this point, he said, “we can now tell women with obesity that in addition to the many other advantages of weight loss, their risk of getting breast cancer will also be reduced.”
The study was supported by the Ontario Bariatric Registry and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ontario Ministry of Long-Term Care. Dr. Doumouras, Dr. Dimick, Dr. Pilewskie, and Dr. Edge reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
In a matched cohort study of more than 69,000 Canadian women, risk for incident breast cancer at 1 year was 40% higher among women who had not undergone bariatric surgery, compared with those who had. The risk remained elevated through 5 years of follow-up.
The findings were “definitely a bit surprising,” study author Aristithes G. Doumouras, MD, MPH, assistant professor of surgery at McMaster University, Hamilton, Ont., said in an interview. “The patients that underwent bariatric surgery had better cancer outcomes than patients who weighed less than they did, so it showed that there was more at play than just weight loss. This effect was durable [and] shows how powerful the surgery is, [as well as] the fact that we haven’t even explored all of its effects.”
The study was published online in JAMA Surgery.
Protective association
To determine whether there is a residual risk for breast cancer following bariatric surgery for obesity, the investigators analyzed clinical and administrative data collected between 2010 and 2016 in Ontario. They retrospectively matched women with obesity who underwent bariatric surgery with women without a history of bariatric surgery. Participants were matched by age and breast cancer screening status. Covariates included diabetes status, neighborhood income quintile, and measures of health care use. The population included 69,260 women (mean age, 45 years).
Among participants who underwent bariatric surgery for obesity, baseline body mass index was greater than 35 for those with related comorbid conditions, and BMI was greater than 40 for those without comorbid conditions. The investigators categorized nonsurgical control patients in accordance with the following four BMI categories: less than 25, 25-29, 30-34, and greater than or equal to 35. Each control group, as well as the surgical group, included 13,852 women.
Participants in the surgical group were followed for 5 years after bariatric surgery. Those in the nonsurgical group were followed for 5 years after the index date (that is, the date of BMI measurement).
In the overall population, 659 cases of breast cancer were diagnosed in the overall population (0.95%) during the study period. This total included 103 (0.74%) cancers in the surgical cohort; 128 (0.92%) in the group with BMI less than 25; 143 (1.03%) among those with BMI 25-29; 150 (1.08%) in the group with BMI 30-34; and 135 (0.97%) among those with BMI greater than or equal to 35.
Most cancers were stage I. There were 65 cases among those with BMI less than 25; 76 for those with BMI of 25-29; 65 for BMI of 30-34; 67 for BMI greater than or equal to 35, and 60 for the surgery group.
Most tumors were of medium grade and were estrogen receptor positive, progesterone receptor positive, and ERBB2 negative. No significant differences were observed across the groups for stage, grade, or hormone status.
There was an increased hazard for incident breast cancer in the nonsurgical group, compared with the postsurgical group after washout periods of 1 year (hazard ratio, 1.40), 2 years (HR, 1.31), and 5 years (HR, 1.38).
In a comparison of the postsurgical cohort with the nonsurgical cohort with BMI less than 25, the hazard of incident breast cancer was not significantly different for any of the washout periods, but there was a reduced hazard for incident breast cancer among postsurgical patients than among nonsurgical patients in all high BMI categories (BMI ≥ 25).
“Taken together, these results demonstrate that the protective association between substantial weight loss via bariatric surgery and breast cancer risk is sustained after 5 years following surgery and that it is associated with a baseline risk similar to that of women with BMI less than 25,” the investigators write.
Nevertheless, Dr. Doumouras said “the interaction between the surgery and individuals is poorly studied, and this level of personalized medicine is simply not there yet. We are working on developing a prospective cohort that has genetic, protein, and microbiome [data] to help answer these questions.”
There are not enough women in subpopulations such as BRCA carriers to study at this point, he added. “This is where more patients and time will really help the research process.”
A universal benefit?
“Although these findings are important overall for the general population at risk for breast cancer, we raise an important caveat: The benefit of surgical weight loss may not be universal,” write Justin B. Dimick, MD, MPH, surgical innovation editor for JAMA Surgery, and Melissa L. Pilewskie, MD, both of the University of Michigan, Ann Arbor, in an accompanying commentary.
“In addition to lifestyle factors, several nonmodifiable risk factors, such as a genetic predisposition, strong family history, personal history of a high-risk breast lesion, or history of chest wall radiation, impart significant elevation in risk, and the data remain mixed on the impact of weight loss for individuals in these high-risk cohorts,” they add.
“Further study to elucidate the underlying mechanism associated with obesity, weight loss, and breast cancer risk should help guide strategies for risk reduction that are specific to unique high-risk cohorts, because modifiable risk factors may not portend the same benefit among all groups.”
Commenting on the findings, Stephen Edge, MD, breast surgeon and vice president for system quality and outcomes at Roswell Park Comprehensive Cancer Center, Buffalo, N.Y., said, “The importance of this study is that it shows that weight loss in midlife can reduce breast cancer risk back to or even below the risk of similar people who were not obese. This has major implications for counseling women.”
The investigators did not have information on the extent of weight loss with surgery or on which participants maintained the lower weight, Dr. Edge noted; “However, overall, most people who have weight reduction surgery have major weight loss.”
At this point, he said, “we can now tell women with obesity that in addition to the many other advantages of weight loss, their risk of getting breast cancer will also be reduced.”
The study was supported by the Ontario Bariatric Registry and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ontario Ministry of Long-Term Care. Dr. Doumouras, Dr. Dimick, Dr. Pilewskie, and Dr. Edge reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
In a matched cohort study of more than 69,000 Canadian women, risk for incident breast cancer at 1 year was 40% higher among women who had not undergone bariatric surgery, compared with those who had. The risk remained elevated through 5 years of follow-up.
The findings were “definitely a bit surprising,” study author Aristithes G. Doumouras, MD, MPH, assistant professor of surgery at McMaster University, Hamilton, Ont., said in an interview. “The patients that underwent bariatric surgery had better cancer outcomes than patients who weighed less than they did, so it showed that there was more at play than just weight loss. This effect was durable [and] shows how powerful the surgery is, [as well as] the fact that we haven’t even explored all of its effects.”
The study was published online in JAMA Surgery.
Protective association
To determine whether there is a residual risk for breast cancer following bariatric surgery for obesity, the investigators analyzed clinical and administrative data collected between 2010 and 2016 in Ontario. They retrospectively matched women with obesity who underwent bariatric surgery with women without a history of bariatric surgery. Participants were matched by age and breast cancer screening status. Covariates included diabetes status, neighborhood income quintile, and measures of health care use. The population included 69,260 women (mean age, 45 years).
Among participants who underwent bariatric surgery for obesity, baseline body mass index was greater than 35 for those with related comorbid conditions, and BMI was greater than 40 for those without comorbid conditions. The investigators categorized nonsurgical control patients in accordance with the following four BMI categories: less than 25, 25-29, 30-34, and greater than or equal to 35. Each control group, as well as the surgical group, included 13,852 women.
Participants in the surgical group were followed for 5 years after bariatric surgery. Those in the nonsurgical group were followed for 5 years after the index date (that is, the date of BMI measurement).
In the overall population, 659 cases of breast cancer were diagnosed in the overall population (0.95%) during the study period. This total included 103 (0.74%) cancers in the surgical cohort; 128 (0.92%) in the group with BMI less than 25; 143 (1.03%) among those with BMI 25-29; 150 (1.08%) in the group with BMI 30-34; and 135 (0.97%) among those with BMI greater than or equal to 35.
Most cancers were stage I. There were 65 cases among those with BMI less than 25; 76 for those with BMI of 25-29; 65 for BMI of 30-34; 67 for BMI greater than or equal to 35, and 60 for the surgery group.
Most tumors were of medium grade and were estrogen receptor positive, progesterone receptor positive, and ERBB2 negative. No significant differences were observed across the groups for stage, grade, or hormone status.
There was an increased hazard for incident breast cancer in the nonsurgical group, compared with the postsurgical group after washout periods of 1 year (hazard ratio, 1.40), 2 years (HR, 1.31), and 5 years (HR, 1.38).
In a comparison of the postsurgical cohort with the nonsurgical cohort with BMI less than 25, the hazard of incident breast cancer was not significantly different for any of the washout periods, but there was a reduced hazard for incident breast cancer among postsurgical patients than among nonsurgical patients in all high BMI categories (BMI ≥ 25).
“Taken together, these results demonstrate that the protective association between substantial weight loss via bariatric surgery and breast cancer risk is sustained after 5 years following surgery and that it is associated with a baseline risk similar to that of women with BMI less than 25,” the investigators write.
Nevertheless, Dr. Doumouras said “the interaction between the surgery and individuals is poorly studied, and this level of personalized medicine is simply not there yet. We are working on developing a prospective cohort that has genetic, protein, and microbiome [data] to help answer these questions.”
There are not enough women in subpopulations such as BRCA carriers to study at this point, he added. “This is where more patients and time will really help the research process.”
A universal benefit?
“Although these findings are important overall for the general population at risk for breast cancer, we raise an important caveat: The benefit of surgical weight loss may not be universal,” write Justin B. Dimick, MD, MPH, surgical innovation editor for JAMA Surgery, and Melissa L. Pilewskie, MD, both of the University of Michigan, Ann Arbor, in an accompanying commentary.
“In addition to lifestyle factors, several nonmodifiable risk factors, such as a genetic predisposition, strong family history, personal history of a high-risk breast lesion, or history of chest wall radiation, impart significant elevation in risk, and the data remain mixed on the impact of weight loss for individuals in these high-risk cohorts,” they add.
“Further study to elucidate the underlying mechanism associated with obesity, weight loss, and breast cancer risk should help guide strategies for risk reduction that are specific to unique high-risk cohorts, because modifiable risk factors may not portend the same benefit among all groups.”
Commenting on the findings, Stephen Edge, MD, breast surgeon and vice president for system quality and outcomes at Roswell Park Comprehensive Cancer Center, Buffalo, N.Y., said, “The importance of this study is that it shows that weight loss in midlife can reduce breast cancer risk back to or even below the risk of similar people who were not obese. This has major implications for counseling women.”
The investigators did not have information on the extent of weight loss with surgery or on which participants maintained the lower weight, Dr. Edge noted; “However, overall, most people who have weight reduction surgery have major weight loss.”
At this point, he said, “we can now tell women with obesity that in addition to the many other advantages of weight loss, their risk of getting breast cancer will also be reduced.”
The study was supported by the Ontario Bariatric Registry and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ontario Ministry of Long-Term Care. Dr. Doumouras, Dr. Dimick, Dr. Pilewskie, and Dr. Edge reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA SURGERY
BMI has greater impact on survival in younger breast cancer patients
new data suggest.
Obesity is a well-known risk factor for breast cancer in postmenopausal women and has been associated with adverse prognosis, said Senna W.M. Lammers, MD, of Maastricht (the Netherlands) University during a presentation at the European Society for Medical Oncology (ESMO) Breast Cancer annual congress. In addition, some studies suggest that patients with higher body mass index (BMI) experience reduced benefits from endocrine therapy, she said.
Dr. Lammers and colleagues conducted a study to determine the prognostic and predictive effect of BMI on disease-free survival in postmenopausal women with hormone receptor–positive (HR+) breast cancer who were treated with extended endocrine therapy.
The study population included participants in the randomized, phase III DATA trial, which evaluated the use of 6 years vs. 3 years of anastrozole in postmenopausal women with HR+ breast cancer who were disease-free after 2-3 years of adjuvant tamoxifen therapy.
Patients were categorized based on BMI as having normal weight (18.5-24.9 kg/m2), overweight (25-29.9 kg/m2), or obese (30 kg/m2 or higher). The primary outcome was disease-free survival (DFS); the median follow-up period was 13.1 years.
DFS for patients with normal weight, overweight, and obesity was 66.2%, 59.5%, and 52.4%, with a P value of less than .001 for the trend, Dr. Lammers said. “These results were confirmed in multivariable analysis,” she said. Overall, patients with overweight and obesity had a worse DFS when compared with patients with normal weight (hazard ratio, 1.16; P = .10, for patients with overweight and HR, 1.26; P = .03 for patients with obesity).
“Next, we aimed to determine whether the prognostic effect of BMI differed by age,” Dr. Lammers said.
In women younger than 60 years, overweight and obesity were significantly associated with worse DFS (HR, 1.29; P = .05 and HR 1.83, P less than .001, respectively). However, this effect was not observed in women aged 60 years and older.
The researchers also examined the treatment effect of extended anastrozole on adapted DFS by weight, and found no significant differences among patients with normal weight, overweight, and obesity (HR, 1.00; HR, 0.74; and HR, 0.97, respectively), said Dr. Lammers.
In the question and answer session, Dr. Lammers was asked about possible explanations for the difference in DFS by age. Potential explanations include possible survival bias “as only the healthier [patients with obesity] survive to old age,” she said. Other potential explanations are biological, such as the potentially higher levels of bone density in older [patients with obesity], she said.
When asked about additional clinical implications, Dr. Lammers emphasized the importance of maintaining a healthy BMI for breast cancer patients of all ages. Other research areas might involve the use of lifestyle interventions, although these are challenging to implement, she noted.
Data draw attention to quality of life and lifestyle factors
The need to “look at drug development with new eyes” is particularly important when reviewing patient-reported outcomes, said Otto Metzger, MD, of the Dana Farber Cancer Institute, Boston, who served as the discussant for the session.
Dr. Metzger brought up the association between age and the effect of BMI on DFS, specifically.
Based on data from multiple studies and meta-analyses, “I do believe that obesity does play a role in prognosis,” he said, but the question is how long will researchers continue to simply record data without acting to add lifestyle interventions while also trying to develop new drugs, he said. Although convincing patients to make lifestyle changes remains a challenge, patients are often more motivated to make such changes after a cancer diagnosis, Dr. Metzger noted.
“I am a firm believer in the use of digital therapeutics in the context of clinical trials,” said Dr. Metzger. Digital technology offers great potential to educate patients on [adverse effects] and also to improve treatment adherence and quality of life, he concluded.
The study was supported by AstraZeneca, and Dr. Lammers disclosed financial relationships with AstraZeneca and Eli Lilly. Dr. Metzger disclosed receiving research funding to his institution from Pfizer, Genentech/Roche, and Sanofi, and serving as an adviser/consultant to AstraZeneca, Merck, Oncoclinicas, Resilience, and Roche.
new data suggest.
Obesity is a well-known risk factor for breast cancer in postmenopausal women and has been associated with adverse prognosis, said Senna W.M. Lammers, MD, of Maastricht (the Netherlands) University during a presentation at the European Society for Medical Oncology (ESMO) Breast Cancer annual congress. In addition, some studies suggest that patients with higher body mass index (BMI) experience reduced benefits from endocrine therapy, she said.
Dr. Lammers and colleagues conducted a study to determine the prognostic and predictive effect of BMI on disease-free survival in postmenopausal women with hormone receptor–positive (HR+) breast cancer who were treated with extended endocrine therapy.
The study population included participants in the randomized, phase III DATA trial, which evaluated the use of 6 years vs. 3 years of anastrozole in postmenopausal women with HR+ breast cancer who were disease-free after 2-3 years of adjuvant tamoxifen therapy.
Patients were categorized based on BMI as having normal weight (18.5-24.9 kg/m2), overweight (25-29.9 kg/m2), or obese (30 kg/m2 or higher). The primary outcome was disease-free survival (DFS); the median follow-up period was 13.1 years.
DFS for patients with normal weight, overweight, and obesity was 66.2%, 59.5%, and 52.4%, with a P value of less than .001 for the trend, Dr. Lammers said. “These results were confirmed in multivariable analysis,” she said. Overall, patients with overweight and obesity had a worse DFS when compared with patients with normal weight (hazard ratio, 1.16; P = .10, for patients with overweight and HR, 1.26; P = .03 for patients with obesity).
“Next, we aimed to determine whether the prognostic effect of BMI differed by age,” Dr. Lammers said.
In women younger than 60 years, overweight and obesity were significantly associated with worse DFS (HR, 1.29; P = .05 and HR 1.83, P less than .001, respectively). However, this effect was not observed in women aged 60 years and older.
The researchers also examined the treatment effect of extended anastrozole on adapted DFS by weight, and found no significant differences among patients with normal weight, overweight, and obesity (HR, 1.00; HR, 0.74; and HR, 0.97, respectively), said Dr. Lammers.
In the question and answer session, Dr. Lammers was asked about possible explanations for the difference in DFS by age. Potential explanations include possible survival bias “as only the healthier [patients with obesity] survive to old age,” she said. Other potential explanations are biological, such as the potentially higher levels of bone density in older [patients with obesity], she said.
When asked about additional clinical implications, Dr. Lammers emphasized the importance of maintaining a healthy BMI for breast cancer patients of all ages. Other research areas might involve the use of lifestyle interventions, although these are challenging to implement, she noted.
Data draw attention to quality of life and lifestyle factors
The need to “look at drug development with new eyes” is particularly important when reviewing patient-reported outcomes, said Otto Metzger, MD, of the Dana Farber Cancer Institute, Boston, who served as the discussant for the session.
Dr. Metzger brought up the association between age and the effect of BMI on DFS, specifically.
Based on data from multiple studies and meta-analyses, “I do believe that obesity does play a role in prognosis,” he said, but the question is how long will researchers continue to simply record data without acting to add lifestyle interventions while also trying to develop new drugs, he said. Although convincing patients to make lifestyle changes remains a challenge, patients are often more motivated to make such changes after a cancer diagnosis, Dr. Metzger noted.
“I am a firm believer in the use of digital therapeutics in the context of clinical trials,” said Dr. Metzger. Digital technology offers great potential to educate patients on [adverse effects] and also to improve treatment adherence and quality of life, he concluded.
The study was supported by AstraZeneca, and Dr. Lammers disclosed financial relationships with AstraZeneca and Eli Lilly. Dr. Metzger disclosed receiving research funding to his institution from Pfizer, Genentech/Roche, and Sanofi, and serving as an adviser/consultant to AstraZeneca, Merck, Oncoclinicas, Resilience, and Roche.
new data suggest.
Obesity is a well-known risk factor for breast cancer in postmenopausal women and has been associated with adverse prognosis, said Senna W.M. Lammers, MD, of Maastricht (the Netherlands) University during a presentation at the European Society for Medical Oncology (ESMO) Breast Cancer annual congress. In addition, some studies suggest that patients with higher body mass index (BMI) experience reduced benefits from endocrine therapy, she said.
Dr. Lammers and colleagues conducted a study to determine the prognostic and predictive effect of BMI on disease-free survival in postmenopausal women with hormone receptor–positive (HR+) breast cancer who were treated with extended endocrine therapy.
The study population included participants in the randomized, phase III DATA trial, which evaluated the use of 6 years vs. 3 years of anastrozole in postmenopausal women with HR+ breast cancer who were disease-free after 2-3 years of adjuvant tamoxifen therapy.
Patients were categorized based on BMI as having normal weight (18.5-24.9 kg/m2), overweight (25-29.9 kg/m2), or obese (30 kg/m2 or higher). The primary outcome was disease-free survival (DFS); the median follow-up period was 13.1 years.
DFS for patients with normal weight, overweight, and obesity was 66.2%, 59.5%, and 52.4%, with a P value of less than .001 for the trend, Dr. Lammers said. “These results were confirmed in multivariable analysis,” she said. Overall, patients with overweight and obesity had a worse DFS when compared with patients with normal weight (hazard ratio, 1.16; P = .10, for patients with overweight and HR, 1.26; P = .03 for patients with obesity).
“Next, we aimed to determine whether the prognostic effect of BMI differed by age,” Dr. Lammers said.
In women younger than 60 years, overweight and obesity were significantly associated with worse DFS (HR, 1.29; P = .05 and HR 1.83, P less than .001, respectively). However, this effect was not observed in women aged 60 years and older.
The researchers also examined the treatment effect of extended anastrozole on adapted DFS by weight, and found no significant differences among patients with normal weight, overweight, and obesity (HR, 1.00; HR, 0.74; and HR, 0.97, respectively), said Dr. Lammers.
In the question and answer session, Dr. Lammers was asked about possible explanations for the difference in DFS by age. Potential explanations include possible survival bias “as only the healthier [patients with obesity] survive to old age,” she said. Other potential explanations are biological, such as the potentially higher levels of bone density in older [patients with obesity], she said.
When asked about additional clinical implications, Dr. Lammers emphasized the importance of maintaining a healthy BMI for breast cancer patients of all ages. Other research areas might involve the use of lifestyle interventions, although these are challenging to implement, she noted.
Data draw attention to quality of life and lifestyle factors
The need to “look at drug development with new eyes” is particularly important when reviewing patient-reported outcomes, said Otto Metzger, MD, of the Dana Farber Cancer Institute, Boston, who served as the discussant for the session.
Dr. Metzger brought up the association between age and the effect of BMI on DFS, specifically.
Based on data from multiple studies and meta-analyses, “I do believe that obesity does play a role in prognosis,” he said, but the question is how long will researchers continue to simply record data without acting to add lifestyle interventions while also trying to develop new drugs, he said. Although convincing patients to make lifestyle changes remains a challenge, patients are often more motivated to make such changes after a cancer diagnosis, Dr. Metzger noted.
“I am a firm believer in the use of digital therapeutics in the context of clinical trials,” said Dr. Metzger. Digital technology offers great potential to educate patients on [adverse effects] and also to improve treatment adherence and quality of life, he concluded.
The study was supported by AstraZeneca, and Dr. Lammers disclosed financial relationships with AstraZeneca and Eli Lilly. Dr. Metzger disclosed receiving research funding to his institution from Pfizer, Genentech/Roche, and Sanofi, and serving as an adviser/consultant to AstraZeneca, Merck, Oncoclinicas, Resilience, and Roche.
FROM ESMO BREAST CANCER 2023
Endoscopic sleeve gastroplasty plus obesity drugs add up to more weight loss
CHICAGO – Antiobesity medications and endoscopic sleeve gastroplasty (ESG) are popular strategies for weight loss on their own. Now researchers are looking at what happens when you combine them.
In a study presented at the annual Digestive Disease Week® (DDW), they found
Starting medication within 6 months of ESG was more ideal than other timing intervals. Initiating medical therapy more than 6 months before ESG was associated with less weight loss.
In the single-center, retrospective study, 224 patients were enrolled, of whom 34% were on monotherapy (ESG alone), 31% had combination therapy (medication prescribed within 6 months prior to or after ESG), and 35% had sequential therapy (medication more than 6 months prior to or after ESG).
Most patients were female, ranging from 74% to 95% of each group, and baseline BMI ranged from a mean 37.5 kg/m2 to 40.1 kg/m2.
The medications involved in the study were phentermine, phentermine/topiramate extended release (Qsymia), orlistat (Xenical, Alli), bupropion/naltrexone ER (Contrave), or the glucagonlike peptide–1 receptor agonist (GLP-1RA) liraglutide (Saxenda, Victoza) or semaglutide (Ozempic, Wegovy, Rybelsus). Of the patients who underwent combination therapy, 30% were prescribed a regimen that included a GLP-1RA. Of the patients who underwent sequential therapy, 81% were prescribed a medication first and 19% underwent ESG first.
At 1 year, the greatest total weight loss was a mean 23.7% with the combination of ESG and a GLP-1RA. Total weight loss was 18% with ESG plus a non–GLP-1RA medication. ESG alone led to 17.3%. Sequential therapy that began with ESG yielded 14.7% total weight loss, whereas sequential therapy that began with medication first resulted in 12% weight loss.
It’s possible that gastroplasty performed second was less impressive because the medications were very effective, and there was not as much weight to lose, said Pichamol Jirapinyo, MD, MPH, a bariatric endoscopist at Brigham and Women’s Hospital, Boston, and lead author of the study.
Researchers stopped medication therapy if people did not experience at least 5% total weight loss after 3 months on a maintenance dose.
Waiting for weight loss to start to plateau after gastroplasty might be an ideal time to add weight loss medication, said Dr. Jirapinyo. “Usually when I see them at 3 months, I plot how fast their weight loss has been. If it’s been going down [steadily], we do not offer an antiobesity medication until I see them again at 6 months.”
The serious adverse event (SAE) rate associated with ESG was similar among the three cohorts: 2.6% with monotherapy group, 1.4% with combination therapy, and 1.3% with sequential therapy. SAEs associated with antiobesity medication occurred in 1.3% of the sequential therapy group and was not reported in either of the other two groups.
“I certainly think combination therapy should be more effective than just gastroplasty alone and is probably better,” said Gregory L. Austin, MD, session comoderator and a gastroenterologist at the UCHealth Digestive Health Center, Denver.
“Whether you start immediately or wait 3 months afterwards is a question that still needs to be answered,” he added.
Dr. Austin agreed that taking an antiobesity medicine more than 6 months before gastroplasty might be associated with enough weight loss to make the gastroplasty look less effective.
He also noted that the study “doesn’t really address the question of whether you should offer gastroplasty to somebody who’s been on [medication] for more than 6 months because you probably still should if they haven’t achieved an appropriate weight loss that’s associated with reduced comorbidity risk going forward.”
Different study, similar result
In a second study, also presented at DDW 2023, investigators looked at timing of liraglutide for weight loss in a randomized controlled trial. They found that administration of GLP-1RA right after transoral outlet reduction endoscopy (TORe) in people with a history of Roux-en-Y gastric bypass extended weight loss longer than a placebo injection. This strategy was also favorable versus waiting to give liraglutide 1 year later.
The researchers randomly assigned 51 people to get weekly subcutaneous liraglutide injections following TORe for 12 months, then placebo injections for 12 months. They assigned 58 patients to receive weekly placebo injections following TORe for 12 months, then liraglutide injections for 12 months.
At 12 months following the procedure, total body weight loss (TBWL) among participants receiving liraglutide was about 22%, compared with about 14% among patients receiving placebo. At 24 months following the procedure (12 months after crossover), TBWL among patients in the liraglutide-first group was almost 35%, compared with about 24% in the placebo-first/liraglutide-second group.
There was a durable effect associated with liraglutide even after switching to placebo, said Ali Lahooti, lead study author and second-year medical student at Weill Cornell Medicine, New York.
“There did seem to be a better benefit of starting on it for the first year and then stopping it,” Dr. Austin noted.
These two studies come at a time when the debate over the timing of different obesity interventions continues. Some experts believe weight loss medications can help with the rebound in weight that some people experience months after bariatric surgery, for example.
‘Wave of the future’
The study by Dr. Jirapinyo and colleagues is “really exciting and interesting,” said Linda S. Lee, MD, medical director of endoscopy, Brigham and Women’s Hospital, Boston, when asked to comment.
Medication begun within 6 months of the endoscopic procedure “led to superior outcomes, compared to just endoscopy alone,” Dr. Lee said. “I think that’s really the wave of the future as far as treating patients with obesity issues. We clearly know that diet and exercise alone for most people is not good enough. Of course, we have surgery, but we also realize that with surgery sometimes the weight starts to creep back up over time.”
Dr. Lee noted that the study was limited because it was retrospective. Ideally, it would be good if future, prospective research randomly assigns people to endoscopy alone or endoscopy plus medication.
Dr. Lee also noted there is a limited number of bariatric endoscopists. By the time people with obesity get to a specialist, they’ve likely tried diet and exercise and “probably have seen all the commercials for these different medications. I think the reality is that most people will ask their primary care physicians about antiobesity medication.
“From my point of view, as long as the medicine is safe and not harming them, then let’s do both of them together,” Dr. Lee added.
Dr. Lee also mentioned another study (Abstract Mo1898) presented at DDW 2023 that showed total weight loss with endoscopic sleeve gastroplasty was durable over 10 years. Follow-up was with only seven patients, however.
Larger numbers are needed to confirm the finding, but it’s “exciting,” she said.
Dr. Jirapinyo receives grant/research support from Apollo Endosurgery, Fractyl, and USGI Medical, and is a consultant for ERBE, GI Dynamics, and Spatz Medical. Dr. Lahooti, Dr. Austin, and Dr. Lee reported no relevant financial relationships.
The meeting is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.
A version of this article first appeared on Medscape.com.
CHICAGO – Antiobesity medications and endoscopic sleeve gastroplasty (ESG) are popular strategies for weight loss on their own. Now researchers are looking at what happens when you combine them.
In a study presented at the annual Digestive Disease Week® (DDW), they found
Starting medication within 6 months of ESG was more ideal than other timing intervals. Initiating medical therapy more than 6 months before ESG was associated with less weight loss.
In the single-center, retrospective study, 224 patients were enrolled, of whom 34% were on monotherapy (ESG alone), 31% had combination therapy (medication prescribed within 6 months prior to or after ESG), and 35% had sequential therapy (medication more than 6 months prior to or after ESG).
Most patients were female, ranging from 74% to 95% of each group, and baseline BMI ranged from a mean 37.5 kg/m2 to 40.1 kg/m2.
The medications involved in the study were phentermine, phentermine/topiramate extended release (Qsymia), orlistat (Xenical, Alli), bupropion/naltrexone ER (Contrave), or the glucagonlike peptide–1 receptor agonist (GLP-1RA) liraglutide (Saxenda, Victoza) or semaglutide (Ozempic, Wegovy, Rybelsus). Of the patients who underwent combination therapy, 30% were prescribed a regimen that included a GLP-1RA. Of the patients who underwent sequential therapy, 81% were prescribed a medication first and 19% underwent ESG first.
At 1 year, the greatest total weight loss was a mean 23.7% with the combination of ESG and a GLP-1RA. Total weight loss was 18% with ESG plus a non–GLP-1RA medication. ESG alone led to 17.3%. Sequential therapy that began with ESG yielded 14.7% total weight loss, whereas sequential therapy that began with medication first resulted in 12% weight loss.
It’s possible that gastroplasty performed second was less impressive because the medications were very effective, and there was not as much weight to lose, said Pichamol Jirapinyo, MD, MPH, a bariatric endoscopist at Brigham and Women’s Hospital, Boston, and lead author of the study.
Researchers stopped medication therapy if people did not experience at least 5% total weight loss after 3 months on a maintenance dose.
Waiting for weight loss to start to plateau after gastroplasty might be an ideal time to add weight loss medication, said Dr. Jirapinyo. “Usually when I see them at 3 months, I plot how fast their weight loss has been. If it’s been going down [steadily], we do not offer an antiobesity medication until I see them again at 6 months.”
The serious adverse event (SAE) rate associated with ESG was similar among the three cohorts: 2.6% with monotherapy group, 1.4% with combination therapy, and 1.3% with sequential therapy. SAEs associated with antiobesity medication occurred in 1.3% of the sequential therapy group and was not reported in either of the other two groups.
“I certainly think combination therapy should be more effective than just gastroplasty alone and is probably better,” said Gregory L. Austin, MD, session comoderator and a gastroenterologist at the UCHealth Digestive Health Center, Denver.
“Whether you start immediately or wait 3 months afterwards is a question that still needs to be answered,” he added.
Dr. Austin agreed that taking an antiobesity medicine more than 6 months before gastroplasty might be associated with enough weight loss to make the gastroplasty look less effective.
He also noted that the study “doesn’t really address the question of whether you should offer gastroplasty to somebody who’s been on [medication] for more than 6 months because you probably still should if they haven’t achieved an appropriate weight loss that’s associated with reduced comorbidity risk going forward.”
Different study, similar result
In a second study, also presented at DDW 2023, investigators looked at timing of liraglutide for weight loss in a randomized controlled trial. They found that administration of GLP-1RA right after transoral outlet reduction endoscopy (TORe) in people with a history of Roux-en-Y gastric bypass extended weight loss longer than a placebo injection. This strategy was also favorable versus waiting to give liraglutide 1 year later.
The researchers randomly assigned 51 people to get weekly subcutaneous liraglutide injections following TORe for 12 months, then placebo injections for 12 months. They assigned 58 patients to receive weekly placebo injections following TORe for 12 months, then liraglutide injections for 12 months.
At 12 months following the procedure, total body weight loss (TBWL) among participants receiving liraglutide was about 22%, compared with about 14% among patients receiving placebo. At 24 months following the procedure (12 months after crossover), TBWL among patients in the liraglutide-first group was almost 35%, compared with about 24% in the placebo-first/liraglutide-second group.
There was a durable effect associated with liraglutide even after switching to placebo, said Ali Lahooti, lead study author and second-year medical student at Weill Cornell Medicine, New York.
“There did seem to be a better benefit of starting on it for the first year and then stopping it,” Dr. Austin noted.
These two studies come at a time when the debate over the timing of different obesity interventions continues. Some experts believe weight loss medications can help with the rebound in weight that some people experience months after bariatric surgery, for example.
‘Wave of the future’
The study by Dr. Jirapinyo and colleagues is “really exciting and interesting,” said Linda S. Lee, MD, medical director of endoscopy, Brigham and Women’s Hospital, Boston, when asked to comment.
Medication begun within 6 months of the endoscopic procedure “led to superior outcomes, compared to just endoscopy alone,” Dr. Lee said. “I think that’s really the wave of the future as far as treating patients with obesity issues. We clearly know that diet and exercise alone for most people is not good enough. Of course, we have surgery, but we also realize that with surgery sometimes the weight starts to creep back up over time.”
Dr. Lee noted that the study was limited because it was retrospective. Ideally, it would be good if future, prospective research randomly assigns people to endoscopy alone or endoscopy plus medication.
Dr. Lee also noted there is a limited number of bariatric endoscopists. By the time people with obesity get to a specialist, they’ve likely tried diet and exercise and “probably have seen all the commercials for these different medications. I think the reality is that most people will ask their primary care physicians about antiobesity medication.
“From my point of view, as long as the medicine is safe and not harming them, then let’s do both of them together,” Dr. Lee added.
Dr. Lee also mentioned another study (Abstract Mo1898) presented at DDW 2023 that showed total weight loss with endoscopic sleeve gastroplasty was durable over 10 years. Follow-up was with only seven patients, however.
Larger numbers are needed to confirm the finding, but it’s “exciting,” she said.
Dr. Jirapinyo receives grant/research support from Apollo Endosurgery, Fractyl, and USGI Medical, and is a consultant for ERBE, GI Dynamics, and Spatz Medical. Dr. Lahooti, Dr. Austin, and Dr. Lee reported no relevant financial relationships.
The meeting is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.
A version of this article first appeared on Medscape.com.
CHICAGO – Antiobesity medications and endoscopic sleeve gastroplasty (ESG) are popular strategies for weight loss on their own. Now researchers are looking at what happens when you combine them.
In a study presented at the annual Digestive Disease Week® (DDW), they found
Starting medication within 6 months of ESG was more ideal than other timing intervals. Initiating medical therapy more than 6 months before ESG was associated with less weight loss.
In the single-center, retrospective study, 224 patients were enrolled, of whom 34% were on monotherapy (ESG alone), 31% had combination therapy (medication prescribed within 6 months prior to or after ESG), and 35% had sequential therapy (medication more than 6 months prior to or after ESG).
Most patients were female, ranging from 74% to 95% of each group, and baseline BMI ranged from a mean 37.5 kg/m2 to 40.1 kg/m2.
The medications involved in the study were phentermine, phentermine/topiramate extended release (Qsymia), orlistat (Xenical, Alli), bupropion/naltrexone ER (Contrave), or the glucagonlike peptide–1 receptor agonist (GLP-1RA) liraglutide (Saxenda, Victoza) or semaglutide (Ozempic, Wegovy, Rybelsus). Of the patients who underwent combination therapy, 30% were prescribed a regimen that included a GLP-1RA. Of the patients who underwent sequential therapy, 81% were prescribed a medication first and 19% underwent ESG first.
At 1 year, the greatest total weight loss was a mean 23.7% with the combination of ESG and a GLP-1RA. Total weight loss was 18% with ESG plus a non–GLP-1RA medication. ESG alone led to 17.3%. Sequential therapy that began with ESG yielded 14.7% total weight loss, whereas sequential therapy that began with medication first resulted in 12% weight loss.
It’s possible that gastroplasty performed second was less impressive because the medications were very effective, and there was not as much weight to lose, said Pichamol Jirapinyo, MD, MPH, a bariatric endoscopist at Brigham and Women’s Hospital, Boston, and lead author of the study.
Researchers stopped medication therapy if people did not experience at least 5% total weight loss after 3 months on a maintenance dose.
Waiting for weight loss to start to plateau after gastroplasty might be an ideal time to add weight loss medication, said Dr. Jirapinyo. “Usually when I see them at 3 months, I plot how fast their weight loss has been. If it’s been going down [steadily], we do not offer an antiobesity medication until I see them again at 6 months.”
The serious adverse event (SAE) rate associated with ESG was similar among the three cohorts: 2.6% with monotherapy group, 1.4% with combination therapy, and 1.3% with sequential therapy. SAEs associated with antiobesity medication occurred in 1.3% of the sequential therapy group and was not reported in either of the other two groups.
“I certainly think combination therapy should be more effective than just gastroplasty alone and is probably better,” said Gregory L. Austin, MD, session comoderator and a gastroenterologist at the UCHealth Digestive Health Center, Denver.
“Whether you start immediately or wait 3 months afterwards is a question that still needs to be answered,” he added.
Dr. Austin agreed that taking an antiobesity medicine more than 6 months before gastroplasty might be associated with enough weight loss to make the gastroplasty look less effective.
He also noted that the study “doesn’t really address the question of whether you should offer gastroplasty to somebody who’s been on [medication] for more than 6 months because you probably still should if they haven’t achieved an appropriate weight loss that’s associated with reduced comorbidity risk going forward.”
Different study, similar result
In a second study, also presented at DDW 2023, investigators looked at timing of liraglutide for weight loss in a randomized controlled trial. They found that administration of GLP-1RA right after transoral outlet reduction endoscopy (TORe) in people with a history of Roux-en-Y gastric bypass extended weight loss longer than a placebo injection. This strategy was also favorable versus waiting to give liraglutide 1 year later.
The researchers randomly assigned 51 people to get weekly subcutaneous liraglutide injections following TORe for 12 months, then placebo injections for 12 months. They assigned 58 patients to receive weekly placebo injections following TORe for 12 months, then liraglutide injections for 12 months.
At 12 months following the procedure, total body weight loss (TBWL) among participants receiving liraglutide was about 22%, compared with about 14% among patients receiving placebo. At 24 months following the procedure (12 months after crossover), TBWL among patients in the liraglutide-first group was almost 35%, compared with about 24% in the placebo-first/liraglutide-second group.
There was a durable effect associated with liraglutide even after switching to placebo, said Ali Lahooti, lead study author and second-year medical student at Weill Cornell Medicine, New York.
“There did seem to be a better benefit of starting on it for the first year and then stopping it,” Dr. Austin noted.
These two studies come at a time when the debate over the timing of different obesity interventions continues. Some experts believe weight loss medications can help with the rebound in weight that some people experience months after bariatric surgery, for example.
‘Wave of the future’
The study by Dr. Jirapinyo and colleagues is “really exciting and interesting,” said Linda S. Lee, MD, medical director of endoscopy, Brigham and Women’s Hospital, Boston, when asked to comment.
Medication begun within 6 months of the endoscopic procedure “led to superior outcomes, compared to just endoscopy alone,” Dr. Lee said. “I think that’s really the wave of the future as far as treating patients with obesity issues. We clearly know that diet and exercise alone for most people is not good enough. Of course, we have surgery, but we also realize that with surgery sometimes the weight starts to creep back up over time.”
Dr. Lee noted that the study was limited because it was retrospective. Ideally, it would be good if future, prospective research randomly assigns people to endoscopy alone or endoscopy plus medication.
Dr. Lee also noted there is a limited number of bariatric endoscopists. By the time people with obesity get to a specialist, they’ve likely tried diet and exercise and “probably have seen all the commercials for these different medications. I think the reality is that most people will ask their primary care physicians about antiobesity medication.
“From my point of view, as long as the medicine is safe and not harming them, then let’s do both of them together,” Dr. Lee added.
Dr. Lee also mentioned another study (Abstract Mo1898) presented at DDW 2023 that showed total weight loss with endoscopic sleeve gastroplasty was durable over 10 years. Follow-up was with only seven patients, however.
Larger numbers are needed to confirm the finding, but it’s “exciting,” she said.
Dr. Jirapinyo receives grant/research support from Apollo Endosurgery, Fractyl, and USGI Medical, and is a consultant for ERBE, GI Dynamics, and Spatz Medical. Dr. Lahooti, Dr. Austin, and Dr. Lee reported no relevant financial relationships.
The meeting is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.
A version of this article first appeared on Medscape.com.
AT DDW 2023
Boys may carry the weight, or overweight, of adults’ infertility
Overweight boy, infertile man?
When it comes to causes of infertility, history and science have generally focused on women. A lot of the research overlooks men, but some previous studies have suggested that male infertility contributes to about half of the cases of couple infertility. The reason for much of that male infertility, however, has been a mystery. Until now.
A group of Italian investigators looked at the declining trend in sperm counts over the past 40 years and the increase of childhood obesity. Is there a correlation? The researchers think so. Childhood obesity can be linked to multiple causes, but the researchers zeroed in on the effect that obesity has on metabolic rates and, therefore, testicular growth.
Collecting data on testicular volume, body mass index (BMI), and insulin resistance from 268 boys aged 2-18 years, the researchers discovered that those with normal weight and normal insulin levels had testicular volumes 1.5 times higher than their overweight counterparts and 1.5-2 times higher than those with hyperinsulinemia, building a case for obesity being a factor for infertility later in life.
Since low testicular volume is associated with lower sperm count and production as an adult, putting two and two together makes a compelling argument for childhood obesity being a major male infertility culprit. It also creates even more urgency for the health care industry and community decision makers to focus on childhood obesity.
It sure would be nice to be able to take one of the many risk factors for future human survival off the table. Maybe by taking something, like cake, off the table.
Fecal transplantation moves to the kitchen
Fecal microbiota transplantation is an effective way to treat Clostridioides difficile infection, but, in the end, it’s still a transplantation procedure involving a nasogastric or colorectal tube or rather large oral capsules with a demanding (30-40 capsules over 2 days) dosage. Please, Science, tell us there’s a better way.
Science, in the form of investigators at the University of Geneva and Lausanne University Hospital in Switzerland, has spoken, and there may be a better way. Presenting fecal beads: All the bacterial goodness of donor stool without the tubal insertions or massive quantities of giant capsules.
We know you’re scoffing out there, but it’s true. All you need is a little alginate, which is a “biocompatible polysaccharide isolated from brown algae” of the Phaeophyceae family. The donor feces is microencapsulated by mixing it with the alginate, dropping that mixture into water containing calcium chloride, turning it into a gel, and then freeze-drying the gel into small (just 2 mm), solid beads.
Sounds plausible enough, but what do you do with them? “These brownish beads can be easily dispersed in a liquid or food that is pleasant to eat. They also have no taste,” senior author Eric Allémann, PhD, said in a statement released by the University of Geneva.
Pleasant to eat? No taste? So which is it? If you really want to know, watch fecal beads week on the new season of “The Great British Baking Show,” when Paul and Prue judge poop baked into crumpets, crepes, and crostatas. Yum.
We’re on the low-oxygen diet
Nine out of ten doctors agree: Oxygen is more important to your continued well-being than food. After all, a human can go weeks without food, but just minutes without oxygen. However, ten out of ten doctors agree that the United States has an obesity problem. They all also agree that previous research has shown soldiers who train at high altitudes lose more weight than those training at lower altitudes.
So, on the one hand, we have a country full of overweight people, and on the other, we have low oxygen levels causing weight loss. The solution, then, is obvious: Stop breathing.
More specifically (and somewhat less facetiously), researchers from Louisiana have launched the Low Oxygen and Weight Status trial and are currently recruiting individuals with BMIs of 30-40 to, uh, suffocate themselves. No, no, it’s okay, it’s just when they’re sleeping.
Fine, straight face. Participants in the LOWS trial will undergo an 8-week period when they will consume a controlled weight-loss diet and spend their nights in a hypoxic sealed tent, where they will sleep in an environment with an oxygen level equivalent to 8,500 feet above sea level (roughly equivalent to Aspen, Colo.). They will be compared with people on the same diet who sleep in a normal, sea-level oxygen environment.
The study’s goal is to determine whether or not spending time in a low-oxygen environment will suppress appetite, increase energy expenditure, and improve weight loss and insulin sensitivity. Excessive weight loss in high-altitude environments isn’t a good thing for soldiers – they kind of need their muscles and body weight to do the whole soldiering thing – but it could be great for people struggling to lose those last few pounds. And it also may prove LOTME’s previous thesis: Air is not good.
Overweight boy, infertile man?
When it comes to causes of infertility, history and science have generally focused on women. A lot of the research overlooks men, but some previous studies have suggested that male infertility contributes to about half of the cases of couple infertility. The reason for much of that male infertility, however, has been a mystery. Until now.
A group of Italian investigators looked at the declining trend in sperm counts over the past 40 years and the increase of childhood obesity. Is there a correlation? The researchers think so. Childhood obesity can be linked to multiple causes, but the researchers zeroed in on the effect that obesity has on metabolic rates and, therefore, testicular growth.
Collecting data on testicular volume, body mass index (BMI), and insulin resistance from 268 boys aged 2-18 years, the researchers discovered that those with normal weight and normal insulin levels had testicular volumes 1.5 times higher than their overweight counterparts and 1.5-2 times higher than those with hyperinsulinemia, building a case for obesity being a factor for infertility later in life.
Since low testicular volume is associated with lower sperm count and production as an adult, putting two and two together makes a compelling argument for childhood obesity being a major male infertility culprit. It also creates even more urgency for the health care industry and community decision makers to focus on childhood obesity.
It sure would be nice to be able to take one of the many risk factors for future human survival off the table. Maybe by taking something, like cake, off the table.
Fecal transplantation moves to the kitchen
Fecal microbiota transplantation is an effective way to treat Clostridioides difficile infection, but, in the end, it’s still a transplantation procedure involving a nasogastric or colorectal tube or rather large oral capsules with a demanding (30-40 capsules over 2 days) dosage. Please, Science, tell us there’s a better way.
Science, in the form of investigators at the University of Geneva and Lausanne University Hospital in Switzerland, has spoken, and there may be a better way. Presenting fecal beads: All the bacterial goodness of donor stool without the tubal insertions or massive quantities of giant capsules.
We know you’re scoffing out there, but it’s true. All you need is a little alginate, which is a “biocompatible polysaccharide isolated from brown algae” of the Phaeophyceae family. The donor feces is microencapsulated by mixing it with the alginate, dropping that mixture into water containing calcium chloride, turning it into a gel, and then freeze-drying the gel into small (just 2 mm), solid beads.
Sounds plausible enough, but what do you do with them? “These brownish beads can be easily dispersed in a liquid or food that is pleasant to eat. They also have no taste,” senior author Eric Allémann, PhD, said in a statement released by the University of Geneva.
Pleasant to eat? No taste? So which is it? If you really want to know, watch fecal beads week on the new season of “The Great British Baking Show,” when Paul and Prue judge poop baked into crumpets, crepes, and crostatas. Yum.
We’re on the low-oxygen diet
Nine out of ten doctors agree: Oxygen is more important to your continued well-being than food. After all, a human can go weeks without food, but just minutes without oxygen. However, ten out of ten doctors agree that the United States has an obesity problem. They all also agree that previous research has shown soldiers who train at high altitudes lose more weight than those training at lower altitudes.
So, on the one hand, we have a country full of overweight people, and on the other, we have low oxygen levels causing weight loss. The solution, then, is obvious: Stop breathing.
More specifically (and somewhat less facetiously), researchers from Louisiana have launched the Low Oxygen and Weight Status trial and are currently recruiting individuals with BMIs of 30-40 to, uh, suffocate themselves. No, no, it’s okay, it’s just when they’re sleeping.
Fine, straight face. Participants in the LOWS trial will undergo an 8-week period when they will consume a controlled weight-loss diet and spend their nights in a hypoxic sealed tent, where they will sleep in an environment with an oxygen level equivalent to 8,500 feet above sea level (roughly equivalent to Aspen, Colo.). They will be compared with people on the same diet who sleep in a normal, sea-level oxygen environment.
The study’s goal is to determine whether or not spending time in a low-oxygen environment will suppress appetite, increase energy expenditure, and improve weight loss and insulin sensitivity. Excessive weight loss in high-altitude environments isn’t a good thing for soldiers – they kind of need their muscles and body weight to do the whole soldiering thing – but it could be great for people struggling to lose those last few pounds. And it also may prove LOTME’s previous thesis: Air is not good.
Overweight boy, infertile man?
When it comes to causes of infertility, history and science have generally focused on women. A lot of the research overlooks men, but some previous studies have suggested that male infertility contributes to about half of the cases of couple infertility. The reason for much of that male infertility, however, has been a mystery. Until now.
A group of Italian investigators looked at the declining trend in sperm counts over the past 40 years and the increase of childhood obesity. Is there a correlation? The researchers think so. Childhood obesity can be linked to multiple causes, but the researchers zeroed in on the effect that obesity has on metabolic rates and, therefore, testicular growth.
Collecting data on testicular volume, body mass index (BMI), and insulin resistance from 268 boys aged 2-18 years, the researchers discovered that those with normal weight and normal insulin levels had testicular volumes 1.5 times higher than their overweight counterparts and 1.5-2 times higher than those with hyperinsulinemia, building a case for obesity being a factor for infertility later in life.
Since low testicular volume is associated with lower sperm count and production as an adult, putting two and two together makes a compelling argument for childhood obesity being a major male infertility culprit. It also creates even more urgency for the health care industry and community decision makers to focus on childhood obesity.
It sure would be nice to be able to take one of the many risk factors for future human survival off the table. Maybe by taking something, like cake, off the table.
Fecal transplantation moves to the kitchen
Fecal microbiota transplantation is an effective way to treat Clostridioides difficile infection, but, in the end, it’s still a transplantation procedure involving a nasogastric or colorectal tube or rather large oral capsules with a demanding (30-40 capsules over 2 days) dosage. Please, Science, tell us there’s a better way.
Science, in the form of investigators at the University of Geneva and Lausanne University Hospital in Switzerland, has spoken, and there may be a better way. Presenting fecal beads: All the bacterial goodness of donor stool without the tubal insertions or massive quantities of giant capsules.
We know you’re scoffing out there, but it’s true. All you need is a little alginate, which is a “biocompatible polysaccharide isolated from brown algae” of the Phaeophyceae family. The donor feces is microencapsulated by mixing it with the alginate, dropping that mixture into water containing calcium chloride, turning it into a gel, and then freeze-drying the gel into small (just 2 mm), solid beads.
Sounds plausible enough, but what do you do with them? “These brownish beads can be easily dispersed in a liquid or food that is pleasant to eat. They also have no taste,” senior author Eric Allémann, PhD, said in a statement released by the University of Geneva.
Pleasant to eat? No taste? So which is it? If you really want to know, watch fecal beads week on the new season of “The Great British Baking Show,” when Paul and Prue judge poop baked into crumpets, crepes, and crostatas. Yum.
We’re on the low-oxygen diet
Nine out of ten doctors agree: Oxygen is more important to your continued well-being than food. After all, a human can go weeks without food, but just minutes without oxygen. However, ten out of ten doctors agree that the United States has an obesity problem. They all also agree that previous research has shown soldiers who train at high altitudes lose more weight than those training at lower altitudes.
So, on the one hand, we have a country full of overweight people, and on the other, we have low oxygen levels causing weight loss. The solution, then, is obvious: Stop breathing.
More specifically (and somewhat less facetiously), researchers from Louisiana have launched the Low Oxygen and Weight Status trial and are currently recruiting individuals with BMIs of 30-40 to, uh, suffocate themselves. No, no, it’s okay, it’s just when they’re sleeping.
Fine, straight face. Participants in the LOWS trial will undergo an 8-week period when they will consume a controlled weight-loss diet and spend their nights in a hypoxic sealed tent, where they will sleep in an environment with an oxygen level equivalent to 8,500 feet above sea level (roughly equivalent to Aspen, Colo.). They will be compared with people on the same diet who sleep in a normal, sea-level oxygen environment.
The study’s goal is to determine whether or not spending time in a low-oxygen environment will suppress appetite, increase energy expenditure, and improve weight loss and insulin sensitivity. Excessive weight loss in high-altitude environments isn’t a good thing for soldiers – they kind of need their muscles and body weight to do the whole soldiering thing – but it could be great for people struggling to lose those last few pounds. And it also may prove LOTME’s previous thesis: Air is not good.
New AACE statement tries to fight weight bias and stigma
SEATTLE –
Highlights from the statement, entitled “Addressing stigma and bias in the diagnosis and management of patients with obesity/adiposity-based chronic disease and assessing bias and stigmatization as determinants of disease severity,” were presented at the annual scientific & clinical congress of the American Association of Clinical Endocrinology. It will be published later this year in Endocrine Practice.
The document reiterates AACE’s previous proposal to use the term “adiposity-based chronic disease (ABCD)” to refer to the spectrum of complications of obesity beyond weight. AACE has incorporated weight bias, stigmatization, psychological health, and social determinants of health into disease staging based on the degree to which these factors impair quality of life and could negatively affect treatment. Another change is the use of a scale from 1 to 3 for ABCD staging, in contrast to the previous scale from 0 to 3, as follows.
Stage 1 (previously 0): No known physical ABCD complications (for example, cardiovascular, biomechanical) but with increased risk that might be reduced by weight loss, and/or internalized weight bias and stigmatization, psychological conditions, and social determinants of health that don’t have immediate adverse health effects but may require individualized care.
Stage 2 (previously 1): One or more mild-moderate ABCD complications plus increased risk of other complications and/or bias/stigma/social determinants that adversely affect quality of life or could impair ABCD treatment.
Stage 3 (previously 2): At least one severe ABCD complication plus increased risk for others, and/or bias/stigma/social determinants with pronounced adverse effects on quality of life or that interfere with weight loss treatment plans or render them harmful.
To accomplish this staging, clinicians are advised to use validated questionnaires to screen patients for the presence and degree of self-stigmatization and internalized weight bias and to refer patients to mental health professionals for related psychological issues. The document also advises clinicians to implement practice policies such as implicit bias training and obesity education for their staff.
“I really hope that this document will increase awareness of the vicious cycle of weight bias, stigma, and internalized weight bias for patients with obesity, both on an individual basis and a bigger chronic care model basis ... By utilizing these concepts in the document, we hope to at least take steps towards reducing the stigma and internalized weight bias and slowing down or reversing that vicious cycle to better care for people with a focus on their health ... It’s not just about a person’s weight,” Karl Nadolsky, DO, the statement’s co-lead author, said.
The new statement builds on previous AACE efforts, including the 2014 publication entitled, “Advanced framework for a new diagnosis of obesity as a chronic disease,” the 2016 management guidelines, and the 2016 position statement, which introduced the ABCD term. All are meant to advance the concept of obesity or ABCD as a medical condition, rather than a cosmetic problem or lifestyle choice.
Now, AACE is explicitly calling attention to the integral role of internal and external weight bias and stigma as both drivers and complications of the condition. The AACE writing panel adopted some of the concepts from a 2020 international consensus statement focusing on obesity stigma, Dr. Nadolsky said.
“We need to focus on health, the biopsychosocial mode. We have to think about the person as a whole. The disease of obesity is really a quintessential disease state that needs a very good holistic approach,” he said.
Asked to comment, Yoni Freedhoff, MD, associate professor, department of family medicine, University of Ottawa, and Medical Director of the Bariatric Medical Institute, said: “I do think staging/categorization are important in the context of bias and stigma and also to combat the notion that the goal is simple medicalization ... It’s good to see the consideration of internalized weight bias as part of an effort to understand the impact of obesity on an individual.”
However, Dr. Freedhoff said he would have preferred that the implicit and internalized bias concepts had been incorporated into the 2009 Edmonton Obesity Staging System, which he believes is easier to use than the AACE staging system.
Dr. Freedhoff also disagrees that it was necessary to remove “0” from the staging (still present in the Edmonton system), done by AACE out of concern that people might mistakenly think it implies zero risk. “It just means no current objective or subjective impact of weight on health or quality of life,” he said.
But, Dr. Nadolsky noted that data on people with “metabolically healthy obesity” suggest that “they might have zero complications but they’re still at high risk, from cancer to stigma and bias, which are a cause of and consequence of obesity and should be part of the ABCD staging system.”
Indeed, Dr. Freedhoff noted, “Obesity confers risk. Just like hypertension. And just like with hypertension, risk is not a guarantee of problems. But we still discuss treatment and people can be symptom- or problem-free when we start it. It can also be ‘borderline’ or mild. But no one gets upset about the idea of treating a known risk factor, or diagnosing a known risk factor, when minor, and when it’s not had any impact on a person’s health. That we don’t do same with obesity is consequent to bias.”
In addition to influencing health care providers and health care systems, the statement also concludes: “Society, including payers and policymakers, should support policies, education, research, and access to care to limit bias and stigma faced by individuals with obesity/ABCD.”
Dr. Nadolsky has reported no relevant financial relationships. Dr. Freedhoff has reported working with the Bariatric Medical Institute and Constant Health, which has received a research grant from Novo Nordisk.
A version of this article originally appeared on Medscape.com.
SEATTLE –
Highlights from the statement, entitled “Addressing stigma and bias in the diagnosis and management of patients with obesity/adiposity-based chronic disease and assessing bias and stigmatization as determinants of disease severity,” were presented at the annual scientific & clinical congress of the American Association of Clinical Endocrinology. It will be published later this year in Endocrine Practice.
The document reiterates AACE’s previous proposal to use the term “adiposity-based chronic disease (ABCD)” to refer to the spectrum of complications of obesity beyond weight. AACE has incorporated weight bias, stigmatization, psychological health, and social determinants of health into disease staging based on the degree to which these factors impair quality of life and could negatively affect treatment. Another change is the use of a scale from 1 to 3 for ABCD staging, in contrast to the previous scale from 0 to 3, as follows.
Stage 1 (previously 0): No known physical ABCD complications (for example, cardiovascular, biomechanical) but with increased risk that might be reduced by weight loss, and/or internalized weight bias and stigmatization, psychological conditions, and social determinants of health that don’t have immediate adverse health effects but may require individualized care.
Stage 2 (previously 1): One or more mild-moderate ABCD complications plus increased risk of other complications and/or bias/stigma/social determinants that adversely affect quality of life or could impair ABCD treatment.
Stage 3 (previously 2): At least one severe ABCD complication plus increased risk for others, and/or bias/stigma/social determinants with pronounced adverse effects on quality of life or that interfere with weight loss treatment plans or render them harmful.
To accomplish this staging, clinicians are advised to use validated questionnaires to screen patients for the presence and degree of self-stigmatization and internalized weight bias and to refer patients to mental health professionals for related psychological issues. The document also advises clinicians to implement practice policies such as implicit bias training and obesity education for their staff.
“I really hope that this document will increase awareness of the vicious cycle of weight bias, stigma, and internalized weight bias for patients with obesity, both on an individual basis and a bigger chronic care model basis ... By utilizing these concepts in the document, we hope to at least take steps towards reducing the stigma and internalized weight bias and slowing down or reversing that vicious cycle to better care for people with a focus on their health ... It’s not just about a person’s weight,” Karl Nadolsky, DO, the statement’s co-lead author, said.
The new statement builds on previous AACE efforts, including the 2014 publication entitled, “Advanced framework for a new diagnosis of obesity as a chronic disease,” the 2016 management guidelines, and the 2016 position statement, which introduced the ABCD term. All are meant to advance the concept of obesity or ABCD as a medical condition, rather than a cosmetic problem or lifestyle choice.
Now, AACE is explicitly calling attention to the integral role of internal and external weight bias and stigma as both drivers and complications of the condition. The AACE writing panel adopted some of the concepts from a 2020 international consensus statement focusing on obesity stigma, Dr. Nadolsky said.
“We need to focus on health, the biopsychosocial mode. We have to think about the person as a whole. The disease of obesity is really a quintessential disease state that needs a very good holistic approach,” he said.
Asked to comment, Yoni Freedhoff, MD, associate professor, department of family medicine, University of Ottawa, and Medical Director of the Bariatric Medical Institute, said: “I do think staging/categorization are important in the context of bias and stigma and also to combat the notion that the goal is simple medicalization ... It’s good to see the consideration of internalized weight bias as part of an effort to understand the impact of obesity on an individual.”
However, Dr. Freedhoff said he would have preferred that the implicit and internalized bias concepts had been incorporated into the 2009 Edmonton Obesity Staging System, which he believes is easier to use than the AACE staging system.
Dr. Freedhoff also disagrees that it was necessary to remove “0” from the staging (still present in the Edmonton system), done by AACE out of concern that people might mistakenly think it implies zero risk. “It just means no current objective or subjective impact of weight on health or quality of life,” he said.
But, Dr. Nadolsky noted that data on people with “metabolically healthy obesity” suggest that “they might have zero complications but they’re still at high risk, from cancer to stigma and bias, which are a cause of and consequence of obesity and should be part of the ABCD staging system.”
Indeed, Dr. Freedhoff noted, “Obesity confers risk. Just like hypertension. And just like with hypertension, risk is not a guarantee of problems. But we still discuss treatment and people can be symptom- or problem-free when we start it. It can also be ‘borderline’ or mild. But no one gets upset about the idea of treating a known risk factor, or diagnosing a known risk factor, when minor, and when it’s not had any impact on a person’s health. That we don’t do same with obesity is consequent to bias.”
In addition to influencing health care providers and health care systems, the statement also concludes: “Society, including payers and policymakers, should support policies, education, research, and access to care to limit bias and stigma faced by individuals with obesity/ABCD.”
Dr. Nadolsky has reported no relevant financial relationships. Dr. Freedhoff has reported working with the Bariatric Medical Institute and Constant Health, which has received a research grant from Novo Nordisk.
A version of this article originally appeared on Medscape.com.
SEATTLE –
Highlights from the statement, entitled “Addressing stigma and bias in the diagnosis and management of patients with obesity/adiposity-based chronic disease and assessing bias and stigmatization as determinants of disease severity,” were presented at the annual scientific & clinical congress of the American Association of Clinical Endocrinology. It will be published later this year in Endocrine Practice.
The document reiterates AACE’s previous proposal to use the term “adiposity-based chronic disease (ABCD)” to refer to the spectrum of complications of obesity beyond weight. AACE has incorporated weight bias, stigmatization, psychological health, and social determinants of health into disease staging based on the degree to which these factors impair quality of life and could negatively affect treatment. Another change is the use of a scale from 1 to 3 for ABCD staging, in contrast to the previous scale from 0 to 3, as follows.
Stage 1 (previously 0): No known physical ABCD complications (for example, cardiovascular, biomechanical) but with increased risk that might be reduced by weight loss, and/or internalized weight bias and stigmatization, psychological conditions, and social determinants of health that don’t have immediate adverse health effects but may require individualized care.
Stage 2 (previously 1): One or more mild-moderate ABCD complications plus increased risk of other complications and/or bias/stigma/social determinants that adversely affect quality of life or could impair ABCD treatment.
Stage 3 (previously 2): At least one severe ABCD complication plus increased risk for others, and/or bias/stigma/social determinants with pronounced adverse effects on quality of life or that interfere with weight loss treatment plans or render them harmful.
To accomplish this staging, clinicians are advised to use validated questionnaires to screen patients for the presence and degree of self-stigmatization and internalized weight bias and to refer patients to mental health professionals for related psychological issues. The document also advises clinicians to implement practice policies such as implicit bias training and obesity education for their staff.
“I really hope that this document will increase awareness of the vicious cycle of weight bias, stigma, and internalized weight bias for patients with obesity, both on an individual basis and a bigger chronic care model basis ... By utilizing these concepts in the document, we hope to at least take steps towards reducing the stigma and internalized weight bias and slowing down or reversing that vicious cycle to better care for people with a focus on their health ... It’s not just about a person’s weight,” Karl Nadolsky, DO, the statement’s co-lead author, said.
The new statement builds on previous AACE efforts, including the 2014 publication entitled, “Advanced framework for a new diagnosis of obesity as a chronic disease,” the 2016 management guidelines, and the 2016 position statement, which introduced the ABCD term. All are meant to advance the concept of obesity or ABCD as a medical condition, rather than a cosmetic problem or lifestyle choice.
Now, AACE is explicitly calling attention to the integral role of internal and external weight bias and stigma as both drivers and complications of the condition. The AACE writing panel adopted some of the concepts from a 2020 international consensus statement focusing on obesity stigma, Dr. Nadolsky said.
“We need to focus on health, the biopsychosocial mode. We have to think about the person as a whole. The disease of obesity is really a quintessential disease state that needs a very good holistic approach,” he said.
Asked to comment, Yoni Freedhoff, MD, associate professor, department of family medicine, University of Ottawa, and Medical Director of the Bariatric Medical Institute, said: “I do think staging/categorization are important in the context of bias and stigma and also to combat the notion that the goal is simple medicalization ... It’s good to see the consideration of internalized weight bias as part of an effort to understand the impact of obesity on an individual.”
However, Dr. Freedhoff said he would have preferred that the implicit and internalized bias concepts had been incorporated into the 2009 Edmonton Obesity Staging System, which he believes is easier to use than the AACE staging system.
Dr. Freedhoff also disagrees that it was necessary to remove “0” from the staging (still present in the Edmonton system), done by AACE out of concern that people might mistakenly think it implies zero risk. “It just means no current objective or subjective impact of weight on health or quality of life,” he said.
But, Dr. Nadolsky noted that data on people with “metabolically healthy obesity” suggest that “they might have zero complications but they’re still at high risk, from cancer to stigma and bias, which are a cause of and consequence of obesity and should be part of the ABCD staging system.”
Indeed, Dr. Freedhoff noted, “Obesity confers risk. Just like hypertension. And just like with hypertension, risk is not a guarantee of problems. But we still discuss treatment and people can be symptom- or problem-free when we start it. It can also be ‘borderline’ or mild. But no one gets upset about the idea of treating a known risk factor, or diagnosing a known risk factor, when minor, and when it’s not had any impact on a person’s health. That we don’t do same with obesity is consequent to bias.”
In addition to influencing health care providers and health care systems, the statement also concludes: “Society, including payers and policymakers, should support policies, education, research, and access to care to limit bias and stigma faced by individuals with obesity/ABCD.”
Dr. Nadolsky has reported no relevant financial relationships. Dr. Freedhoff has reported working with the Bariatric Medical Institute and Constant Health, which has received a research grant from Novo Nordisk.
A version of this article originally appeared on Medscape.com.
AT AACE 2023
Study shows higher obesity-related cancer mortality in areas with more fast food
based on data from a new cross-sectional study of more than 3,000 communities.
Although increased healthy eating has been associated with reduced risk of obesity and with reduced cancer incidence and mortality, access to healthier eating remains a challenge in communities with less access to grocery stores and healthy food options (food deserts) and/or easy access to convenience stores and fast food (food swamps), Malcolm Seth Bevel, PhD, of the Medical College of Georgia, Augusta, and colleagues, wrote in their paper, published in JAMA Oncology.
In addition, data on the association between food deserts and swamps and obesity-related cancer mortality are limited, they said.
“We felt that the study was important given the fact that obesity is an epidemic in the United States, and multiple factors contribute to obesity, especially adverse food environments,” Dr. Bevel said in an interview. “Also, I lived in these areas my whole life, and saw how it affected underserved populations. There was a story that needed to be told, so we’re telling it,” he said in an interview.
In a study, the researchers analyzed food access and cancer mortality data from 3,038 counties across the United States. The food access data came from the U.S. Department of Agriculture Food Environment Atlas (FEA) for the years 2012, 2014, 2015, 2017, and 2020. Data on obesity-related cancer mortality came from the Centers for Disease Control and Prevention for the years from 2010 to 2020.
Food desert scores were calculated through data from the FEA, and food swamp scores were based on the ratio of fast-food restaurants and convenience stores to grocery stores and farmers markets in a modification of the Retail Food Environment Index score.
The researchers used an age-adjusted, multiple regression model to determine the association between food desert and food swamp scores and obesity-related cancer mortality rates. Higher food swamp and food desert scores (defined as 20.0 to 58.0 or higher) were used to classify counties as having fewer healthy food resources. The primary outcome was obesity-related cancer mortality, defined as high or low (71.8 or higher per 100,000 individuals and less than 71.8 per 100,000 individuals, respectively).
Overall, high rates of obesity-related cancer mortality were 77% more likely in the counties that met the criteria for high food swamp scores (adjusted odds ratio 1.77). In addition, researchers found a positive dose-response relationship among three levels of both food desert scores and food swamp scores and obesity-related cancer mortality.
A total of 758 counties had obesity-related cancer mortality rates in the highest quartile. Compared to counties with low rates of obesity-related cancer mortality, counties with high rates of obesity-related cancer mortality also had a higher percentage of non-Hispanic Black residents (3.26% vs. 1.77%), higher percentage of adults older than 65 years (15.71% vs. 15.40%), higher rates of adult obesity (33.0% vs. 32.10%), and higher rates of adult diabetes (12.50% vs. 10.70%).
Possible explanations for the results include the lack of interest in grocery stores in neighborhoods with a population with a lower socioeconomic status, which can create a food desert, the researchers wrote in their discussion. “Coupled with the increasing growth rate of fast-food restaurants in recent years and the intentional advertisement of unhealthy foods in urban neighborhoods with [people of lower income], the food desert may transform into a food swamp,” they said.
The findings were limited by several factors including the study design, which did not allow for showing a causal association of food deserts and food swamps with obesity-related cancer mortality, the researchers noted. Other limitations included the use of groups rather than individuals, the potential misclassification of food stores, and the use of county-level data on race, ethnicity, and income, they wrote.
The results indicate that “food swamps appear to be a growing epidemic across the U.S., likely because of systemic issues, and should draw concern and conversation from local and state officials,” the researchers concluded.
Community-level investments can benefit individual health
Dr. Bevel said he was not surprised by the findings, as he has seen firsthand the lack of healthy food options and growth of unhealthy food options, especially for certain populations in certain communities. “Typically, these are people who have lower socioeconomic status, primarily non-Hispanic Black or African American or Hispanic American,” he said “I have watched people have to choose between getting fruits/vegetables versus their medications or running to fast food places to feed their families. What is truly surprising is that we’re not talking about people’s lived environment enough for my taste,” he said.
“I hope that our data and results can inform local and state policymakers to truly invest in all communities, such as funding for community gardens, and realize that adverse food environments, including the barriers in navigating these environments, have significant consequences on real people,” said Dr. Bevel. “Also, I hope that the results can help clinicians realize that a patient’s lived environment can truly affect their obesity and/or obesity-related cancer status; being cognizant of that is the first step in holistic, comprehensive care,” he said.
“One role that oncologists might be able to play in improving patients’ access to healthier food is to create and/or implement healthy lifestyle programs with gardening components to combat the poorest food environments that their patients likely reside in,” said Dr. Bevel. Clinicians also could consider the innovative approach of “food prescriptions” to help reduce the effects of deprived, built environments, he noted.
Looking ahead, next steps for research include determining the severity of association between food swamps and obesity-related cancer by varying factors such as cancer type, and examining any potential racial disparities between people living in these environments and obesity-related cancer, Dr. Bevel added.
Data provide foundation for multilevel interventions
The current study findings “raise a clarion call to elevate the discussion on food availability and access to ensure an equitable emphasis on both the importance of lifestyle factors and the upstream structural, economic, and environmental contexts that shape these behaviors at the individual level,” Karriem S. Watson, DHSc, MS, MPH, of the National Institutes of Health, Bethesda, Md., and Angela Odoms-Young, PhD, of Cornell University, Ithaca, N.Y., wrote in an accompanying editorial.
The findings provide a foundation for studies of obesity-related cancer outcomes that take the community environment into consideration, they added.
The causes of both obesity and cancer are complex, and the study findings suggest that the links between unhealthy food environments and obesity-related cancer may go beyond dietary consumption alone and extend to social and psychological factors, the editorialists noted.
“Whether dealing with the lack of access to healthy foods or an overabundance of unhealthy food, there is a critical need to develop additional research that explores the associations between obesity-related cancer mortality and food inequities,” they concluded.
The study received no outside funding. The researchers and the editorialists had no financial conflicts to disclose.
based on data from a new cross-sectional study of more than 3,000 communities.
Although increased healthy eating has been associated with reduced risk of obesity and with reduced cancer incidence and mortality, access to healthier eating remains a challenge in communities with less access to grocery stores and healthy food options (food deserts) and/or easy access to convenience stores and fast food (food swamps), Malcolm Seth Bevel, PhD, of the Medical College of Georgia, Augusta, and colleagues, wrote in their paper, published in JAMA Oncology.
In addition, data on the association between food deserts and swamps and obesity-related cancer mortality are limited, they said.
“We felt that the study was important given the fact that obesity is an epidemic in the United States, and multiple factors contribute to obesity, especially adverse food environments,” Dr. Bevel said in an interview. “Also, I lived in these areas my whole life, and saw how it affected underserved populations. There was a story that needed to be told, so we’re telling it,” he said in an interview.
In a study, the researchers analyzed food access and cancer mortality data from 3,038 counties across the United States. The food access data came from the U.S. Department of Agriculture Food Environment Atlas (FEA) for the years 2012, 2014, 2015, 2017, and 2020. Data on obesity-related cancer mortality came from the Centers for Disease Control and Prevention for the years from 2010 to 2020.
Food desert scores were calculated through data from the FEA, and food swamp scores were based on the ratio of fast-food restaurants and convenience stores to grocery stores and farmers markets in a modification of the Retail Food Environment Index score.
The researchers used an age-adjusted, multiple regression model to determine the association between food desert and food swamp scores and obesity-related cancer mortality rates. Higher food swamp and food desert scores (defined as 20.0 to 58.0 or higher) were used to classify counties as having fewer healthy food resources. The primary outcome was obesity-related cancer mortality, defined as high or low (71.8 or higher per 100,000 individuals and less than 71.8 per 100,000 individuals, respectively).
Overall, high rates of obesity-related cancer mortality were 77% more likely in the counties that met the criteria for high food swamp scores (adjusted odds ratio 1.77). In addition, researchers found a positive dose-response relationship among three levels of both food desert scores and food swamp scores and obesity-related cancer mortality.
A total of 758 counties had obesity-related cancer mortality rates in the highest quartile. Compared to counties with low rates of obesity-related cancer mortality, counties with high rates of obesity-related cancer mortality also had a higher percentage of non-Hispanic Black residents (3.26% vs. 1.77%), higher percentage of adults older than 65 years (15.71% vs. 15.40%), higher rates of adult obesity (33.0% vs. 32.10%), and higher rates of adult diabetes (12.50% vs. 10.70%).
Possible explanations for the results include the lack of interest in grocery stores in neighborhoods with a population with a lower socioeconomic status, which can create a food desert, the researchers wrote in their discussion. “Coupled with the increasing growth rate of fast-food restaurants in recent years and the intentional advertisement of unhealthy foods in urban neighborhoods with [people of lower income], the food desert may transform into a food swamp,” they said.
The findings were limited by several factors including the study design, which did not allow for showing a causal association of food deserts and food swamps with obesity-related cancer mortality, the researchers noted. Other limitations included the use of groups rather than individuals, the potential misclassification of food stores, and the use of county-level data on race, ethnicity, and income, they wrote.
The results indicate that “food swamps appear to be a growing epidemic across the U.S., likely because of systemic issues, and should draw concern and conversation from local and state officials,” the researchers concluded.
Community-level investments can benefit individual health
Dr. Bevel said he was not surprised by the findings, as he has seen firsthand the lack of healthy food options and growth of unhealthy food options, especially for certain populations in certain communities. “Typically, these are people who have lower socioeconomic status, primarily non-Hispanic Black or African American or Hispanic American,” he said “I have watched people have to choose between getting fruits/vegetables versus their medications or running to fast food places to feed their families. What is truly surprising is that we’re not talking about people’s lived environment enough for my taste,” he said.
“I hope that our data and results can inform local and state policymakers to truly invest in all communities, such as funding for community gardens, and realize that adverse food environments, including the barriers in navigating these environments, have significant consequences on real people,” said Dr. Bevel. “Also, I hope that the results can help clinicians realize that a patient’s lived environment can truly affect their obesity and/or obesity-related cancer status; being cognizant of that is the first step in holistic, comprehensive care,” he said.
“One role that oncologists might be able to play in improving patients’ access to healthier food is to create and/or implement healthy lifestyle programs with gardening components to combat the poorest food environments that their patients likely reside in,” said Dr. Bevel. Clinicians also could consider the innovative approach of “food prescriptions” to help reduce the effects of deprived, built environments, he noted.
Looking ahead, next steps for research include determining the severity of association between food swamps and obesity-related cancer by varying factors such as cancer type, and examining any potential racial disparities between people living in these environments and obesity-related cancer, Dr. Bevel added.
Data provide foundation for multilevel interventions
The current study findings “raise a clarion call to elevate the discussion on food availability and access to ensure an equitable emphasis on both the importance of lifestyle factors and the upstream structural, economic, and environmental contexts that shape these behaviors at the individual level,” Karriem S. Watson, DHSc, MS, MPH, of the National Institutes of Health, Bethesda, Md., and Angela Odoms-Young, PhD, of Cornell University, Ithaca, N.Y., wrote in an accompanying editorial.
The findings provide a foundation for studies of obesity-related cancer outcomes that take the community environment into consideration, they added.
The causes of both obesity and cancer are complex, and the study findings suggest that the links between unhealthy food environments and obesity-related cancer may go beyond dietary consumption alone and extend to social and psychological factors, the editorialists noted.
“Whether dealing with the lack of access to healthy foods or an overabundance of unhealthy food, there is a critical need to develop additional research that explores the associations between obesity-related cancer mortality and food inequities,” they concluded.
The study received no outside funding. The researchers and the editorialists had no financial conflicts to disclose.
based on data from a new cross-sectional study of more than 3,000 communities.
Although increased healthy eating has been associated with reduced risk of obesity and with reduced cancer incidence and mortality, access to healthier eating remains a challenge in communities with less access to grocery stores and healthy food options (food deserts) and/or easy access to convenience stores and fast food (food swamps), Malcolm Seth Bevel, PhD, of the Medical College of Georgia, Augusta, and colleagues, wrote in their paper, published in JAMA Oncology.
In addition, data on the association between food deserts and swamps and obesity-related cancer mortality are limited, they said.
“We felt that the study was important given the fact that obesity is an epidemic in the United States, and multiple factors contribute to obesity, especially adverse food environments,” Dr. Bevel said in an interview. “Also, I lived in these areas my whole life, and saw how it affected underserved populations. There was a story that needed to be told, so we’re telling it,” he said in an interview.
In a study, the researchers analyzed food access and cancer mortality data from 3,038 counties across the United States. The food access data came from the U.S. Department of Agriculture Food Environment Atlas (FEA) for the years 2012, 2014, 2015, 2017, and 2020. Data on obesity-related cancer mortality came from the Centers for Disease Control and Prevention for the years from 2010 to 2020.
Food desert scores were calculated through data from the FEA, and food swamp scores were based on the ratio of fast-food restaurants and convenience stores to grocery stores and farmers markets in a modification of the Retail Food Environment Index score.
The researchers used an age-adjusted, multiple regression model to determine the association between food desert and food swamp scores and obesity-related cancer mortality rates. Higher food swamp and food desert scores (defined as 20.0 to 58.0 or higher) were used to classify counties as having fewer healthy food resources. The primary outcome was obesity-related cancer mortality, defined as high or low (71.8 or higher per 100,000 individuals and less than 71.8 per 100,000 individuals, respectively).
Overall, high rates of obesity-related cancer mortality were 77% more likely in the counties that met the criteria for high food swamp scores (adjusted odds ratio 1.77). In addition, researchers found a positive dose-response relationship among three levels of both food desert scores and food swamp scores and obesity-related cancer mortality.
A total of 758 counties had obesity-related cancer mortality rates in the highest quartile. Compared to counties with low rates of obesity-related cancer mortality, counties with high rates of obesity-related cancer mortality also had a higher percentage of non-Hispanic Black residents (3.26% vs. 1.77%), higher percentage of adults older than 65 years (15.71% vs. 15.40%), higher rates of adult obesity (33.0% vs. 32.10%), and higher rates of adult diabetes (12.50% vs. 10.70%).
Possible explanations for the results include the lack of interest in grocery stores in neighborhoods with a population with a lower socioeconomic status, which can create a food desert, the researchers wrote in their discussion. “Coupled with the increasing growth rate of fast-food restaurants in recent years and the intentional advertisement of unhealthy foods in urban neighborhoods with [people of lower income], the food desert may transform into a food swamp,” they said.
The findings were limited by several factors including the study design, which did not allow for showing a causal association of food deserts and food swamps with obesity-related cancer mortality, the researchers noted. Other limitations included the use of groups rather than individuals, the potential misclassification of food stores, and the use of county-level data on race, ethnicity, and income, they wrote.
The results indicate that “food swamps appear to be a growing epidemic across the U.S., likely because of systemic issues, and should draw concern and conversation from local and state officials,” the researchers concluded.
Community-level investments can benefit individual health
Dr. Bevel said he was not surprised by the findings, as he has seen firsthand the lack of healthy food options and growth of unhealthy food options, especially for certain populations in certain communities. “Typically, these are people who have lower socioeconomic status, primarily non-Hispanic Black or African American or Hispanic American,” he said “I have watched people have to choose between getting fruits/vegetables versus their medications or running to fast food places to feed their families. What is truly surprising is that we’re not talking about people’s lived environment enough for my taste,” he said.
“I hope that our data and results can inform local and state policymakers to truly invest in all communities, such as funding for community gardens, and realize that adverse food environments, including the barriers in navigating these environments, have significant consequences on real people,” said Dr. Bevel. “Also, I hope that the results can help clinicians realize that a patient’s lived environment can truly affect their obesity and/or obesity-related cancer status; being cognizant of that is the first step in holistic, comprehensive care,” he said.
“One role that oncologists might be able to play in improving patients’ access to healthier food is to create and/or implement healthy lifestyle programs with gardening components to combat the poorest food environments that their patients likely reside in,” said Dr. Bevel. Clinicians also could consider the innovative approach of “food prescriptions” to help reduce the effects of deprived, built environments, he noted.
Looking ahead, next steps for research include determining the severity of association between food swamps and obesity-related cancer by varying factors such as cancer type, and examining any potential racial disparities between people living in these environments and obesity-related cancer, Dr. Bevel added.
Data provide foundation for multilevel interventions
The current study findings “raise a clarion call to elevate the discussion on food availability and access to ensure an equitable emphasis on both the importance of lifestyle factors and the upstream structural, economic, and environmental contexts that shape these behaviors at the individual level,” Karriem S. Watson, DHSc, MS, MPH, of the National Institutes of Health, Bethesda, Md., and Angela Odoms-Young, PhD, of Cornell University, Ithaca, N.Y., wrote in an accompanying editorial.
The findings provide a foundation for studies of obesity-related cancer outcomes that take the community environment into consideration, they added.
The causes of both obesity and cancer are complex, and the study findings suggest that the links between unhealthy food environments and obesity-related cancer may go beyond dietary consumption alone and extend to social and psychological factors, the editorialists noted.
“Whether dealing with the lack of access to healthy foods or an overabundance of unhealthy food, there is a critical need to develop additional research that explores the associations between obesity-related cancer mortality and food inequities,” they concluded.
The study received no outside funding. The researchers and the editorialists had no financial conflicts to disclose.
FROM JAMA ONCOLOGY