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Type 1 diabetes no longer a disease of the thin: Lifestyle advice needed
About two-thirds of people with type 1 diabetes in the United States have overweight or obesity, nearly the same proportion as Americans without diabetes, new nationwide survey data suggest.
What’s more, among people with overweight or obesity, those with type 1 diabetes are less likely to receive lifestyle recommendations from health care professionals than those with type 2 diabetes, and are less likely to actually engage in lifestyle weight management activities than others with overweight or obesity, with or without type 2 diabetes.
“Among U.S. adults with type 1 diabetes, the burden of overweight and obesity is substantial and remains poorly managed,” write Michael Fang, PhD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, and colleagues.
Their data, from the National Health Interview Survey (NHIS), were published online in Annals of Internal Medicine.
The need for insulin complicates weight management in people with type 1 diabetes because changes in diet and physical activity typically require adjustments to insulin timing and dosage to prevent hypoglycemia. There is little evidence to guide this for weight management, Dr. Fang and colleagues explain.
Consequently, “the lack of evidence for safe, effective methods of diet- and exercise-based weight control in people with type 1 diabetes may be keeping doctors from recommending such methods,” Dr. Fang said in a statement.
“Large clinical trials have been done in type 2 diabetes patients to establish guidelines for diet- and exercise-based weight management, and we now need something similar for type 1 diabetes patients.”
Asked to comment, M. Sue Kirkman, MD, told this news organization: “The days when we could teach simple concepts about diabetes type like ‘those with type 1 are lean and those with type 2 are overweight’ are long gone. … Of concern, fewer adults with type 1 diabetes and overweight/obesity report that they are engaging in physical activity or caloric restriction than those without diabetes or those with type 2 diabetes.”
There are several likely reasons for the low rates of obesity/overweight lifestyle modification advice and implementation for those with type 1 diabetes, noted Dr. Kirkman, of the University of North Carolina at Chapel Hill, who coauthored joint American/European guidance on type 1 diabetes management.
“Medical visits are often primarily focused on glycemic management and complications screening, and we know that physicians in general are not very knowledgeable about how to counsel people – even those without diabetes – on weight loss. When you add in potential worries, real or not, about hypoglycemia, ketosis with carbohydrate restriction … it’s no wonder that this may not be addressed in busy visits.”
She also observed, “In years of going to diabetes meetings, I’ve noticed occasional sessions on managing ‘elite athletes’ with type 1 diabetes, but rarely are there sessions on how to counsel people about everyday healthy living.”
Many with type 1 diabetes have overweight/obesity
Dr. Fang and colleagues analyzed NHIS data for the years 2016, 2017, 2019, 2020, and 2021, when diabetes subtype data were available, for 128,571 adults. Diabetes type and height/weight data were self-reported. In the 2016, 2017, and 2020 surveys, participants were asked whether their physicians had recommended increasing physical activity and/or reducing calorie or fat consumption, and whether they were currently engaging in those activities.
The study population comprised 733 people with type 1 diabetes, 12,397 with type 2 diabetes, and 115,441 without diabetes. The proportions with overweight (body mass index, 25 to < 30 kg/m2) or obesity (≥ 30 kg/m2) were 62% among those with type 1 diabetes and 64% among those without diabetes, compared with 86% among those with type 2 diabetes.
Among those with overweight or obesity, the proportions who reported having received lifestyle recommendations were greatest among those with type 2 diabetes and least among those without diabetes, with the type 1 diabetes group in the middle.
After adjustment for age, sex, and race/ethnicity, the adjusted prevalence of receiving a provider recommendation to increase physical activity was 60% for those with type 2 diabetes, 54% for type 1 diabetes, and 44% for those without diabetes. Proportions for receiving recommendations for reducing fat/caloric intake were similar, at 60%, 51%, and 41%, respectively.
The proportions who reported actually engaging in lifestyle activities for weight management were lowest among those with type 1 diabetes, with 52% and 56% of them reporting having increased their physical activity and reducing fat/calories, respectively, compared with proportions ranging from 56% to 63% among the other two groups.
Regarding those findings, Dr. Kirkman commented, “In addition to the factors regarding physician interactions, people with type 1 diabetes may see this as a lower-priority health issue after years of being told that glucose control is the main priority.”
“I also wonder if the many, many tasks people with type 1 diabetes must do every day to manage their diabetes – along with other life issues all adults face – mean that there is just too much on the plate to add more lifestyle changes,” she added.
Asked about the potential for off-label use of glucagonlike peptide–1 agonists for weight management for people with type 1 diabetes, Dr. Kirkman said they could probably help some patients. However, she also pointed to two clinical trials in which liraglutide added to insulin therapy helped with glycemic control and weight reduction, but also increased the risk for hypoglycemia and diabetic ketoacidosis.
“It’s really important that researchers engage with adults with type 1 diabetes to better understand the unique priorities and barriers they face in addressing body weight,” Dr. Kirkman said.
Senior study author Elizabeth Selvin, PhD, professor of epidemiology at the Bloomberg School, said in the statement: “Our study busts the myth that people with type 1 diabetes are not being affected by the global obesity epidemic. … These findings should be a wake-up call that we need to be aggressive in addressing the obesity epidemic in persons with type 1 diabetes.”
The study was funded by the U.S. National Institutes of Health. Dr. Fang and Dr. Kirkman have reported no relevant financial relationships. Dr. Selvin has reported receiving royalty payments from Wolters Kluwer for chapters and laboratory monographs in UpToDate. She also reports receiving honoraria for editorial work on journals published by the American Diabetes Association and European Association for the Study of Diabetes.
A version of this article originally appeared on Medscape.com.
About two-thirds of people with type 1 diabetes in the United States have overweight or obesity, nearly the same proportion as Americans without diabetes, new nationwide survey data suggest.
What’s more, among people with overweight or obesity, those with type 1 diabetes are less likely to receive lifestyle recommendations from health care professionals than those with type 2 diabetes, and are less likely to actually engage in lifestyle weight management activities than others with overweight or obesity, with or without type 2 diabetes.
“Among U.S. adults with type 1 diabetes, the burden of overweight and obesity is substantial and remains poorly managed,” write Michael Fang, PhD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, and colleagues.
Their data, from the National Health Interview Survey (NHIS), were published online in Annals of Internal Medicine.
The need for insulin complicates weight management in people with type 1 diabetes because changes in diet and physical activity typically require adjustments to insulin timing and dosage to prevent hypoglycemia. There is little evidence to guide this for weight management, Dr. Fang and colleagues explain.
Consequently, “the lack of evidence for safe, effective methods of diet- and exercise-based weight control in people with type 1 diabetes may be keeping doctors from recommending such methods,” Dr. Fang said in a statement.
“Large clinical trials have been done in type 2 diabetes patients to establish guidelines for diet- and exercise-based weight management, and we now need something similar for type 1 diabetes patients.”
Asked to comment, M. Sue Kirkman, MD, told this news organization: “The days when we could teach simple concepts about diabetes type like ‘those with type 1 are lean and those with type 2 are overweight’ are long gone. … Of concern, fewer adults with type 1 diabetes and overweight/obesity report that they are engaging in physical activity or caloric restriction than those without diabetes or those with type 2 diabetes.”
There are several likely reasons for the low rates of obesity/overweight lifestyle modification advice and implementation for those with type 1 diabetes, noted Dr. Kirkman, of the University of North Carolina at Chapel Hill, who coauthored joint American/European guidance on type 1 diabetes management.
“Medical visits are often primarily focused on glycemic management and complications screening, and we know that physicians in general are not very knowledgeable about how to counsel people – even those without diabetes – on weight loss. When you add in potential worries, real or not, about hypoglycemia, ketosis with carbohydrate restriction … it’s no wonder that this may not be addressed in busy visits.”
She also observed, “In years of going to diabetes meetings, I’ve noticed occasional sessions on managing ‘elite athletes’ with type 1 diabetes, but rarely are there sessions on how to counsel people about everyday healthy living.”
Many with type 1 diabetes have overweight/obesity
Dr. Fang and colleagues analyzed NHIS data for the years 2016, 2017, 2019, 2020, and 2021, when diabetes subtype data were available, for 128,571 adults. Diabetes type and height/weight data were self-reported. In the 2016, 2017, and 2020 surveys, participants were asked whether their physicians had recommended increasing physical activity and/or reducing calorie or fat consumption, and whether they were currently engaging in those activities.
The study population comprised 733 people with type 1 diabetes, 12,397 with type 2 diabetes, and 115,441 without diabetes. The proportions with overweight (body mass index, 25 to < 30 kg/m2) or obesity (≥ 30 kg/m2) were 62% among those with type 1 diabetes and 64% among those without diabetes, compared with 86% among those with type 2 diabetes.
Among those with overweight or obesity, the proportions who reported having received lifestyle recommendations were greatest among those with type 2 diabetes and least among those without diabetes, with the type 1 diabetes group in the middle.
After adjustment for age, sex, and race/ethnicity, the adjusted prevalence of receiving a provider recommendation to increase physical activity was 60% for those with type 2 diabetes, 54% for type 1 diabetes, and 44% for those without diabetes. Proportions for receiving recommendations for reducing fat/caloric intake were similar, at 60%, 51%, and 41%, respectively.
The proportions who reported actually engaging in lifestyle activities for weight management were lowest among those with type 1 diabetes, with 52% and 56% of them reporting having increased their physical activity and reducing fat/calories, respectively, compared with proportions ranging from 56% to 63% among the other two groups.
Regarding those findings, Dr. Kirkman commented, “In addition to the factors regarding physician interactions, people with type 1 diabetes may see this as a lower-priority health issue after years of being told that glucose control is the main priority.”
“I also wonder if the many, many tasks people with type 1 diabetes must do every day to manage their diabetes – along with other life issues all adults face – mean that there is just too much on the plate to add more lifestyle changes,” she added.
Asked about the potential for off-label use of glucagonlike peptide–1 agonists for weight management for people with type 1 diabetes, Dr. Kirkman said they could probably help some patients. However, she also pointed to two clinical trials in which liraglutide added to insulin therapy helped with glycemic control and weight reduction, but also increased the risk for hypoglycemia and diabetic ketoacidosis.
“It’s really important that researchers engage with adults with type 1 diabetes to better understand the unique priorities and barriers they face in addressing body weight,” Dr. Kirkman said.
Senior study author Elizabeth Selvin, PhD, professor of epidemiology at the Bloomberg School, said in the statement: “Our study busts the myth that people with type 1 diabetes are not being affected by the global obesity epidemic. … These findings should be a wake-up call that we need to be aggressive in addressing the obesity epidemic in persons with type 1 diabetes.”
The study was funded by the U.S. National Institutes of Health. Dr. Fang and Dr. Kirkman have reported no relevant financial relationships. Dr. Selvin has reported receiving royalty payments from Wolters Kluwer for chapters and laboratory monographs in UpToDate. She also reports receiving honoraria for editorial work on journals published by the American Diabetes Association and European Association for the Study of Diabetes.
A version of this article originally appeared on Medscape.com.
About two-thirds of people with type 1 diabetes in the United States have overweight or obesity, nearly the same proportion as Americans without diabetes, new nationwide survey data suggest.
What’s more, among people with overweight or obesity, those with type 1 diabetes are less likely to receive lifestyle recommendations from health care professionals than those with type 2 diabetes, and are less likely to actually engage in lifestyle weight management activities than others with overweight or obesity, with or without type 2 diabetes.
“Among U.S. adults with type 1 diabetes, the burden of overweight and obesity is substantial and remains poorly managed,” write Michael Fang, PhD, of the Johns Hopkins Bloomberg School of Public Health, Baltimore, and colleagues.
Their data, from the National Health Interview Survey (NHIS), were published online in Annals of Internal Medicine.
The need for insulin complicates weight management in people with type 1 diabetes because changes in diet and physical activity typically require adjustments to insulin timing and dosage to prevent hypoglycemia. There is little evidence to guide this for weight management, Dr. Fang and colleagues explain.
Consequently, “the lack of evidence for safe, effective methods of diet- and exercise-based weight control in people with type 1 diabetes may be keeping doctors from recommending such methods,” Dr. Fang said in a statement.
“Large clinical trials have been done in type 2 diabetes patients to establish guidelines for diet- and exercise-based weight management, and we now need something similar for type 1 diabetes patients.”
Asked to comment, M. Sue Kirkman, MD, told this news organization: “The days when we could teach simple concepts about diabetes type like ‘those with type 1 are lean and those with type 2 are overweight’ are long gone. … Of concern, fewer adults with type 1 diabetes and overweight/obesity report that they are engaging in physical activity or caloric restriction than those without diabetes or those with type 2 diabetes.”
There are several likely reasons for the low rates of obesity/overweight lifestyle modification advice and implementation for those with type 1 diabetes, noted Dr. Kirkman, of the University of North Carolina at Chapel Hill, who coauthored joint American/European guidance on type 1 diabetes management.
“Medical visits are often primarily focused on glycemic management and complications screening, and we know that physicians in general are not very knowledgeable about how to counsel people – even those without diabetes – on weight loss. When you add in potential worries, real or not, about hypoglycemia, ketosis with carbohydrate restriction … it’s no wonder that this may not be addressed in busy visits.”
She also observed, “In years of going to diabetes meetings, I’ve noticed occasional sessions on managing ‘elite athletes’ with type 1 diabetes, but rarely are there sessions on how to counsel people about everyday healthy living.”
Many with type 1 diabetes have overweight/obesity
Dr. Fang and colleagues analyzed NHIS data for the years 2016, 2017, 2019, 2020, and 2021, when diabetes subtype data were available, for 128,571 adults. Diabetes type and height/weight data were self-reported. In the 2016, 2017, and 2020 surveys, participants were asked whether their physicians had recommended increasing physical activity and/or reducing calorie or fat consumption, and whether they were currently engaging in those activities.
The study population comprised 733 people with type 1 diabetes, 12,397 with type 2 diabetes, and 115,441 without diabetes. The proportions with overweight (body mass index, 25 to < 30 kg/m2) or obesity (≥ 30 kg/m2) were 62% among those with type 1 diabetes and 64% among those without diabetes, compared with 86% among those with type 2 diabetes.
Among those with overweight or obesity, the proportions who reported having received lifestyle recommendations were greatest among those with type 2 diabetes and least among those without diabetes, with the type 1 diabetes group in the middle.
After adjustment for age, sex, and race/ethnicity, the adjusted prevalence of receiving a provider recommendation to increase physical activity was 60% for those with type 2 diabetes, 54% for type 1 diabetes, and 44% for those without diabetes. Proportions for receiving recommendations for reducing fat/caloric intake were similar, at 60%, 51%, and 41%, respectively.
The proportions who reported actually engaging in lifestyle activities for weight management were lowest among those with type 1 diabetes, with 52% and 56% of them reporting having increased their physical activity and reducing fat/calories, respectively, compared with proportions ranging from 56% to 63% among the other two groups.
Regarding those findings, Dr. Kirkman commented, “In addition to the factors regarding physician interactions, people with type 1 diabetes may see this as a lower-priority health issue after years of being told that glucose control is the main priority.”
“I also wonder if the many, many tasks people with type 1 diabetes must do every day to manage their diabetes – along with other life issues all adults face – mean that there is just too much on the plate to add more lifestyle changes,” she added.
Asked about the potential for off-label use of glucagonlike peptide–1 agonists for weight management for people with type 1 diabetes, Dr. Kirkman said they could probably help some patients. However, she also pointed to two clinical trials in which liraglutide added to insulin therapy helped with glycemic control and weight reduction, but also increased the risk for hypoglycemia and diabetic ketoacidosis.
“It’s really important that researchers engage with adults with type 1 diabetes to better understand the unique priorities and barriers they face in addressing body weight,” Dr. Kirkman said.
Senior study author Elizabeth Selvin, PhD, professor of epidemiology at the Bloomberg School, said in the statement: “Our study busts the myth that people with type 1 diabetes are not being affected by the global obesity epidemic. … These findings should be a wake-up call that we need to be aggressive in addressing the obesity epidemic in persons with type 1 diabetes.”
The study was funded by the U.S. National Institutes of Health. Dr. Fang and Dr. Kirkman have reported no relevant financial relationships. Dr. Selvin has reported receiving royalty payments from Wolters Kluwer for chapters and laboratory monographs in UpToDate. She also reports receiving honoraria for editorial work on journals published by the American Diabetes Association and European Association for the Study of Diabetes.
A version of this article originally appeared on Medscape.com.
FROM ANNALS OF INTERNAL MEDICINE
AAP vs. AED on obesity treatment: Is there a middle ground?
While there is little controversy that both obesity and eating disorders represent important public health concerns, each deserving of clinical attention, how best to address one without worsening the other has been the crux of the discussion.
Sparking the dispute was a recent publication from the American Academy of Pediatrics that outlines the scope of the obesity problem and makes specific recommendations for assessment and treatment.1 The ambitious 100-page document, with 801 citations, puts new emphasis on the medical and psychological costs associated with obesity and advocates that pediatric primary care clinicians be more assertive in its treatment. While the guidelines certainly don’t urge the use of medications or surgery options as first-line treatment, the new recommendations do put them on the table as options.
In response, the Academy of Eating Disorders issued a public statement outlining several concerns regarding these guidelines that centered around a lack of a detailed plan to screen and address eating disorders; concerns that pediatricians don’t have the level of training and “skills” to conduct these conversations with patients and families with enough sensitivity; and worries about the premature use of antiobesity medications and surgeries in this population.2
It is fair to say that the critique was sharply worded, invoking physicians’ Hippocratic oath, criticizing their training, and suggesting that the guidelines could be biased by pharmaceutical industry influence (of note, the authors of the guidelines reported no ties to any pharmaceutical company). The AED urged that the guidelines be “revised” after consultation with other groups, including them.
Not unexpectedly, this response, especially coming from a group whose leadership and members are primarily nonphysicians, triggered its own sharp rebukes, including a recent commentary that counter-accused some of the eating disorder clinicians of being more concerned with their pet diets than actual health improvements.3
After everyone takes some deep breaths, it’s worth looking to see if there is some middle ground to explore here. The AAP document, to my reading, shows some important acknowledgments of the stigma associated with being overweight, even coming from pediatricians themselves. One passage reads, “Pediatricians and other PHCPs [primary health care providers] have been – and remain – a source of weight bias. They first need to uncover and address their own attitudes regarding children with obesity. Understanding weight stigma and bias, and learning how to reduce it in the clinical setting, sets the stage for productive discussions and improved relationships between families and pediatricians or other PHCPs.”
The guidelines also include some suggestions for how to talk to youth and families about obesity in less stigmatizing ways and offer a fairly lengthy summary of motivational interviewing techniques as they might apply to obesity discussions and lifestyle change. There is also a section on the interface between obesity and eating disorders with suggestions for further reading on their assessment and management.4
Indeed, research has looked specifically at how to minimize the triggering of eating disorders when addressing weight problems, a concern that has been raised by pediatricians themselves as documented in a qualitative study that also invoked the “do no harm” principle.5 One study asked more than 2,000 teens about how various conversations about weight affected their behavior.6 A main finding from that study was that conversations that focused on healthy eating rather than weight per se were less likely to be associated with unhealthy weight control behaviors. This message was emphasized in a publication that came from the AAP itself; it addresses the interaction between eating disorders and obesity.7 Strangely, however, the suggestion to try to minimize the focus on weight in discussions with patients isn’t well emphasized in the publication.
Overall, though, the AAP guidelines offer a well-informed and balanced approach to helping overweight youth. Pediatricians and other pediatric primary care clinicians are frequently called upon to engage in extremely sensitive and difficult discussions with patients and families on a wide variety of topics and most do so quite skillfully, especially when given the proper time and tools. While it is an area in which many of us, including mental health professionals, could do better, it’s no surprise that the AED’s disparaging of pediatricians’ communication competence came off as insulting. Similarly, productive dialogue would be likely enhanced if both sides avoided unfounded speculation about bias and motive and worked from a good faith perspective that all of us are engaged in this important discussion because of a desire to improve the lives of kids.
From my reading, it is quite a stretch to conclude that this document is urging a hasty and financially driven descent into GLP-1 analogues and bariatric surgery. That said, this wouldn’t be the first time a professional organization issues detailed, thoughtful, and nuanced care guidelines only to have them “condensed” within the practical confines of a busy office practice. Leaders would do well to remember that there remains much work to do to empower clinicians to be able to follow these guidelines as intended.
Dr. Rettew is a child and adolescent psychiatrist with Lane County Behavioral Health in Eugene, Ore., and Oregon Health & Science University, Portland. His latest book is “Parenting Made Complicated: What Science Really Knows About the Greatest Debates of Early Childhood.”
References
1. Hampl SE et al. Pediatrics. 2023;151(2):e2022060640.
2. Academy of Eating Disorders. Jan. 26, 2023. Accessed February 2, 2023. Available at The Academy for Eating Disorders Releases a Statement on the Recent American Academy of Pediatrics Clinical Practice Guideline for Weight-Related Care: First, Do No Harm (newswise.com).
3. Freedhoff Y. MDedge Pediatrics 2023. Available at https://www.mdedge.com/pediatrics/article/260894/obesity/weight-bias-affects-views-kids-obesity-recommendations?channel=52.
4. Hornberger LL, Lane MA et al. Pediatrics. 2021;147(1):e202004027989.
5. Loth KA, Lebow J et al. Global Pediatric Health. 2021;8:1-9.
6. Berge JM et al. JAMA Pediatrics. 2013;167(8):746-53.
7. Golden NH et al. Pediatrics. 2016;138(3):e20161649.
While there is little controversy that both obesity and eating disorders represent important public health concerns, each deserving of clinical attention, how best to address one without worsening the other has been the crux of the discussion.
Sparking the dispute was a recent publication from the American Academy of Pediatrics that outlines the scope of the obesity problem and makes specific recommendations for assessment and treatment.1 The ambitious 100-page document, with 801 citations, puts new emphasis on the medical and psychological costs associated with obesity and advocates that pediatric primary care clinicians be more assertive in its treatment. While the guidelines certainly don’t urge the use of medications or surgery options as first-line treatment, the new recommendations do put them on the table as options.
In response, the Academy of Eating Disorders issued a public statement outlining several concerns regarding these guidelines that centered around a lack of a detailed plan to screen and address eating disorders; concerns that pediatricians don’t have the level of training and “skills” to conduct these conversations with patients and families with enough sensitivity; and worries about the premature use of antiobesity medications and surgeries in this population.2
It is fair to say that the critique was sharply worded, invoking physicians’ Hippocratic oath, criticizing their training, and suggesting that the guidelines could be biased by pharmaceutical industry influence (of note, the authors of the guidelines reported no ties to any pharmaceutical company). The AED urged that the guidelines be “revised” after consultation with other groups, including them.
Not unexpectedly, this response, especially coming from a group whose leadership and members are primarily nonphysicians, triggered its own sharp rebukes, including a recent commentary that counter-accused some of the eating disorder clinicians of being more concerned with their pet diets than actual health improvements.3
After everyone takes some deep breaths, it’s worth looking to see if there is some middle ground to explore here. The AAP document, to my reading, shows some important acknowledgments of the stigma associated with being overweight, even coming from pediatricians themselves. One passage reads, “Pediatricians and other PHCPs [primary health care providers] have been – and remain – a source of weight bias. They first need to uncover and address their own attitudes regarding children with obesity. Understanding weight stigma and bias, and learning how to reduce it in the clinical setting, sets the stage for productive discussions and improved relationships between families and pediatricians or other PHCPs.”
The guidelines also include some suggestions for how to talk to youth and families about obesity in less stigmatizing ways and offer a fairly lengthy summary of motivational interviewing techniques as they might apply to obesity discussions and lifestyle change. There is also a section on the interface between obesity and eating disorders with suggestions for further reading on their assessment and management.4
Indeed, research has looked specifically at how to minimize the triggering of eating disorders when addressing weight problems, a concern that has been raised by pediatricians themselves as documented in a qualitative study that also invoked the “do no harm” principle.5 One study asked more than 2,000 teens about how various conversations about weight affected their behavior.6 A main finding from that study was that conversations that focused on healthy eating rather than weight per se were less likely to be associated with unhealthy weight control behaviors. This message was emphasized in a publication that came from the AAP itself; it addresses the interaction between eating disorders and obesity.7 Strangely, however, the suggestion to try to minimize the focus on weight in discussions with patients isn’t well emphasized in the publication.
Overall, though, the AAP guidelines offer a well-informed and balanced approach to helping overweight youth. Pediatricians and other pediatric primary care clinicians are frequently called upon to engage in extremely sensitive and difficult discussions with patients and families on a wide variety of topics and most do so quite skillfully, especially when given the proper time and tools. While it is an area in which many of us, including mental health professionals, could do better, it’s no surprise that the AED’s disparaging of pediatricians’ communication competence came off as insulting. Similarly, productive dialogue would be likely enhanced if both sides avoided unfounded speculation about bias and motive and worked from a good faith perspective that all of us are engaged in this important discussion because of a desire to improve the lives of kids.
From my reading, it is quite a stretch to conclude that this document is urging a hasty and financially driven descent into GLP-1 analogues and bariatric surgery. That said, this wouldn’t be the first time a professional organization issues detailed, thoughtful, and nuanced care guidelines only to have them “condensed” within the practical confines of a busy office practice. Leaders would do well to remember that there remains much work to do to empower clinicians to be able to follow these guidelines as intended.
Dr. Rettew is a child and adolescent psychiatrist with Lane County Behavioral Health in Eugene, Ore., and Oregon Health & Science University, Portland. His latest book is “Parenting Made Complicated: What Science Really Knows About the Greatest Debates of Early Childhood.”
References
1. Hampl SE et al. Pediatrics. 2023;151(2):e2022060640.
2. Academy of Eating Disorders. Jan. 26, 2023. Accessed February 2, 2023. Available at The Academy for Eating Disorders Releases a Statement on the Recent American Academy of Pediatrics Clinical Practice Guideline for Weight-Related Care: First, Do No Harm (newswise.com).
3. Freedhoff Y. MDedge Pediatrics 2023. Available at https://www.mdedge.com/pediatrics/article/260894/obesity/weight-bias-affects-views-kids-obesity-recommendations?channel=52.
4. Hornberger LL, Lane MA et al. Pediatrics. 2021;147(1):e202004027989.
5. Loth KA, Lebow J et al. Global Pediatric Health. 2021;8:1-9.
6. Berge JM et al. JAMA Pediatrics. 2013;167(8):746-53.
7. Golden NH et al. Pediatrics. 2016;138(3):e20161649.
While there is little controversy that both obesity and eating disorders represent important public health concerns, each deserving of clinical attention, how best to address one without worsening the other has been the crux of the discussion.
Sparking the dispute was a recent publication from the American Academy of Pediatrics that outlines the scope of the obesity problem and makes specific recommendations for assessment and treatment.1 The ambitious 100-page document, with 801 citations, puts new emphasis on the medical and psychological costs associated with obesity and advocates that pediatric primary care clinicians be more assertive in its treatment. While the guidelines certainly don’t urge the use of medications or surgery options as first-line treatment, the new recommendations do put them on the table as options.
In response, the Academy of Eating Disorders issued a public statement outlining several concerns regarding these guidelines that centered around a lack of a detailed plan to screen and address eating disorders; concerns that pediatricians don’t have the level of training and “skills” to conduct these conversations with patients and families with enough sensitivity; and worries about the premature use of antiobesity medications and surgeries in this population.2
It is fair to say that the critique was sharply worded, invoking physicians’ Hippocratic oath, criticizing their training, and suggesting that the guidelines could be biased by pharmaceutical industry influence (of note, the authors of the guidelines reported no ties to any pharmaceutical company). The AED urged that the guidelines be “revised” after consultation with other groups, including them.
Not unexpectedly, this response, especially coming from a group whose leadership and members are primarily nonphysicians, triggered its own sharp rebukes, including a recent commentary that counter-accused some of the eating disorder clinicians of being more concerned with their pet diets than actual health improvements.3
After everyone takes some deep breaths, it’s worth looking to see if there is some middle ground to explore here. The AAP document, to my reading, shows some important acknowledgments of the stigma associated with being overweight, even coming from pediatricians themselves. One passage reads, “Pediatricians and other PHCPs [primary health care providers] have been – and remain – a source of weight bias. They first need to uncover and address their own attitudes regarding children with obesity. Understanding weight stigma and bias, and learning how to reduce it in the clinical setting, sets the stage for productive discussions and improved relationships between families and pediatricians or other PHCPs.”
The guidelines also include some suggestions for how to talk to youth and families about obesity in less stigmatizing ways and offer a fairly lengthy summary of motivational interviewing techniques as they might apply to obesity discussions and lifestyle change. There is also a section on the interface between obesity and eating disorders with suggestions for further reading on their assessment and management.4
Indeed, research has looked specifically at how to minimize the triggering of eating disorders when addressing weight problems, a concern that has been raised by pediatricians themselves as documented in a qualitative study that also invoked the “do no harm” principle.5 One study asked more than 2,000 teens about how various conversations about weight affected their behavior.6 A main finding from that study was that conversations that focused on healthy eating rather than weight per se were less likely to be associated with unhealthy weight control behaviors. This message was emphasized in a publication that came from the AAP itself; it addresses the interaction between eating disorders and obesity.7 Strangely, however, the suggestion to try to minimize the focus on weight in discussions with patients isn’t well emphasized in the publication.
Overall, though, the AAP guidelines offer a well-informed and balanced approach to helping overweight youth. Pediatricians and other pediatric primary care clinicians are frequently called upon to engage in extremely sensitive and difficult discussions with patients and families on a wide variety of topics and most do so quite skillfully, especially when given the proper time and tools. While it is an area in which many of us, including mental health professionals, could do better, it’s no surprise that the AED’s disparaging of pediatricians’ communication competence came off as insulting. Similarly, productive dialogue would be likely enhanced if both sides avoided unfounded speculation about bias and motive and worked from a good faith perspective that all of us are engaged in this important discussion because of a desire to improve the lives of kids.
From my reading, it is quite a stretch to conclude that this document is urging a hasty and financially driven descent into GLP-1 analogues and bariatric surgery. That said, this wouldn’t be the first time a professional organization issues detailed, thoughtful, and nuanced care guidelines only to have them “condensed” within the practical confines of a busy office practice. Leaders would do well to remember that there remains much work to do to empower clinicians to be able to follow these guidelines as intended.
Dr. Rettew is a child and adolescent psychiatrist with Lane County Behavioral Health in Eugene, Ore., and Oregon Health & Science University, Portland. His latest book is “Parenting Made Complicated: What Science Really Knows About the Greatest Debates of Early Childhood.”
References
1. Hampl SE et al. Pediatrics. 2023;151(2):e2022060640.
2. Academy of Eating Disorders. Jan. 26, 2023. Accessed February 2, 2023. Available at The Academy for Eating Disorders Releases a Statement on the Recent American Academy of Pediatrics Clinical Practice Guideline for Weight-Related Care: First, Do No Harm (newswise.com).
3. Freedhoff Y. MDedge Pediatrics 2023. Available at https://www.mdedge.com/pediatrics/article/260894/obesity/weight-bias-affects-views-kids-obesity-recommendations?channel=52.
4. Hornberger LL, Lane MA et al. Pediatrics. 2021;147(1):e202004027989.
5. Loth KA, Lebow J et al. Global Pediatric Health. 2021;8:1-9.
6. Berge JM et al. JAMA Pediatrics. 2013;167(8):746-53.
7. Golden NH et al. Pediatrics. 2016;138(3):e20161649.
Longer life after bariatric surgery, but suicide risk in young
Death from cardiovascular disease, cancer, and diabetes was 29%, 43%, and 72% lower, respectively, in the bariatric surgery patients versus nonsurgery peers, during a mean follow-up of 13 years (all P > .001).
However, the youngest group of bariatric surgery patients – who were 18-34 years old – had a fivefold increased risk of suicide during follow-up compared with their peers who did not undergo surgery (P = .001).
These findings are from a retrospective study in Utah that matched close to 22,000 patients with severe obesity who underwent Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch from 1982 to 2018 with an equal number of nonsurgery individuals.
The study, by Ted D. Adams, PhD, MPH, and colleagues, was published online in Obesity.
‘Impressive’ data, in men too, but psychological screening important
The overall improved survival and decreased deaths from diabetes, heart disease, and cancer over this long follow-up are “impressive,” Dr. Adams, of Intermountain Surgical Specialties/Digestive Health Clinical Program, Salt Lake City, said in an interview.
Previous studies have not shown a survival benefit from bariatric surgery versus no surgery in men, he said. However, “because we had a fair number of male patients and because of the length of follow-up, we did show that the improved mortality was not only evident for the female patients but also for the male patients,” Dr. Adams stressed.
Finding increased suicide rates among bariatric surgical patients who underwent surgery at a younger age (18-34 years) shows that “we need to try and determine who is at risk for suicide,” according to Dr. Adams.
Patients with severe obesity, especially younger ones, “may need more aggressive presurgical psychological screening and postsurgery follow-up,” wrote Dr. Adams and colleagues.
The findings may also “stimulate important research related to the discovery of physiologic and biomolecular mechanisms leading to nonsurgical treatment that results in weight loss and improved mortality similar to that achieved by bariatric surgery,” they suggested.
Close to 1 in 10 Americans has severe obesity
The prevalence of severe obesity (BMI ≥ 40 kg/m2) in the United States has increased from 4.7% during 1999-2000 to 9.2% during 2017-2018, based on National Health and Nutrition Examination Survey (NHANES) data, the researchers noted.
They previously published a study of long-term mortality in 7,925 patients who had gastric bypass surgery from 1984 to 2002 matched with patients with the same BMI who did not have bariatric surgery and were followed out to 2002.
The current study extends the follow-up through 2021, doubles the number of bypass patients, and includes three newer types of bariatric surgery.
The researchers matched 21,873 patients aged 18-80 who had Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch during 1982-2018 in Utah (from the Utah Population Database) with people of the same BMI category, age category (18-34, 35-44, 45-54, and 55-80 years), and sex (from Utah driver license data).
Most patients were women (79%) and most were White (94% and 85%). They had a mean age of 42 years and a mean BMI of 46 kg/m2.
Most patients had Roux-en-Y gastric bypass (69%), and the rest had sleeve gastrectomy (14%), gastric banding (12%), and duodenal switch (4.8%).
During follow-up, 13.5% of patients in the bariatric surgery group and 14.6% of people in the nonsurgery group died.
Overall, all-cause mortality was 16% lower in patients who had bariatric surgery versus matched nonsurgical participants; it was 14% lower in women and 21% lower in men (all P < .001).
All-cause mortality was significantly lower in patients who had bariatric surgery when they were 35-44, 45-54, and 55-80 years old compared with matched peers who did not have surgery.
However, the findings “should not imply patients necessarily postpone surgery until older age,” the researchers cautioned, “as postsurgical complications have been shown to increase with increasing age at surgery and surgical postponement may result in worsened clinical status related to certain conditions such as orthopedic joint health.”
The researchers found significantly improved all-cause mortality following either type of surgery (gastric bypass, gastric banding, and sleeve gastrectomy) compared with no surgery.
Along with fewer deaths from cardiovascular disease, cancer, and diabetes, deaths from lung disease were 39% lower in the surgery group than in the nonsurgery group.
However, in the youngest group (age 18-34), deaths from cirrhosis of the liver were significantly higher in the patients who had bariatric surgery, and rates of suicide were significantly greater for both females and males, compared with similar people who did not undergo surgery.
The study was supported by grants from Ethicon Endo-Surgery (Johnson & Johnson); the National Institute of Diabetes and Digestive and Kidney Diseases, a division of the National Institutes of Health; U.S. Public Health Service; and Intermountain Research and Medical Foundation of Intermountain Healthcare. Dr. Adams disclosed ties to Ethicon Endo-Surgery and Intermountain Healthcare. A coauthor reported ties with Biomedical Research Program at Weill Cornell Medicine in Qatar, a program funded by the Qatar Foundation. The other authors have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Death from cardiovascular disease, cancer, and diabetes was 29%, 43%, and 72% lower, respectively, in the bariatric surgery patients versus nonsurgery peers, during a mean follow-up of 13 years (all P > .001).
However, the youngest group of bariatric surgery patients – who were 18-34 years old – had a fivefold increased risk of suicide during follow-up compared with their peers who did not undergo surgery (P = .001).
These findings are from a retrospective study in Utah that matched close to 22,000 patients with severe obesity who underwent Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch from 1982 to 2018 with an equal number of nonsurgery individuals.
The study, by Ted D. Adams, PhD, MPH, and colleagues, was published online in Obesity.
‘Impressive’ data, in men too, but psychological screening important
The overall improved survival and decreased deaths from diabetes, heart disease, and cancer over this long follow-up are “impressive,” Dr. Adams, of Intermountain Surgical Specialties/Digestive Health Clinical Program, Salt Lake City, said in an interview.
Previous studies have not shown a survival benefit from bariatric surgery versus no surgery in men, he said. However, “because we had a fair number of male patients and because of the length of follow-up, we did show that the improved mortality was not only evident for the female patients but also for the male patients,” Dr. Adams stressed.
Finding increased suicide rates among bariatric surgical patients who underwent surgery at a younger age (18-34 years) shows that “we need to try and determine who is at risk for suicide,” according to Dr. Adams.
Patients with severe obesity, especially younger ones, “may need more aggressive presurgical psychological screening and postsurgery follow-up,” wrote Dr. Adams and colleagues.
The findings may also “stimulate important research related to the discovery of physiologic and biomolecular mechanisms leading to nonsurgical treatment that results in weight loss and improved mortality similar to that achieved by bariatric surgery,” they suggested.
Close to 1 in 10 Americans has severe obesity
The prevalence of severe obesity (BMI ≥ 40 kg/m2) in the United States has increased from 4.7% during 1999-2000 to 9.2% during 2017-2018, based on National Health and Nutrition Examination Survey (NHANES) data, the researchers noted.
They previously published a study of long-term mortality in 7,925 patients who had gastric bypass surgery from 1984 to 2002 matched with patients with the same BMI who did not have bariatric surgery and were followed out to 2002.
The current study extends the follow-up through 2021, doubles the number of bypass patients, and includes three newer types of bariatric surgery.
The researchers matched 21,873 patients aged 18-80 who had Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch during 1982-2018 in Utah (from the Utah Population Database) with people of the same BMI category, age category (18-34, 35-44, 45-54, and 55-80 years), and sex (from Utah driver license data).
Most patients were women (79%) and most were White (94% and 85%). They had a mean age of 42 years and a mean BMI of 46 kg/m2.
Most patients had Roux-en-Y gastric bypass (69%), and the rest had sleeve gastrectomy (14%), gastric banding (12%), and duodenal switch (4.8%).
During follow-up, 13.5% of patients in the bariatric surgery group and 14.6% of people in the nonsurgery group died.
Overall, all-cause mortality was 16% lower in patients who had bariatric surgery versus matched nonsurgical participants; it was 14% lower in women and 21% lower in men (all P < .001).
All-cause mortality was significantly lower in patients who had bariatric surgery when they were 35-44, 45-54, and 55-80 years old compared with matched peers who did not have surgery.
However, the findings “should not imply patients necessarily postpone surgery until older age,” the researchers cautioned, “as postsurgical complications have been shown to increase with increasing age at surgery and surgical postponement may result in worsened clinical status related to certain conditions such as orthopedic joint health.”
The researchers found significantly improved all-cause mortality following either type of surgery (gastric bypass, gastric banding, and sleeve gastrectomy) compared with no surgery.
Along with fewer deaths from cardiovascular disease, cancer, and diabetes, deaths from lung disease were 39% lower in the surgery group than in the nonsurgery group.
However, in the youngest group (age 18-34), deaths from cirrhosis of the liver were significantly higher in the patients who had bariatric surgery, and rates of suicide were significantly greater for both females and males, compared with similar people who did not undergo surgery.
The study was supported by grants from Ethicon Endo-Surgery (Johnson & Johnson); the National Institute of Diabetes and Digestive and Kidney Diseases, a division of the National Institutes of Health; U.S. Public Health Service; and Intermountain Research and Medical Foundation of Intermountain Healthcare. Dr. Adams disclosed ties to Ethicon Endo-Surgery and Intermountain Healthcare. A coauthor reported ties with Biomedical Research Program at Weill Cornell Medicine in Qatar, a program funded by the Qatar Foundation. The other authors have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Death from cardiovascular disease, cancer, and diabetes was 29%, 43%, and 72% lower, respectively, in the bariatric surgery patients versus nonsurgery peers, during a mean follow-up of 13 years (all P > .001).
However, the youngest group of bariatric surgery patients – who were 18-34 years old – had a fivefold increased risk of suicide during follow-up compared with their peers who did not undergo surgery (P = .001).
These findings are from a retrospective study in Utah that matched close to 22,000 patients with severe obesity who underwent Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch from 1982 to 2018 with an equal number of nonsurgery individuals.
The study, by Ted D. Adams, PhD, MPH, and colleagues, was published online in Obesity.
‘Impressive’ data, in men too, but psychological screening important
The overall improved survival and decreased deaths from diabetes, heart disease, and cancer over this long follow-up are “impressive,” Dr. Adams, of Intermountain Surgical Specialties/Digestive Health Clinical Program, Salt Lake City, said in an interview.
Previous studies have not shown a survival benefit from bariatric surgery versus no surgery in men, he said. However, “because we had a fair number of male patients and because of the length of follow-up, we did show that the improved mortality was not only evident for the female patients but also for the male patients,” Dr. Adams stressed.
Finding increased suicide rates among bariatric surgical patients who underwent surgery at a younger age (18-34 years) shows that “we need to try and determine who is at risk for suicide,” according to Dr. Adams.
Patients with severe obesity, especially younger ones, “may need more aggressive presurgical psychological screening and postsurgery follow-up,” wrote Dr. Adams and colleagues.
The findings may also “stimulate important research related to the discovery of physiologic and biomolecular mechanisms leading to nonsurgical treatment that results in weight loss and improved mortality similar to that achieved by bariatric surgery,” they suggested.
Close to 1 in 10 Americans has severe obesity
The prevalence of severe obesity (BMI ≥ 40 kg/m2) in the United States has increased from 4.7% during 1999-2000 to 9.2% during 2017-2018, based on National Health and Nutrition Examination Survey (NHANES) data, the researchers noted.
They previously published a study of long-term mortality in 7,925 patients who had gastric bypass surgery from 1984 to 2002 matched with patients with the same BMI who did not have bariatric surgery and were followed out to 2002.
The current study extends the follow-up through 2021, doubles the number of bypass patients, and includes three newer types of bariatric surgery.
The researchers matched 21,873 patients aged 18-80 who had Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch during 1982-2018 in Utah (from the Utah Population Database) with people of the same BMI category, age category (18-34, 35-44, 45-54, and 55-80 years), and sex (from Utah driver license data).
Most patients were women (79%) and most were White (94% and 85%). They had a mean age of 42 years and a mean BMI of 46 kg/m2.
Most patients had Roux-en-Y gastric bypass (69%), and the rest had sleeve gastrectomy (14%), gastric banding (12%), and duodenal switch (4.8%).
During follow-up, 13.5% of patients in the bariatric surgery group and 14.6% of people in the nonsurgery group died.
Overall, all-cause mortality was 16% lower in patients who had bariatric surgery versus matched nonsurgical participants; it was 14% lower in women and 21% lower in men (all P < .001).
All-cause mortality was significantly lower in patients who had bariatric surgery when they were 35-44, 45-54, and 55-80 years old compared with matched peers who did not have surgery.
However, the findings “should not imply patients necessarily postpone surgery until older age,” the researchers cautioned, “as postsurgical complications have been shown to increase with increasing age at surgery and surgical postponement may result in worsened clinical status related to certain conditions such as orthopedic joint health.”
The researchers found significantly improved all-cause mortality following either type of surgery (gastric bypass, gastric banding, and sleeve gastrectomy) compared with no surgery.
Along with fewer deaths from cardiovascular disease, cancer, and diabetes, deaths from lung disease were 39% lower in the surgery group than in the nonsurgery group.
However, in the youngest group (age 18-34), deaths from cirrhosis of the liver were significantly higher in the patients who had bariatric surgery, and rates of suicide were significantly greater for both females and males, compared with similar people who did not undergo surgery.
The study was supported by grants from Ethicon Endo-Surgery (Johnson & Johnson); the National Institute of Diabetes and Digestive and Kidney Diseases, a division of the National Institutes of Health; U.S. Public Health Service; and Intermountain Research and Medical Foundation of Intermountain Healthcare. Dr. Adams disclosed ties to Ethicon Endo-Surgery and Intermountain Healthcare. A coauthor reported ties with Biomedical Research Program at Weill Cornell Medicine in Qatar, a program funded by the Qatar Foundation. The other authors have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM OBESITY
Study documents link between preadolescent acne and elevated BMI
The that used age- and sex-matched controls.
The investigators also identified “a potential association” with precocious puberty that they said “should be considered, especially among those presenting [with acne] under 8 or 9 years old.” The study was published in Pediatric Dermatology .
Senior author Megha M. Tollefson, MD, and coauthors used resources of the Rochester Epidemiology Project to identify all residents of Olmstead County, Minn., who were diagnosed with acne between the ages of 7 and 12 years during 2010-2018. They then randomly selected two age and sex-matched community controls in order to evaluate the relationship of preadolescent acne and BMI.
They confirmed 643 acne cases, and calculated an annual age- and sex-adjusted incidence rate for ages 7-12 of 58 per 10,000 person-years (95% confidence interval, 53.5-62.5). The incidence rate was significantly higher in females than males (89.2 vs. 28.2 per 10,000 person-years; P < .001), and it significantly increased with age (incidence rates of 4.3, 24.4, and 144.3 per 10,000 person-years among those ages 7-8, 9-10, and 11-12 years, respectively).
The median BMI percentile among children with acne was significantly higher than those without an acne diagnosis (75.0 vs. 65.0; P <.001). They also were much more likely to be obese: 16.7% of the children with acne had a BMI in at least the 95th percentile, compared with 12.2% among controls with no acne diagnosis (P = .01). (The qualifying 581 acne cases for this analysis had BMIs recorded within 8 months of the index data, in addition to not having pre-existing acne-relevant endocrine disorders.)
“High BMI is a strong risk factor for acne development and severity in adults, but until now pediatric studies have revealed mixed information ... [and have been] largely retrospective reviews without controls,” Dr. Tollefson, professor of pediatrics and dermatology at the Mayo Clinic, Rochester, Minn., and colleagues wrote.
‘Valuable’ data
Leah Lalor, MD, a pediatric dermatologist not involved with the research, said she is happy to see it. “It’s really valuable,” she said in an interview. “It’s actually the first study that gives us incidence data for preadolescent acne. We all have [had our estimates], but this study quantifies it ... and it will set the stage for further studies of preadolescents in the future.”
The study also documents that “girls are more likely to present to the clinic with acne, and to do so at younger ages, which we’ve suspected and which makes physiologic sense since girls tend to go through puberty earlier than boys,” said Dr. Lalor, assistant professor of dermatology and pediatrics at the Medical College of Wisconsin and the Children’s Wisconsin Clinics, both in Milwaukee. “And most interestingly, it really reveals that BMI is higher among preadolescents with acne than those without.”
The important caveat, she emphasized, is that the study population in Olmstead County, Minn. has a relatively higher level of education, wealth, and employment than the rest of the United States.
The investigators also found that use of systemic acne medications increased with increasing BMI (odds ratio, 1.43 per 5 kg/m2 increase in BMI; 95% CI, 1.07-1.92; P = .015). Approximately 5% of underweight or normal children were prescribed systemic acne medications, compared with 8.1% of overweight children, and 10.3% of those who were obese – data that suggest that most preadolescents with acne had mild to moderate disease and that more severe acne may be associated with increasing BMI percentiles, the authors wrote.
Approximately 4% of the 643 preadolescents with acne were diagnosed with an acne-relevant endocrine disorder prior to or at the time of acne diagnosis – most commonly precocious puberty. Of the 24 diagnoses of precocious puberty, 22 were in females, with a mean age at diagnosis of 7.3 years.
Puberty before age 8 in girls and 9 in boys is classified as precocious puberty. “Thus, a thorough review of systems and exam should be done in this population [with acne] to look for precocious puberty with a low threshold for systemic evaluation if indicated,” the authors wrote, also noting that 19 or the 482 female patients with acne were subsequently diagnosed with polycystic ovary syndrome.
Dr. Lalor said she “automatically” refers children with acne who are younger than 7 for an endocrine workup, but not necessarily children ages 7, 8, or 9 because “that’s considered within the normal realm of starting to get some acne.” Acne in the context of other symptoms such as body odor, hair, or thelarche may prompt referral in these ages, however, she said.
Future research
Obesity may influence preadolescent acne development through its effect on puberty, as overweight and obese girls achieve puberty earlier than those with normal BMI. And “insulin resistance, which may be related to obesity, has been implicated with inducing or worsening acne potentially related to shifts in IGF-1 [insulin-like growth factor 1] signaling and hyperandrogenemia,” Dr. Tollefson and colleagues wrote. Nutrition is also a possible confounder in the study.
“Patients and families have long felt that certain foods or practices contribute to acne, though this has been difficult to prove,” Dr. Lalor said. “We know that excess skim milk seems to contribute ... and there’s a correlation between high glycemic load diets [and acne].”
Assessing dietary habits in conjunction with BMI, and acne incidence and severity, would be valuable. So would research to determine “if decreasing the BMI percentile [in children with acne] would improve or prevent acne, without doing any acne treatments,” she said.
The study was supported by the National Institute on Aging and the Rochester Epidemiology Project. The authors reported no conflicts of interest. Dr. Lalor also reported no conflicts of interest.
The that used age- and sex-matched controls.
The investigators also identified “a potential association” with precocious puberty that they said “should be considered, especially among those presenting [with acne] under 8 or 9 years old.” The study was published in Pediatric Dermatology .
Senior author Megha M. Tollefson, MD, and coauthors used resources of the Rochester Epidemiology Project to identify all residents of Olmstead County, Minn., who were diagnosed with acne between the ages of 7 and 12 years during 2010-2018. They then randomly selected two age and sex-matched community controls in order to evaluate the relationship of preadolescent acne and BMI.
They confirmed 643 acne cases, and calculated an annual age- and sex-adjusted incidence rate for ages 7-12 of 58 per 10,000 person-years (95% confidence interval, 53.5-62.5). The incidence rate was significantly higher in females than males (89.2 vs. 28.2 per 10,000 person-years; P < .001), and it significantly increased with age (incidence rates of 4.3, 24.4, and 144.3 per 10,000 person-years among those ages 7-8, 9-10, and 11-12 years, respectively).
The median BMI percentile among children with acne was significantly higher than those without an acne diagnosis (75.0 vs. 65.0; P <.001). They also were much more likely to be obese: 16.7% of the children with acne had a BMI in at least the 95th percentile, compared with 12.2% among controls with no acne diagnosis (P = .01). (The qualifying 581 acne cases for this analysis had BMIs recorded within 8 months of the index data, in addition to not having pre-existing acne-relevant endocrine disorders.)
“High BMI is a strong risk factor for acne development and severity in adults, but until now pediatric studies have revealed mixed information ... [and have been] largely retrospective reviews without controls,” Dr. Tollefson, professor of pediatrics and dermatology at the Mayo Clinic, Rochester, Minn., and colleagues wrote.
‘Valuable’ data
Leah Lalor, MD, a pediatric dermatologist not involved with the research, said she is happy to see it. “It’s really valuable,” she said in an interview. “It’s actually the first study that gives us incidence data for preadolescent acne. We all have [had our estimates], but this study quantifies it ... and it will set the stage for further studies of preadolescents in the future.”
The study also documents that “girls are more likely to present to the clinic with acne, and to do so at younger ages, which we’ve suspected and which makes physiologic sense since girls tend to go through puberty earlier than boys,” said Dr. Lalor, assistant professor of dermatology and pediatrics at the Medical College of Wisconsin and the Children’s Wisconsin Clinics, both in Milwaukee. “And most interestingly, it really reveals that BMI is higher among preadolescents with acne than those without.”
The important caveat, she emphasized, is that the study population in Olmstead County, Minn. has a relatively higher level of education, wealth, and employment than the rest of the United States.
The investigators also found that use of systemic acne medications increased with increasing BMI (odds ratio, 1.43 per 5 kg/m2 increase in BMI; 95% CI, 1.07-1.92; P = .015). Approximately 5% of underweight or normal children were prescribed systemic acne medications, compared with 8.1% of overweight children, and 10.3% of those who were obese – data that suggest that most preadolescents with acne had mild to moderate disease and that more severe acne may be associated with increasing BMI percentiles, the authors wrote.
Approximately 4% of the 643 preadolescents with acne were diagnosed with an acne-relevant endocrine disorder prior to or at the time of acne diagnosis – most commonly precocious puberty. Of the 24 diagnoses of precocious puberty, 22 were in females, with a mean age at diagnosis of 7.3 years.
Puberty before age 8 in girls and 9 in boys is classified as precocious puberty. “Thus, a thorough review of systems and exam should be done in this population [with acne] to look for precocious puberty with a low threshold for systemic evaluation if indicated,” the authors wrote, also noting that 19 or the 482 female patients with acne were subsequently diagnosed with polycystic ovary syndrome.
Dr. Lalor said she “automatically” refers children with acne who are younger than 7 for an endocrine workup, but not necessarily children ages 7, 8, or 9 because “that’s considered within the normal realm of starting to get some acne.” Acne in the context of other symptoms such as body odor, hair, or thelarche may prompt referral in these ages, however, she said.
Future research
Obesity may influence preadolescent acne development through its effect on puberty, as overweight and obese girls achieve puberty earlier than those with normal BMI. And “insulin resistance, which may be related to obesity, has been implicated with inducing or worsening acne potentially related to shifts in IGF-1 [insulin-like growth factor 1] signaling and hyperandrogenemia,” Dr. Tollefson and colleagues wrote. Nutrition is also a possible confounder in the study.
“Patients and families have long felt that certain foods or practices contribute to acne, though this has been difficult to prove,” Dr. Lalor said. “We know that excess skim milk seems to contribute ... and there’s a correlation between high glycemic load diets [and acne].”
Assessing dietary habits in conjunction with BMI, and acne incidence and severity, would be valuable. So would research to determine “if decreasing the BMI percentile [in children with acne] would improve or prevent acne, without doing any acne treatments,” she said.
The study was supported by the National Institute on Aging and the Rochester Epidemiology Project. The authors reported no conflicts of interest. Dr. Lalor also reported no conflicts of interest.
The that used age- and sex-matched controls.
The investigators also identified “a potential association” with precocious puberty that they said “should be considered, especially among those presenting [with acne] under 8 or 9 years old.” The study was published in Pediatric Dermatology .
Senior author Megha M. Tollefson, MD, and coauthors used resources of the Rochester Epidemiology Project to identify all residents of Olmstead County, Minn., who were diagnosed with acne between the ages of 7 and 12 years during 2010-2018. They then randomly selected two age and sex-matched community controls in order to evaluate the relationship of preadolescent acne and BMI.
They confirmed 643 acne cases, and calculated an annual age- and sex-adjusted incidence rate for ages 7-12 of 58 per 10,000 person-years (95% confidence interval, 53.5-62.5). The incidence rate was significantly higher in females than males (89.2 vs. 28.2 per 10,000 person-years; P < .001), and it significantly increased with age (incidence rates of 4.3, 24.4, and 144.3 per 10,000 person-years among those ages 7-8, 9-10, and 11-12 years, respectively).
The median BMI percentile among children with acne was significantly higher than those without an acne diagnosis (75.0 vs. 65.0; P <.001). They also were much more likely to be obese: 16.7% of the children with acne had a BMI in at least the 95th percentile, compared with 12.2% among controls with no acne diagnosis (P = .01). (The qualifying 581 acne cases for this analysis had BMIs recorded within 8 months of the index data, in addition to not having pre-existing acne-relevant endocrine disorders.)
“High BMI is a strong risk factor for acne development and severity in adults, but until now pediatric studies have revealed mixed information ... [and have been] largely retrospective reviews without controls,” Dr. Tollefson, professor of pediatrics and dermatology at the Mayo Clinic, Rochester, Minn., and colleagues wrote.
‘Valuable’ data
Leah Lalor, MD, a pediatric dermatologist not involved with the research, said she is happy to see it. “It’s really valuable,” she said in an interview. “It’s actually the first study that gives us incidence data for preadolescent acne. We all have [had our estimates], but this study quantifies it ... and it will set the stage for further studies of preadolescents in the future.”
The study also documents that “girls are more likely to present to the clinic with acne, and to do so at younger ages, which we’ve suspected and which makes physiologic sense since girls tend to go through puberty earlier than boys,” said Dr. Lalor, assistant professor of dermatology and pediatrics at the Medical College of Wisconsin and the Children’s Wisconsin Clinics, both in Milwaukee. “And most interestingly, it really reveals that BMI is higher among preadolescents with acne than those without.”
The important caveat, she emphasized, is that the study population in Olmstead County, Minn. has a relatively higher level of education, wealth, and employment than the rest of the United States.
The investigators also found that use of systemic acne medications increased with increasing BMI (odds ratio, 1.43 per 5 kg/m2 increase in BMI; 95% CI, 1.07-1.92; P = .015). Approximately 5% of underweight or normal children were prescribed systemic acne medications, compared with 8.1% of overweight children, and 10.3% of those who were obese – data that suggest that most preadolescents with acne had mild to moderate disease and that more severe acne may be associated with increasing BMI percentiles, the authors wrote.
Approximately 4% of the 643 preadolescents with acne were diagnosed with an acne-relevant endocrine disorder prior to or at the time of acne diagnosis – most commonly precocious puberty. Of the 24 diagnoses of precocious puberty, 22 were in females, with a mean age at diagnosis of 7.3 years.
Puberty before age 8 in girls and 9 in boys is classified as precocious puberty. “Thus, a thorough review of systems and exam should be done in this population [with acne] to look for precocious puberty with a low threshold for systemic evaluation if indicated,” the authors wrote, also noting that 19 or the 482 female patients with acne were subsequently diagnosed with polycystic ovary syndrome.
Dr. Lalor said she “automatically” refers children with acne who are younger than 7 for an endocrine workup, but not necessarily children ages 7, 8, or 9 because “that’s considered within the normal realm of starting to get some acne.” Acne in the context of other symptoms such as body odor, hair, or thelarche may prompt referral in these ages, however, she said.
Future research
Obesity may influence preadolescent acne development through its effect on puberty, as overweight and obese girls achieve puberty earlier than those with normal BMI. And “insulin resistance, which may be related to obesity, has been implicated with inducing or worsening acne potentially related to shifts in IGF-1 [insulin-like growth factor 1] signaling and hyperandrogenemia,” Dr. Tollefson and colleagues wrote. Nutrition is also a possible confounder in the study.
“Patients and families have long felt that certain foods or practices contribute to acne, though this has been difficult to prove,” Dr. Lalor said. “We know that excess skim milk seems to contribute ... and there’s a correlation between high glycemic load diets [and acne].”
Assessing dietary habits in conjunction with BMI, and acne incidence and severity, would be valuable. So would research to determine “if decreasing the BMI percentile [in children with acne] would improve or prevent acne, without doing any acne treatments,” she said.
The study was supported by the National Institute on Aging and the Rochester Epidemiology Project. The authors reported no conflicts of interest. Dr. Lalor also reported no conflicts of interest.
FROM PEDIATRIC DERMATOLOGY
Keto for life? Reasons to think twice
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.
Almonds may be a good diet option
according to researchers at the University of South Australia’s Alliance for Research in Exercise, Nutrition and Activity.
What to know
People who consume as few as 30-50 g of almonds, as opposed to an energy-equivalent carbohydrate snack, can lower their energy intake significantly at the subsequent meal.
People who eat almonds can experience changes in their appetite-regulating hormones that may contribute to less food intake.
Almond consumption can lower C-peptide responses, which can improve insulin sensitivity and reduce the risk of developing diabetes and cardiovascular disease.
Eating almonds can raise levels of glucose-dependent insulinotropic polypeptide glucagon, which can send satiety signals to the brain, and pancreatic polypeptide, which slows digestion, which may reduce food intake, supporting weight loss.
Almonds are high in protein, fiber, and unsaturated fatty acids, which may contribute to their satiating properties and help explain why fewer calories are consumed.
A version of this article originally appeared on Medscape.com.
This is a summary of the article “Acute Feeding With Almonds Compared to a Carbohydrate-Based Snack Improves Appetite-Regulating Hormones With No Effect on Self-reported Appetite Sensations: A Randomised Controlled Trial,” published in the European Journal of Nutrition on Oct. 11, 2022. The full article can be found on link.springer.com.
according to researchers at the University of South Australia’s Alliance for Research in Exercise, Nutrition and Activity.
What to know
People who consume as few as 30-50 g of almonds, as opposed to an energy-equivalent carbohydrate snack, can lower their energy intake significantly at the subsequent meal.
People who eat almonds can experience changes in their appetite-regulating hormones that may contribute to less food intake.
Almond consumption can lower C-peptide responses, which can improve insulin sensitivity and reduce the risk of developing diabetes and cardiovascular disease.
Eating almonds can raise levels of glucose-dependent insulinotropic polypeptide glucagon, which can send satiety signals to the brain, and pancreatic polypeptide, which slows digestion, which may reduce food intake, supporting weight loss.
Almonds are high in protein, fiber, and unsaturated fatty acids, which may contribute to their satiating properties and help explain why fewer calories are consumed.
A version of this article originally appeared on Medscape.com.
This is a summary of the article “Acute Feeding With Almonds Compared to a Carbohydrate-Based Snack Improves Appetite-Regulating Hormones With No Effect on Self-reported Appetite Sensations: A Randomised Controlled Trial,” published in the European Journal of Nutrition on Oct. 11, 2022. The full article can be found on link.springer.com.
according to researchers at the University of South Australia’s Alliance for Research in Exercise, Nutrition and Activity.
What to know
People who consume as few as 30-50 g of almonds, as opposed to an energy-equivalent carbohydrate snack, can lower their energy intake significantly at the subsequent meal.
People who eat almonds can experience changes in their appetite-regulating hormones that may contribute to less food intake.
Almond consumption can lower C-peptide responses, which can improve insulin sensitivity and reduce the risk of developing diabetes and cardiovascular disease.
Eating almonds can raise levels of glucose-dependent insulinotropic polypeptide glucagon, which can send satiety signals to the brain, and pancreatic polypeptide, which slows digestion, which may reduce food intake, supporting weight loss.
Almonds are high in protein, fiber, and unsaturated fatty acids, which may contribute to their satiating properties and help explain why fewer calories are consumed.
A version of this article originally appeared on Medscape.com.
This is a summary of the article “Acute Feeding With Almonds Compared to a Carbohydrate-Based Snack Improves Appetite-Regulating Hormones With No Effect on Self-reported Appetite Sensations: A Randomised Controlled Trial,” published in the European Journal of Nutrition on Oct. 11, 2022. The full article can be found on link.springer.com.
FROM THE EUROPEAN JOURNAL OF NUTRITION
Commenting on weight’s not rude. It’s dangerous.
It was the start of the fall semester of my sophomore year of college.
At my small women’s college, the previous semester’s gossip had been about our classmate, S*. She had gone from being very thin to noticeably gaining a lot of weight in a few months. The rumors were that S was pregnant and gave birth over summer break. As a busy biology premed major, this was my first time hearing the news. So when I saw her standing in the hallway, back to her previous weight, I was excited for her.
In true extravert fashion, I commented on the baby and her new size. But no sooner had the words left my mouth than I regretted them.
The hall grew awkwardly silent as S’s face flushed and she asked, “Excuse me?!” Instantly I knew that the rumors weren’t true.
Thankfully, at that moment, the classroom opened and we walked in. Whew! After class, S asked if we could talk. She explained that she had a thyroid tumor and struggled to adjust to the treatments, which caused her weight fluctuations. She had never been pregnant.
My awkward statement had been the first time anyone on campus had directly mentioned her weight, though she suspected that people were talking about her. We became fast friends after this rocky beginning. Although we lost touch after college, S taught me an invaluable lesson about making assumptions about people’s weight: Ask before you assume.
Now, years later, as an internist and obesity specialist, this lesson continues to be reinforced daily.
In daily life, comments about weight can be perceived as rude. In the clinical setting, however, assumptions about weight are a form of weight bias. Weight bias can lead to weight stigma and even be dangerous to health care.
Let’s discuss the insidious influence of weight bias in health care through two commonly used phrases and then look at a few solutions to address weight bias in health care individually and systematically.
Common weight bias assumptions
“Great job, you lost weight!” In checking your patient’s vital signs, you notice that this patient with obesity has a significant weight change. You congratulate them upon entering the room. Unfortunately, their weight loss was a result of minimal eating after losing a loved one. This isn’t healthy weight loss. One of the adverse effects of weight bias is that it infers that weight loss is always a good thing, especially in people with larger bodies. This is a dangerous presumption. Let’s remember that the body favors fat storage, hence why “unintentional weight loss” is a recognized medical condition prompting evaluation. We have to be careful not to celebrate weight loss “at all costs,” such as fad diets that haven’t been shown to improve health outcomes.
Furthermore, patients who lose weight quickly (more than 4-8 lb/month) require closer follow-up and evaluation for secondary causes of weight loss. Patients may lose weight at a faster rate with the new antiobesity medications, but clinicians still should ensure that age-appropriate health maintenance screening is done and be vigilant for secondary causes of weight changes.
“Have you tried losing weight yet?” Three times. That’s how many times Chanté Burkett went to her doctor about her painful, enlarging firm stomach. She was advised to continue working on weight loss, which she did diligently. But Ms. Burkett’s abdomen kept growing and her concerns were dismissed. A visit to urgent care and a CT scan revealed that Ms. Burkett’s excess abdominal “fat” was a 13-lb mucinous cystadenoma. Sadly, cases like hers aren’t rare, isolated events. Weight bias can cause anchoring on one diagnosis, preventing consideration of other diagnostic possibilities. Even worse, anchoring will lead to the wrong intervention, such as prescribing weight loss for presumed increased adiposity instead of ordering the appropriate testing.
It’s also essential to recognize that, even if someone does have the disease of obesity, weight loss isn’t the solution to every medical concern. Even if weight loss is helpful, other, more pressing treatments may still be necessary. Telling a person with obesity who has an acute complaint to “just lose weight” is comparable to telling a patient with coronary artery disease who presents with an 80% vessel occlusion and chest pain to follow a low-fat diet. In both cases, you need to address the acute concern appropriately, then focus on the chronic treatment.
Ways to reduce clinical weight bias
How do you reduce clinical weight bias?
Ask, don’t assume. The information from the scale is simply data. Instead of judging it positively or negatively and creating a story, ask the patient. An unbiased way to approach the conversation is to say, “Great to see you. You seem [positive adjective of choice]. How have you been?” Wait until the vitals section to objectively discuss weight unless the patient offers the discussion earlier or their chief complaint lists a weight-related concern.
Order necessary tests to evaluate weight. Weight is the vital sign that people wear externally, so we feel that we can readily interpret it without any further assessment. However, resist the urge to interpret scale data without context. Keeping an open mind helps prevent anchoring and missing critical clues in the clinical history.
Address weight changes effectively. Sometimes there is an indication to prescribe weight loss as part of the treatment plan. However, remember that weight loss isn’t simply “calories in vs. calories out.” Obesity is a complex medical disease that requires a multimodal treatment approach. As clinicians, we have access to the most powerful tools for weight loss. Unfortunately, weight bias contributes to limited prescribing of metabolic medications (“antiobesity medications” or AOMs). In addition, systemic weight bias prevents insurance coverage of AOMs. The Treat and Reduce Obesity Act has been introduced into Congress to help improve life-transforming access to AOMs.
Acknowledge your bias. Our experiences make us all susceptible to bias. The Harvard Weight Implicit Association Test is free and a helpful way to assess your level of weight bias. I take it annually to ensure that I remain objective in my practice.
Addressing weight bias needs to extend beyond the individual level.
Systemically, health care needs to address the following:
Language. Use people-centered language. For example, “People aren’t obese. They have obesity.”
Accessibility. Health care settings must be comfortable and accessible for people of all sizes. Furthermore, improvements to access the services that comprehensive obesity care requires, such as AOMs, bariatric procedures and bariatric surgery, mental health care, nutrition, fitness specialists, health coaches, and more, are needed.
Education. Medical students and trainees have to learn the newest obesity science and know how to treat obesity effectively. Acknowledge and address biased tools. Recent data have shown that some of our screening tools, such as body mass index, have inherent bias. It’s time to focus on using improved diagnostic tools and personalized treatments.
We are at a pivotal time in our scientific understanding of body weight regulation and the disease of obesity. Clinical weight bias is primarily rooted in flawed science influenced by biased cultural norms and other forms of discrimination, such as racial and gender bias. We must move past assumptions to give our patients the optimal individualized care they need. So next time you observe a weight change, instead of commenting on their weight, say, “Great to see you! How have you been?”
S*: Initial has been changed to protect privacy.
Dr. Gonsahn-Bollie is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Connect with her at www.embraceyouweightloss.com or on Instagram @embraceyoumd. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness”, was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She has disclosed no relevant financial relationships. A version of this article originally appeared on Medscape.com.
It was the start of the fall semester of my sophomore year of college.
At my small women’s college, the previous semester’s gossip had been about our classmate, S*. She had gone from being very thin to noticeably gaining a lot of weight in a few months. The rumors were that S was pregnant and gave birth over summer break. As a busy biology premed major, this was my first time hearing the news. So when I saw her standing in the hallway, back to her previous weight, I was excited for her.
In true extravert fashion, I commented on the baby and her new size. But no sooner had the words left my mouth than I regretted them.
The hall grew awkwardly silent as S’s face flushed and she asked, “Excuse me?!” Instantly I knew that the rumors weren’t true.
Thankfully, at that moment, the classroom opened and we walked in. Whew! After class, S asked if we could talk. She explained that she had a thyroid tumor and struggled to adjust to the treatments, which caused her weight fluctuations. She had never been pregnant.
My awkward statement had been the first time anyone on campus had directly mentioned her weight, though she suspected that people were talking about her. We became fast friends after this rocky beginning. Although we lost touch after college, S taught me an invaluable lesson about making assumptions about people’s weight: Ask before you assume.
Now, years later, as an internist and obesity specialist, this lesson continues to be reinforced daily.
In daily life, comments about weight can be perceived as rude. In the clinical setting, however, assumptions about weight are a form of weight bias. Weight bias can lead to weight stigma and even be dangerous to health care.
Let’s discuss the insidious influence of weight bias in health care through two commonly used phrases and then look at a few solutions to address weight bias in health care individually and systematically.
Common weight bias assumptions
“Great job, you lost weight!” In checking your patient’s vital signs, you notice that this patient with obesity has a significant weight change. You congratulate them upon entering the room. Unfortunately, their weight loss was a result of minimal eating after losing a loved one. This isn’t healthy weight loss. One of the adverse effects of weight bias is that it infers that weight loss is always a good thing, especially in people with larger bodies. This is a dangerous presumption. Let’s remember that the body favors fat storage, hence why “unintentional weight loss” is a recognized medical condition prompting evaluation. We have to be careful not to celebrate weight loss “at all costs,” such as fad diets that haven’t been shown to improve health outcomes.
Furthermore, patients who lose weight quickly (more than 4-8 lb/month) require closer follow-up and evaluation for secondary causes of weight loss. Patients may lose weight at a faster rate with the new antiobesity medications, but clinicians still should ensure that age-appropriate health maintenance screening is done and be vigilant for secondary causes of weight changes.
“Have you tried losing weight yet?” Three times. That’s how many times Chanté Burkett went to her doctor about her painful, enlarging firm stomach. She was advised to continue working on weight loss, which she did diligently. But Ms. Burkett’s abdomen kept growing and her concerns were dismissed. A visit to urgent care and a CT scan revealed that Ms. Burkett’s excess abdominal “fat” was a 13-lb mucinous cystadenoma. Sadly, cases like hers aren’t rare, isolated events. Weight bias can cause anchoring on one diagnosis, preventing consideration of other diagnostic possibilities. Even worse, anchoring will lead to the wrong intervention, such as prescribing weight loss for presumed increased adiposity instead of ordering the appropriate testing.
It’s also essential to recognize that, even if someone does have the disease of obesity, weight loss isn’t the solution to every medical concern. Even if weight loss is helpful, other, more pressing treatments may still be necessary. Telling a person with obesity who has an acute complaint to “just lose weight” is comparable to telling a patient with coronary artery disease who presents with an 80% vessel occlusion and chest pain to follow a low-fat diet. In both cases, you need to address the acute concern appropriately, then focus on the chronic treatment.
Ways to reduce clinical weight bias
How do you reduce clinical weight bias?
Ask, don’t assume. The information from the scale is simply data. Instead of judging it positively or negatively and creating a story, ask the patient. An unbiased way to approach the conversation is to say, “Great to see you. You seem [positive adjective of choice]. How have you been?” Wait until the vitals section to objectively discuss weight unless the patient offers the discussion earlier or their chief complaint lists a weight-related concern.
Order necessary tests to evaluate weight. Weight is the vital sign that people wear externally, so we feel that we can readily interpret it without any further assessment. However, resist the urge to interpret scale data without context. Keeping an open mind helps prevent anchoring and missing critical clues in the clinical history.
Address weight changes effectively. Sometimes there is an indication to prescribe weight loss as part of the treatment plan. However, remember that weight loss isn’t simply “calories in vs. calories out.” Obesity is a complex medical disease that requires a multimodal treatment approach. As clinicians, we have access to the most powerful tools for weight loss. Unfortunately, weight bias contributes to limited prescribing of metabolic medications (“antiobesity medications” or AOMs). In addition, systemic weight bias prevents insurance coverage of AOMs. The Treat and Reduce Obesity Act has been introduced into Congress to help improve life-transforming access to AOMs.
Acknowledge your bias. Our experiences make us all susceptible to bias. The Harvard Weight Implicit Association Test is free and a helpful way to assess your level of weight bias. I take it annually to ensure that I remain objective in my practice.
Addressing weight bias needs to extend beyond the individual level.
Systemically, health care needs to address the following:
Language. Use people-centered language. For example, “People aren’t obese. They have obesity.”
Accessibility. Health care settings must be comfortable and accessible for people of all sizes. Furthermore, improvements to access the services that comprehensive obesity care requires, such as AOMs, bariatric procedures and bariatric surgery, mental health care, nutrition, fitness specialists, health coaches, and more, are needed.
Education. Medical students and trainees have to learn the newest obesity science and know how to treat obesity effectively. Acknowledge and address biased tools. Recent data have shown that some of our screening tools, such as body mass index, have inherent bias. It’s time to focus on using improved diagnostic tools and personalized treatments.
We are at a pivotal time in our scientific understanding of body weight regulation and the disease of obesity. Clinical weight bias is primarily rooted in flawed science influenced by biased cultural norms and other forms of discrimination, such as racial and gender bias. We must move past assumptions to give our patients the optimal individualized care they need. So next time you observe a weight change, instead of commenting on their weight, say, “Great to see you! How have you been?”
S*: Initial has been changed to protect privacy.
Dr. Gonsahn-Bollie is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Connect with her at www.embraceyouweightloss.com or on Instagram @embraceyoumd. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness”, was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She has disclosed no relevant financial relationships. A version of this article originally appeared on Medscape.com.
It was the start of the fall semester of my sophomore year of college.
At my small women’s college, the previous semester’s gossip had been about our classmate, S*. She had gone from being very thin to noticeably gaining a lot of weight in a few months. The rumors were that S was pregnant and gave birth over summer break. As a busy biology premed major, this was my first time hearing the news. So when I saw her standing in the hallway, back to her previous weight, I was excited for her.
In true extravert fashion, I commented on the baby and her new size. But no sooner had the words left my mouth than I regretted them.
The hall grew awkwardly silent as S’s face flushed and she asked, “Excuse me?!” Instantly I knew that the rumors weren’t true.
Thankfully, at that moment, the classroom opened and we walked in. Whew! After class, S asked if we could talk. She explained that she had a thyroid tumor and struggled to adjust to the treatments, which caused her weight fluctuations. She had never been pregnant.
My awkward statement had been the first time anyone on campus had directly mentioned her weight, though she suspected that people were talking about her. We became fast friends after this rocky beginning. Although we lost touch after college, S taught me an invaluable lesson about making assumptions about people’s weight: Ask before you assume.
Now, years later, as an internist and obesity specialist, this lesson continues to be reinforced daily.
In daily life, comments about weight can be perceived as rude. In the clinical setting, however, assumptions about weight are a form of weight bias. Weight bias can lead to weight stigma and even be dangerous to health care.
Let’s discuss the insidious influence of weight bias in health care through two commonly used phrases and then look at a few solutions to address weight bias in health care individually and systematically.
Common weight bias assumptions
“Great job, you lost weight!” In checking your patient’s vital signs, you notice that this patient with obesity has a significant weight change. You congratulate them upon entering the room. Unfortunately, their weight loss was a result of minimal eating after losing a loved one. This isn’t healthy weight loss. One of the adverse effects of weight bias is that it infers that weight loss is always a good thing, especially in people with larger bodies. This is a dangerous presumption. Let’s remember that the body favors fat storage, hence why “unintentional weight loss” is a recognized medical condition prompting evaluation. We have to be careful not to celebrate weight loss “at all costs,” such as fad diets that haven’t been shown to improve health outcomes.
Furthermore, patients who lose weight quickly (more than 4-8 lb/month) require closer follow-up and evaluation for secondary causes of weight loss. Patients may lose weight at a faster rate with the new antiobesity medications, but clinicians still should ensure that age-appropriate health maintenance screening is done and be vigilant for secondary causes of weight changes.
“Have you tried losing weight yet?” Three times. That’s how many times Chanté Burkett went to her doctor about her painful, enlarging firm stomach. She was advised to continue working on weight loss, which she did diligently. But Ms. Burkett’s abdomen kept growing and her concerns were dismissed. A visit to urgent care and a CT scan revealed that Ms. Burkett’s excess abdominal “fat” was a 13-lb mucinous cystadenoma. Sadly, cases like hers aren’t rare, isolated events. Weight bias can cause anchoring on one diagnosis, preventing consideration of other diagnostic possibilities. Even worse, anchoring will lead to the wrong intervention, such as prescribing weight loss for presumed increased adiposity instead of ordering the appropriate testing.
It’s also essential to recognize that, even if someone does have the disease of obesity, weight loss isn’t the solution to every medical concern. Even if weight loss is helpful, other, more pressing treatments may still be necessary. Telling a person with obesity who has an acute complaint to “just lose weight” is comparable to telling a patient with coronary artery disease who presents with an 80% vessel occlusion and chest pain to follow a low-fat diet. In both cases, you need to address the acute concern appropriately, then focus on the chronic treatment.
Ways to reduce clinical weight bias
How do you reduce clinical weight bias?
Ask, don’t assume. The information from the scale is simply data. Instead of judging it positively or negatively and creating a story, ask the patient. An unbiased way to approach the conversation is to say, “Great to see you. You seem [positive adjective of choice]. How have you been?” Wait until the vitals section to objectively discuss weight unless the patient offers the discussion earlier or their chief complaint lists a weight-related concern.
Order necessary tests to evaluate weight. Weight is the vital sign that people wear externally, so we feel that we can readily interpret it without any further assessment. However, resist the urge to interpret scale data without context. Keeping an open mind helps prevent anchoring and missing critical clues in the clinical history.
Address weight changes effectively. Sometimes there is an indication to prescribe weight loss as part of the treatment plan. However, remember that weight loss isn’t simply “calories in vs. calories out.” Obesity is a complex medical disease that requires a multimodal treatment approach. As clinicians, we have access to the most powerful tools for weight loss. Unfortunately, weight bias contributes to limited prescribing of metabolic medications (“antiobesity medications” or AOMs). In addition, systemic weight bias prevents insurance coverage of AOMs. The Treat and Reduce Obesity Act has been introduced into Congress to help improve life-transforming access to AOMs.
Acknowledge your bias. Our experiences make us all susceptible to bias. The Harvard Weight Implicit Association Test is free and a helpful way to assess your level of weight bias. I take it annually to ensure that I remain objective in my practice.
Addressing weight bias needs to extend beyond the individual level.
Systemically, health care needs to address the following:
Language. Use people-centered language. For example, “People aren’t obese. They have obesity.”
Accessibility. Health care settings must be comfortable and accessible for people of all sizes. Furthermore, improvements to access the services that comprehensive obesity care requires, such as AOMs, bariatric procedures and bariatric surgery, mental health care, nutrition, fitness specialists, health coaches, and more, are needed.
Education. Medical students and trainees have to learn the newest obesity science and know how to treat obesity effectively. Acknowledge and address biased tools. Recent data have shown that some of our screening tools, such as body mass index, have inherent bias. It’s time to focus on using improved diagnostic tools and personalized treatments.
We are at a pivotal time in our scientific understanding of body weight regulation and the disease of obesity. Clinical weight bias is primarily rooted in flawed science influenced by biased cultural norms and other forms of discrimination, such as racial and gender bias. We must move past assumptions to give our patients the optimal individualized care they need. So next time you observe a weight change, instead of commenting on their weight, say, “Great to see you! How have you been?”
S*: Initial has been changed to protect privacy.
Dr. Gonsahn-Bollie is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Connect with her at www.embraceyouweightloss.com or on Instagram @embraceyoumd. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness”, was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She has disclosed no relevant financial relationships. A version of this article originally appeared on Medscape.com.
‘Ozempic face’: Accepting wrinkles for improved health
This transcript has been edited for clarity.
Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.
I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.
Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.
The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.
What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.
It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.
Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.
I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.
Thank you.
Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.
I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.
Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.
The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.
What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.
It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.
Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.
I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.
Thank you.
Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.
I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.
Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.
The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.
What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.
It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.
Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.
I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.
Thank you.
Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.
Could boosting fat taste receptors help cut calories?
Desire for dietary lipids has been traced to the taste receptors CD36 and GPR120, and these have been found to be malfunctioning in both obese animals and humans, leading to low perception of fat levels in food.
The study was published online in Cellular and Molecular Gastroenterology and Hepatology. “Ours is the first study on targeting fat taste receptors, leading to [the] activation of tongue-gut loop as a therapeutic approach, and it opens new vistas to synthesize more potent chemical compounds to decrease progressive weight gain under [high-fat diet] consumption,” the authors wrote.
The perception of fat has recently been identified as a potential sixth basic taste quality, joining sweet, sour, bitter, salt, and umami. CD36 is expressed by taste cells, where it senses dietary long-chain fatty acids (LCFAs), and its deletion led mice to ignore LCFAs and oily solutions that they would otherwise prefer. GPR120 has also been proposed as a lipid sensor.
Previous researchers had suggested that CD36 may play a role in the preference for eating fats, while GPR120 could have a role in lipid satiation following consumption. “Our team also supported these conclusions and proposed that CD36 might be involved in immediate early detection [of fat in foods], whereas GPR120 will be responsible for post-ingestive regulation of lipid food intake,” the authors wrote.
The researchers showed that lipids bind to CD36 when they are present in low concentrations, but at high concentrations they bind to GPR120, suggesting that the two receptors are nonoverlapping but nevertheless complement one another during fatty acid–mediated signaling with taste bud cells (TBC). They are also coexpressed within the same type of TBC.
Experiments in rodents suggest that obese animals have reduced capacity to sense dietary fatty acids, which drives consumption of greater amounts. Fat-rich diets can also reduce fat taste perception, and this has been shown cross-sectionally in obese human subjects, and a single nucleotide polymorphism in CD36 that leads to a reduction in expression is linked to reduced perception of dietary fatty acids.
To test the idea that altering the receptors could change behavior, the researchers synthesized two novel fat taste receptor agonists (FTAs) that are derived from the LCFA linoleic acid, which is abundant in Western diets.
Using nerve recordings, the researchers confirmed that a message from TBCs is sent to the brain via the chorda tympani nerve, and the two FTAs increased the nerve signal. The signals from LCFAs alone were boosted with the addition of the FTAs, suggesting that these molecules can be effective even in the presence of dietary lipids. They also confirmed that FTAs activate the tongue-brain-gut loop by increasing pancreato-bile secretion more than linoleic acid alone.
Given the choice between two bottles, mice preferred the one containing FTAs, and the experiments indicated that FTAs are 95-142 times more potent than natural LCFA as food attractants.
It is well known that diet and lifestyle interventions rarely result in long-term weight loss, and products designed to mimic ‘fat-like’ texture – such as maltodextrin, inulin, and plant fibers – have had limited success because they do not have a fat-like taste and can lead to gastrointestinal side effects. Agonists of CD36 and GPR120 added to low- or noncaloric foods could boost their appeal and lead to earlier satiation.
Importantly, in obese mice, both TFAs led to decreased food intake as well as reduced weight gain and fat mass, without affecting lean mass. One of the agents also promoted a higher metabolic rate through increased energy expenditure.
The researchers also examined the agents’ effects on the microbiota of the obese mice, which contain high concentrations of bacteria belonging to the Lachnospiraceae family. Both inhibitors reduced the numbers of Lachnospiraceae bacteria, and promoted other bacterial families that may contribute to an anti-inflammatory effect. Obese animals exposed to TFAs also showed improvements in dyslipidemia, and there was evidence that they could reduce liver lipid concentrations.
There was no evidence of any mutagenicity, genotoxicity, or endocrine disruption. In sum, these new agonists might enable the development of novel treatments of obesity, which would have a major impact on human health.
The authors stated that they have no financial conflicts of interest. The study received financial support from institutions including the Société d'Accélération du Transfert de Technologies and the University of Burgundy.
This article was updated 2/15/23.
The obesity epidemic represents a significant public health crisis that has spread to most countries on the planet. In addition to being a major risk factor for diabetes and cardiovascular disease, obesity also impacts the incidence of gastrointestinal cancers. Despite major efforts of health professionals and public health messaging, it remains very difficult for patients to achieve sustained weight loss by changing diet and increasing physical activity alone. Novel approaches to regulate food intake and thus obesity are urgently needed.
While these are preclinical studies, it will now be fascinating to determine if these or similar compounds can be developed into drugs or food additives to impact human food intake and thus become an additional tool in the fight against the obesity epidemic.
Klaus H. Kaestner, PhD, MS, is with the department of genetics and Center for Molecular Studies in Digestive and Liver Diseases, University of Pennsylvania, Philadelphia. He has no financial conflicts of interest.
The obesity epidemic represents a significant public health crisis that has spread to most countries on the planet. In addition to being a major risk factor for diabetes and cardiovascular disease, obesity also impacts the incidence of gastrointestinal cancers. Despite major efforts of health professionals and public health messaging, it remains very difficult for patients to achieve sustained weight loss by changing diet and increasing physical activity alone. Novel approaches to regulate food intake and thus obesity are urgently needed.
While these are preclinical studies, it will now be fascinating to determine if these or similar compounds can be developed into drugs or food additives to impact human food intake and thus become an additional tool in the fight against the obesity epidemic.
Klaus H. Kaestner, PhD, MS, is with the department of genetics and Center for Molecular Studies in Digestive and Liver Diseases, University of Pennsylvania, Philadelphia. He has no financial conflicts of interest.
The obesity epidemic represents a significant public health crisis that has spread to most countries on the planet. In addition to being a major risk factor for diabetes and cardiovascular disease, obesity also impacts the incidence of gastrointestinal cancers. Despite major efforts of health professionals and public health messaging, it remains very difficult for patients to achieve sustained weight loss by changing diet and increasing physical activity alone. Novel approaches to regulate food intake and thus obesity are urgently needed.
While these are preclinical studies, it will now be fascinating to determine if these or similar compounds can be developed into drugs or food additives to impact human food intake and thus become an additional tool in the fight against the obesity epidemic.
Klaus H. Kaestner, PhD, MS, is with the department of genetics and Center for Molecular Studies in Digestive and Liver Diseases, University of Pennsylvania, Philadelphia. He has no financial conflicts of interest.
Desire for dietary lipids has been traced to the taste receptors CD36 and GPR120, and these have been found to be malfunctioning in both obese animals and humans, leading to low perception of fat levels in food.
The study was published online in Cellular and Molecular Gastroenterology and Hepatology. “Ours is the first study on targeting fat taste receptors, leading to [the] activation of tongue-gut loop as a therapeutic approach, and it opens new vistas to synthesize more potent chemical compounds to decrease progressive weight gain under [high-fat diet] consumption,” the authors wrote.
The perception of fat has recently been identified as a potential sixth basic taste quality, joining sweet, sour, bitter, salt, and umami. CD36 is expressed by taste cells, where it senses dietary long-chain fatty acids (LCFAs), and its deletion led mice to ignore LCFAs and oily solutions that they would otherwise prefer. GPR120 has also been proposed as a lipid sensor.
Previous researchers had suggested that CD36 may play a role in the preference for eating fats, while GPR120 could have a role in lipid satiation following consumption. “Our team also supported these conclusions and proposed that CD36 might be involved in immediate early detection [of fat in foods], whereas GPR120 will be responsible for post-ingestive regulation of lipid food intake,” the authors wrote.
The researchers showed that lipids bind to CD36 when they are present in low concentrations, but at high concentrations they bind to GPR120, suggesting that the two receptors are nonoverlapping but nevertheless complement one another during fatty acid–mediated signaling with taste bud cells (TBC). They are also coexpressed within the same type of TBC.
Experiments in rodents suggest that obese animals have reduced capacity to sense dietary fatty acids, which drives consumption of greater amounts. Fat-rich diets can also reduce fat taste perception, and this has been shown cross-sectionally in obese human subjects, and a single nucleotide polymorphism in CD36 that leads to a reduction in expression is linked to reduced perception of dietary fatty acids.
To test the idea that altering the receptors could change behavior, the researchers synthesized two novel fat taste receptor agonists (FTAs) that are derived from the LCFA linoleic acid, which is abundant in Western diets.
Using nerve recordings, the researchers confirmed that a message from TBCs is sent to the brain via the chorda tympani nerve, and the two FTAs increased the nerve signal. The signals from LCFAs alone were boosted with the addition of the FTAs, suggesting that these molecules can be effective even in the presence of dietary lipids. They also confirmed that FTAs activate the tongue-brain-gut loop by increasing pancreato-bile secretion more than linoleic acid alone.
Given the choice between two bottles, mice preferred the one containing FTAs, and the experiments indicated that FTAs are 95-142 times more potent than natural LCFA as food attractants.
It is well known that diet and lifestyle interventions rarely result in long-term weight loss, and products designed to mimic ‘fat-like’ texture – such as maltodextrin, inulin, and plant fibers – have had limited success because they do not have a fat-like taste and can lead to gastrointestinal side effects. Agonists of CD36 and GPR120 added to low- or noncaloric foods could boost their appeal and lead to earlier satiation.
Importantly, in obese mice, both TFAs led to decreased food intake as well as reduced weight gain and fat mass, without affecting lean mass. One of the agents also promoted a higher metabolic rate through increased energy expenditure.
The researchers also examined the agents’ effects on the microbiota of the obese mice, which contain high concentrations of bacteria belonging to the Lachnospiraceae family. Both inhibitors reduced the numbers of Lachnospiraceae bacteria, and promoted other bacterial families that may contribute to an anti-inflammatory effect. Obese animals exposed to TFAs also showed improvements in dyslipidemia, and there was evidence that they could reduce liver lipid concentrations.
There was no evidence of any mutagenicity, genotoxicity, or endocrine disruption. In sum, these new agonists might enable the development of novel treatments of obesity, which would have a major impact on human health.
The authors stated that they have no financial conflicts of interest. The study received financial support from institutions including the Société d'Accélération du Transfert de Technologies and the University of Burgundy.
This article was updated 2/15/23.
Desire for dietary lipids has been traced to the taste receptors CD36 and GPR120, and these have been found to be malfunctioning in both obese animals and humans, leading to low perception of fat levels in food.
The study was published online in Cellular and Molecular Gastroenterology and Hepatology. “Ours is the first study on targeting fat taste receptors, leading to [the] activation of tongue-gut loop as a therapeutic approach, and it opens new vistas to synthesize more potent chemical compounds to decrease progressive weight gain under [high-fat diet] consumption,” the authors wrote.
The perception of fat has recently been identified as a potential sixth basic taste quality, joining sweet, sour, bitter, salt, and umami. CD36 is expressed by taste cells, where it senses dietary long-chain fatty acids (LCFAs), and its deletion led mice to ignore LCFAs and oily solutions that they would otherwise prefer. GPR120 has also been proposed as a lipid sensor.
Previous researchers had suggested that CD36 may play a role in the preference for eating fats, while GPR120 could have a role in lipid satiation following consumption. “Our team also supported these conclusions and proposed that CD36 might be involved in immediate early detection [of fat in foods], whereas GPR120 will be responsible for post-ingestive regulation of lipid food intake,” the authors wrote.
The researchers showed that lipids bind to CD36 when they are present in low concentrations, but at high concentrations they bind to GPR120, suggesting that the two receptors are nonoverlapping but nevertheless complement one another during fatty acid–mediated signaling with taste bud cells (TBC). They are also coexpressed within the same type of TBC.
Experiments in rodents suggest that obese animals have reduced capacity to sense dietary fatty acids, which drives consumption of greater amounts. Fat-rich diets can also reduce fat taste perception, and this has been shown cross-sectionally in obese human subjects, and a single nucleotide polymorphism in CD36 that leads to a reduction in expression is linked to reduced perception of dietary fatty acids.
To test the idea that altering the receptors could change behavior, the researchers synthesized two novel fat taste receptor agonists (FTAs) that are derived from the LCFA linoleic acid, which is abundant in Western diets.
Using nerve recordings, the researchers confirmed that a message from TBCs is sent to the brain via the chorda tympani nerve, and the two FTAs increased the nerve signal. The signals from LCFAs alone were boosted with the addition of the FTAs, suggesting that these molecules can be effective even in the presence of dietary lipids. They also confirmed that FTAs activate the tongue-brain-gut loop by increasing pancreato-bile secretion more than linoleic acid alone.
Given the choice between two bottles, mice preferred the one containing FTAs, and the experiments indicated that FTAs are 95-142 times more potent than natural LCFA as food attractants.
It is well known that diet and lifestyle interventions rarely result in long-term weight loss, and products designed to mimic ‘fat-like’ texture – such as maltodextrin, inulin, and plant fibers – have had limited success because they do not have a fat-like taste and can lead to gastrointestinal side effects. Agonists of CD36 and GPR120 added to low- or noncaloric foods could boost their appeal and lead to earlier satiation.
Importantly, in obese mice, both TFAs led to decreased food intake as well as reduced weight gain and fat mass, without affecting lean mass. One of the agents also promoted a higher metabolic rate through increased energy expenditure.
The researchers also examined the agents’ effects on the microbiota of the obese mice, which contain high concentrations of bacteria belonging to the Lachnospiraceae family. Both inhibitors reduced the numbers of Lachnospiraceae bacteria, and promoted other bacterial families that may contribute to an anti-inflammatory effect. Obese animals exposed to TFAs also showed improvements in dyslipidemia, and there was evidence that they could reduce liver lipid concentrations.
There was no evidence of any mutagenicity, genotoxicity, or endocrine disruption. In sum, these new agonists might enable the development of novel treatments of obesity, which would have a major impact on human health.
The authors stated that they have no financial conflicts of interest. The study received financial support from institutions including the Société d'Accélération du Transfert de Technologies and the University of Burgundy.
This article was updated 2/15/23.
FROM CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
Eating potatoes is healthy, study finds
according to researchers at Louisiana State University’s Pennington Biomedical Research Center, Baton Rouge.
What to know
Potatoes are filled with key nutrients, packed with health benefits, and do not increase the risk of type 2 diabetes, as has been assumed.
People tend to eat the same weight of food regardless of calorie content to feel full, so by eating foods that are heavier in weight and that are low in calories, you can reduce the number of calories you consume.
Study participants found themselves fuller, and full more quickly, and often did not even finish their meal when the high-calorie items of their meals were replaced with potatoes.
Participants had overweight, obesity, or insulin resistance, but their blood glucose levels were not negatively affected by the potato consumption, and all of those involved actually lost weight.
People typically do not stick with a diet they don’t like or that isn't varied enough, but potatoes can be prepared in numerous ways for variety in a diet, and they are a fairly inexpensive vegetable to incorporate into a diet.
This is a summary of the article, "Low-Energy Dense Potato- and Bean-Based Diets Reduce Body Weight and Insulin Resistance: A Randomized, Feeding, Equivalence Trial," published in the Journal of Medicinal Food on November 11, 2022. The full article can be found on pubmed.ncbi.nlm.nih.gov.
A version of this article first appeared on Medscape.com.
according to researchers at Louisiana State University’s Pennington Biomedical Research Center, Baton Rouge.
What to know
Potatoes are filled with key nutrients, packed with health benefits, and do not increase the risk of type 2 diabetes, as has been assumed.
People tend to eat the same weight of food regardless of calorie content to feel full, so by eating foods that are heavier in weight and that are low in calories, you can reduce the number of calories you consume.
Study participants found themselves fuller, and full more quickly, and often did not even finish their meal when the high-calorie items of their meals were replaced with potatoes.
Participants had overweight, obesity, or insulin resistance, but their blood glucose levels were not negatively affected by the potato consumption, and all of those involved actually lost weight.
People typically do not stick with a diet they don’t like or that isn't varied enough, but potatoes can be prepared in numerous ways for variety in a diet, and they are a fairly inexpensive vegetable to incorporate into a diet.
This is a summary of the article, "Low-Energy Dense Potato- and Bean-Based Diets Reduce Body Weight and Insulin Resistance: A Randomized, Feeding, Equivalence Trial," published in the Journal of Medicinal Food on November 11, 2022. The full article can be found on pubmed.ncbi.nlm.nih.gov.
A version of this article first appeared on Medscape.com.
according to researchers at Louisiana State University’s Pennington Biomedical Research Center, Baton Rouge.
What to know
Potatoes are filled with key nutrients, packed with health benefits, and do not increase the risk of type 2 diabetes, as has been assumed.
People tend to eat the same weight of food regardless of calorie content to feel full, so by eating foods that are heavier in weight and that are low in calories, you can reduce the number of calories you consume.
Study participants found themselves fuller, and full more quickly, and often did not even finish their meal when the high-calorie items of their meals were replaced with potatoes.
Participants had overweight, obesity, or insulin resistance, but their blood glucose levels were not negatively affected by the potato consumption, and all of those involved actually lost weight.
People typically do not stick with a diet they don’t like or that isn't varied enough, but potatoes can be prepared in numerous ways for variety in a diet, and they are a fairly inexpensive vegetable to incorporate into a diet.
This is a summary of the article, "Low-Energy Dense Potato- and Bean-Based Diets Reduce Body Weight and Insulin Resistance: A Randomized, Feeding, Equivalence Trial," published in the Journal of Medicinal Food on November 11, 2022. The full article can be found on pubmed.ncbi.nlm.nih.gov.
A version of this article first appeared on Medscape.com.