Obesity

Almonds might affect appetite during a weight loss diet and may assist with weight management in the long term, 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.

Almonds might affect appetite during a weight loss diet and may assist with weight management in the long term, 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.

Almonds might affect appetite during a weight loss diet and may assist with weight management in the long term, 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.

“Congratulations on the baby. You look great!” I enthusiastically proclaimed to my classmate. 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.

“Congratulations on the baby. You look great!” I enthusiastically proclaimed to my classmate. 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.

“Congratulations on the baby. You look great!” I enthusiastically proclaimed to my classmate. 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.

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.

Two novel molecules that act as tongue taste receptor agonists led to a reduction in fat-rich food intake and countered body weight gain in mice. The agents are believed to enhance the taste of fat and initiate the tongue-gut satiation loop.

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. 

Two novel molecules that act as tongue taste receptor agonists led to a reduction in fat-rich food intake and countered body weight gain in mice. The agents are believed to enhance the taste of fat and initiate the tongue-gut satiation loop.

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. 

Two novel molecules that act as tongue taste receptor agonists led to a reduction in fat-rich food intake and countered body weight gain in mice. The agents are believed to enhance the taste of fat and initiate the tongue-gut satiation loop.

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. 

Contrary to common belief, potatoes do not have a negative effect on blood glucose levels and can actually help people lose weight, 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.

Contrary to common belief, potatoes do not have a negative effect on blood glucose levels and can actually help people lose weight, 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.

Contrary to common belief, potatoes do not have a negative effect on blood glucose levels and can actually help people lose weight, 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.

A 12-month program of moderate to vigorous exercise reduced the risk of type 2 diabetes by approximately 50% in adults with obesity over 10 years, according to a new analysis of a study.

“Physical exercise combined with diet restriction has been proven to be effective in prevention of diabetes. However, the long-term effect of exercise on prevention of diabetes, and the difference of exercise intensity in prevention of diabetes have not been well studied,” said corresponding author Xiaoying Li, MD, of Zhongshan Hospital, Fudan University, Shanghai, in an interview.

In the research letter published in JAMA Internal Medicine, Dr. Li and colleagues analyzed the results of a study of 220 adults with central obesity and nonalcoholic fatty liver disease, but no incident diabetes, randomized to a 12-month program of vigorous exercise (73 patients), moderate aerobic exercise (73 patients) or no exercise (74 patients).

A total of 208 participants completed the 1-year intervention; of these, 195 and 178 remained to provide data at 2 years and 10 years, respectively. The mean age of the participants was 53.9 years, 32.3% were male, and the mean waist circumference was 96.1 cm at baseline.

The cumulative incidence of type 2 diabetes in the vigorous exercise, moderate exercise, and nonexercise groups was 2.1 per 100 person-years 1.9 per 100 person-years, and 4.1 per 100 person-years, respectively, over the 10-year follow-up period. This translated to a reduction in type 2 diabetes risk of 49% in the vigorous exercise group and 53% in the moderate exercise group compared with the nonexercise group.

In addition, individuals in the vigorous and moderate exercise groups significantly reduced their HbA1c and waist circumference compared with the nonexercisers. Levels of plasma fasting glucose and weight regain were lower in both exercise groups compared with nonexercisers, but these differences were not significant.

The exercise intervention was described in a 2016 study, which was also published in JAMA Internal Medicine. That study’s purpose was to compare the effects of exercise on patients with nonalcoholic fatty liver disease. Participants were coached and supervised for their exercise programs. The program for the vigorous group involved jogging for 150 minutes per week at 65%-80% of maximum heart rate for 6 months and brisk walking 150 minutes per week at 45%-55% of maximum heart rate for another 6 months. The program for the moderate exercise group involved brisk walking 150 minutes per week for 12 months.

Both exercise groups showed a trend towards higher levels of leisure time physical activity after 10 years compared with the nonexercise groups, although the difference was not significant.

The main limitation of the study was that incident prediabetes was not prespecified, which may have led to some confounding, the researchers noted. In addition, the participants were highly supervised for a 12-month program only. However, the results support the long-term value of physical exercise as a method of obesity management and to delay progression to type 2 diabetes in obese individuals, they said. Vigorous and moderate aerobic exercise programs could be implemented for this patient population, they concluded.

“Surprisingly, our findings demonstrated that a 12-month vigorous aerobic exercise or moderate aerobic exercise could significantly reduce the risk of incident diabetes by 50% over the 10-year follow-up,” Dr. Li said in an interview. The results suggest that physical exercise for some period of time can produce a long-term beneficial effect in prevention of type 2 diabetes, he said.

Potential barriers to the routine use of an exercise intervention in patients with obesity include the unwillingness of this population to engage in vigorous exercise, and the potential for musculoskeletal injury, said Dr. Li. In these cases, obese patients should be encouraged to pursue moderate exercise, Dr. Li said.

Looking ahead, more research is needed to examine the potential mechanism behind the effect of exercise on diabetes prevention, said Dr. Li.

Findings fill gap in long-term outcome data

The current study is important because of the long-term follow-up data, said Jill Kanaley, PhD, professor and interim chair of nutrition and exercise physiology at the University of Missouri, in an interview. “We seldom follow up on our training studies, thus it is important to see if there is any long-term impact of these interventions,” she said.

Dr. Kanaley said she was surprised to see the residual benefits of the exercise intervention 10 years later.

“We often wonder how long the impact of the exercise training will stay with someone so that they continue to exercise and watch their weight; this study seems to indicate that there is an educational component that stays with them,” she said.

The main clinical takeaway from the current study was the minimal weight gain over time, Dr. Kanaley said.

Although time may be a barrier to the routine use of an exercise intervention, patients have to realize that they can usually find the time, especially given the multiple benefits, said Dr. Kanaley. “The exercise interventions provide more benefits than just weight control and glucose levels,” she said.

“The 30-60 minutes of exercise does not have to come all at the same time,” Dr. Kanaley noted. “It could be three 15-minute bouts of exercise/physical activity to get their 45 minutes in,” she noted. Exercise does not have to be heavy vigorous exercise, even walking is beneficial, she said. For people who complain of boredom with an exercise routine, Dr. Kanaley encourages mixing it up, with activities such as different exercise classes, running, or walking on a different day of any given week.

Although the current study was conducted in China, the findings may translate to a U.S. population, Dr. Kanaley said in an interview. However, “frequently our Western diet is less healthy than the traditional Chinese diet. This may have provided an immeasurable benefit to these subjects,” although study participants did not make specific adjustments to their diets, she said.  

Additional research is needed to confirm the findings, said Dr. Kanaley. “Ideally, the study should be repeated in a population with a Western diet,” she noted.

Next steps for research include maintenance of activity

Evidence on the long-term benefits of exercise programs is limited, said Amanda Paluch, PhD, a physical activity epidemiologist at the University of Massachusetts, Amherst, in an interview.

“Chronic diseases such as diabetes can take years to develop, so understanding these important health outcomes requires years of follow-up. This study followed their study participants for 10 years, which gives us a nice glimpse of the long-term benefits of exercise training on diabetes prevention,” she said.

Data from previous observational studies of individuals’ current activity levels (without an intervention) suggest that adults who are more physically active have a lower risk of diabetes over time, said Dr. Paluch. However, the current study is one of the few with rigorous exercise interventions with extensive follow-up on diabetes risk, and it provides important evidence that a 12-month structured exercise program in inactive adults with obesity can result in meaningful long-term health benefits by lowering the risk of diabetes, she said.

“The individuals in the current study participated in a structured exercise program where their exercise sessions were supervised and coached,” Dr. Paluch noted. “Having a personalized coach may not be within the budget or time constraints for many people,” she said. Her message to clinicians for their patients: “When looking to start an exercise routine, identify an activity you enjoy and find feasible to fit into your existing life and schedule,” she said.

“Although this study was conducted in China, the results are meaningful for the U.S. population, as we would expect the physiological benefit of exercise to be consistent across various populations,” Dr. Paluch said. “However, there are certainly differences across countries at the individual level to the larger community-wide level that may influence a person’s ability to maintain physical activity and prevent diabetes, so replicating similar studies in other countries, including the U.S., would be of value.” 

“Additionally, we need more research on how to encourage maintenance of physical activity in the long-term, after the initial exercise program is over,” she said.

“From this current study, we cannot tease out whether diabetes risk is reduced because of the 12-month exercise intervention or the benefit is from maintaining physical activity regularly over the 10 years of follow-up, or a combination of the two,” said Dr. Paluch. Future studies should consider teasing out participants who were only active during the exercise intervention, then ceased being active vs. participants who continued with vigorous activity long-term, she said.

The study was supported by the National Nature Science Foundation, the National Key Research and Development Program of China, and the Shanghai Municipal Science and Technology Major Project. The researchers, Dr. Kanaley, and Dr. Paluch had no financial conflicts to disclose.

A 12-month program of moderate to vigorous exercise reduced the risk of type 2 diabetes by approximately 50% in adults with obesity over 10 years, according to a new analysis of a study.

“Physical exercise combined with diet restriction has been proven to be effective in prevention of diabetes. However, the long-term effect of exercise on prevention of diabetes, and the difference of exercise intensity in prevention of diabetes have not been well studied,” said corresponding author Xiaoying Li, MD, of Zhongshan Hospital, Fudan University, Shanghai, in an interview.

In the research letter published in JAMA Internal Medicine, Dr. Li and colleagues analyzed the results of a study of 220 adults with central obesity and nonalcoholic fatty liver disease, but no incident diabetes, randomized to a 12-month program of vigorous exercise (73 patients), moderate aerobic exercise (73 patients) or no exercise (74 patients).

A total of 208 participants completed the 1-year intervention; of these, 195 and 178 remained to provide data at 2 years and 10 years, respectively. The mean age of the participants was 53.9 years, 32.3% were male, and the mean waist circumference was 96.1 cm at baseline.

The cumulative incidence of type 2 diabetes in the vigorous exercise, moderate exercise, and nonexercise groups was 2.1 per 100 person-years 1.9 per 100 person-years, and 4.1 per 100 person-years, respectively, over the 10-year follow-up period. This translated to a reduction in type 2 diabetes risk of 49% in the vigorous exercise group and 53% in the moderate exercise group compared with the nonexercise group.

In addition, individuals in the vigorous and moderate exercise groups significantly reduced their HbA1c and waist circumference compared with the nonexercisers. Levels of plasma fasting glucose and weight regain were lower in both exercise groups compared with nonexercisers, but these differences were not significant.

The exercise intervention was described in a 2016 study, which was also published in JAMA Internal Medicine. That study’s purpose was to compare the effects of exercise on patients with nonalcoholic fatty liver disease. Participants were coached and supervised for their exercise programs. The program for the vigorous group involved jogging for 150 minutes per week at 65%-80% of maximum heart rate for 6 months and brisk walking 150 minutes per week at 45%-55% of maximum heart rate for another 6 months. The program for the moderate exercise group involved brisk walking 150 minutes per week for 12 months.

Both exercise groups showed a trend towards higher levels of leisure time physical activity after 10 years compared with the nonexercise groups, although the difference was not significant.

The main limitation of the study was that incident prediabetes was not prespecified, which may have led to some confounding, the researchers noted. In addition, the participants were highly supervised for a 12-month program only. However, the results support the long-term value of physical exercise as a method of obesity management and to delay progression to type 2 diabetes in obese individuals, they said. Vigorous and moderate aerobic exercise programs could be implemented for this patient population, they concluded.

“Surprisingly, our findings demonstrated that a 12-month vigorous aerobic exercise or moderate aerobic exercise could significantly reduce the risk of incident diabetes by 50% over the 10-year follow-up,” Dr. Li said in an interview. The results suggest that physical exercise for some period of time can produce a long-term beneficial effect in prevention of type 2 diabetes, he said.

Potential barriers to the routine use of an exercise intervention in patients with obesity include the unwillingness of this population to engage in vigorous exercise, and the potential for musculoskeletal injury, said Dr. Li. In these cases, obese patients should be encouraged to pursue moderate exercise, Dr. Li said.

Looking ahead, more research is needed to examine the potential mechanism behind the effect of exercise on diabetes prevention, said Dr. Li.

Findings fill gap in long-term outcome data

The current study is important because of the long-term follow-up data, said Jill Kanaley, PhD, professor and interim chair of nutrition and exercise physiology at the University of Missouri, in an interview. “We seldom follow up on our training studies, thus it is important to see if there is any long-term impact of these interventions,” she said.

Dr. Kanaley said she was surprised to see the residual benefits of the exercise intervention 10 years later.

“We often wonder how long the impact of the exercise training will stay with someone so that they continue to exercise and watch their weight; this study seems to indicate that there is an educational component that stays with them,” she said.

The main clinical takeaway from the current study was the minimal weight gain over time, Dr. Kanaley said.

Although time may be a barrier to the routine use of an exercise intervention, patients have to realize that they can usually find the time, especially given the multiple benefits, said Dr. Kanaley. “The exercise interventions provide more benefits than just weight control and glucose levels,” she said.

“The 30-60 minutes of exercise does not have to come all at the same time,” Dr. Kanaley noted. “It could be three 15-minute bouts of exercise/physical activity to get their 45 minutes in,” she noted. Exercise does not have to be heavy vigorous exercise, even walking is beneficial, she said. For people who complain of boredom with an exercise routine, Dr. Kanaley encourages mixing it up, with activities such as different exercise classes, running, or walking on a different day of any given week.

Although the current study was conducted in China, the findings may translate to a U.S. population, Dr. Kanaley said in an interview. However, “frequently our Western diet is less healthy than the traditional Chinese diet. This may have provided an immeasurable benefit to these subjects,” although study participants did not make specific adjustments to their diets, she said.  

Additional research is needed to confirm the findings, said Dr. Kanaley. “Ideally, the study should be repeated in a population with a Western diet,” she noted.

Next steps for research include maintenance of activity

Evidence on the long-term benefits of exercise programs is limited, said Amanda Paluch, PhD, a physical activity epidemiologist at the University of Massachusetts, Amherst, in an interview.

“Chronic diseases such as diabetes can take years to develop, so understanding these important health outcomes requires years of follow-up. This study followed their study participants for 10 years, which gives us a nice glimpse of the long-term benefits of exercise training on diabetes prevention,” she said.

Data from previous observational studies of individuals’ current activity levels (without an intervention) suggest that adults who are more physically active have a lower risk of diabetes over time, said Dr. Paluch. However, the current study is one of the few with rigorous exercise interventions with extensive follow-up on diabetes risk, and it provides important evidence that a 12-month structured exercise program in inactive adults with obesity can result in meaningful long-term health benefits by lowering the risk of diabetes, she said.

“The individuals in the current study participated in a structured exercise program where their exercise sessions were supervised and coached,” Dr. Paluch noted. “Having a personalized coach may not be within the budget or time constraints for many people,” she said. Her message to clinicians for their patients: “When looking to start an exercise routine, identify an activity you enjoy and find feasible to fit into your existing life and schedule,” she said.

“Although this study was conducted in China, the results are meaningful for the U.S. population, as we would expect the physiological benefit of exercise to be consistent across various populations,” Dr. Paluch said. “However, there are certainly differences across countries at the individual level to the larger community-wide level that may influence a person’s ability to maintain physical activity and prevent diabetes, so replicating similar studies in other countries, including the U.S., would be of value.” 

“Additionally, we need more research on how to encourage maintenance of physical activity in the long-term, after the initial exercise program is over,” she said.

“From this current study, we cannot tease out whether diabetes risk is reduced because of the 12-month exercise intervention or the benefit is from maintaining physical activity regularly over the 10 years of follow-up, or a combination of the two,” said Dr. Paluch. Future studies should consider teasing out participants who were only active during the exercise intervention, then ceased being active vs. participants who continued with vigorous activity long-term, she said.

The study was supported by the National Nature Science Foundation, the National Key Research and Development Program of China, and the Shanghai Municipal Science and Technology Major Project. The researchers, Dr. Kanaley, and Dr. Paluch had no financial conflicts to disclose.

A 12-month program of moderate to vigorous exercise reduced the risk of type 2 diabetes by approximately 50% in adults with obesity over 10 years, according to a new analysis of a study.

“Physical exercise combined with diet restriction has been proven to be effective in prevention of diabetes. However, the long-term effect of exercise on prevention of diabetes, and the difference of exercise intensity in prevention of diabetes have not been well studied,” said corresponding author Xiaoying Li, MD, of Zhongshan Hospital, Fudan University, Shanghai, in an interview.

In the research letter published in JAMA Internal Medicine, Dr. Li and colleagues analyzed the results of a study of 220 adults with central obesity and nonalcoholic fatty liver disease, but no incident diabetes, randomized to a 12-month program of vigorous exercise (73 patients), moderate aerobic exercise (73 patients) or no exercise (74 patients).

A total of 208 participants completed the 1-year intervention; of these, 195 and 178 remained to provide data at 2 years and 10 years, respectively. The mean age of the participants was 53.9 years, 32.3% were male, and the mean waist circumference was 96.1 cm at baseline.

The cumulative incidence of type 2 diabetes in the vigorous exercise, moderate exercise, and nonexercise groups was 2.1 per 100 person-years 1.9 per 100 person-years, and 4.1 per 100 person-years, respectively, over the 10-year follow-up period. This translated to a reduction in type 2 diabetes risk of 49% in the vigorous exercise group and 53% in the moderate exercise group compared with the nonexercise group.

In addition, individuals in the vigorous and moderate exercise groups significantly reduced their HbA1c and waist circumference compared with the nonexercisers. Levels of plasma fasting glucose and weight regain were lower in both exercise groups compared with nonexercisers, but these differences were not significant.

The exercise intervention was described in a 2016 study, which was also published in JAMA Internal Medicine. That study’s purpose was to compare the effects of exercise on patients with nonalcoholic fatty liver disease. Participants were coached and supervised for their exercise programs. The program for the vigorous group involved jogging for 150 minutes per week at 65%-80% of maximum heart rate for 6 months and brisk walking 150 minutes per week at 45%-55% of maximum heart rate for another 6 months. The program for the moderate exercise group involved brisk walking 150 minutes per week for 12 months.

Both exercise groups showed a trend towards higher levels of leisure time physical activity after 10 years compared with the nonexercise groups, although the difference was not significant.

The main limitation of the study was that incident prediabetes was not prespecified, which may have led to some confounding, the researchers noted. In addition, the participants were highly supervised for a 12-month program only. However, the results support the long-term value of physical exercise as a method of obesity management and to delay progression to type 2 diabetes in obese individuals, they said. Vigorous and moderate aerobic exercise programs could be implemented for this patient population, they concluded.

“Surprisingly, our findings demonstrated that a 12-month vigorous aerobic exercise or moderate aerobic exercise could significantly reduce the risk of incident diabetes by 50% over the 10-year follow-up,” Dr. Li said in an interview. The results suggest that physical exercise for some period of time can produce a long-term beneficial effect in prevention of type 2 diabetes, he said.

Potential barriers to the routine use of an exercise intervention in patients with obesity include the unwillingness of this population to engage in vigorous exercise, and the potential for musculoskeletal injury, said Dr. Li. In these cases, obese patients should be encouraged to pursue moderate exercise, Dr. Li said.

Looking ahead, more research is needed to examine the potential mechanism behind the effect of exercise on diabetes prevention, said Dr. Li.

Findings fill gap in long-term outcome data

The current study is important because of the long-term follow-up data, said Jill Kanaley, PhD, professor and interim chair of nutrition and exercise physiology at the University of Missouri, in an interview. “We seldom follow up on our training studies, thus it is important to see if there is any long-term impact of these interventions,” she said.

Dr. Kanaley said she was surprised to see the residual benefits of the exercise intervention 10 years later.

“We often wonder how long the impact of the exercise training will stay with someone so that they continue to exercise and watch their weight; this study seems to indicate that there is an educational component that stays with them,” she said.

The main clinical takeaway from the current study was the minimal weight gain over time, Dr. Kanaley said.

Although time may be a barrier to the routine use of an exercise intervention, patients have to realize that they can usually find the time, especially given the multiple benefits, said Dr. Kanaley. “The exercise interventions provide more benefits than just weight control and glucose levels,” she said.

“The 30-60 minutes of exercise does not have to come all at the same time,” Dr. Kanaley noted. “It could be three 15-minute bouts of exercise/physical activity to get their 45 minutes in,” she noted. Exercise does not have to be heavy vigorous exercise, even walking is beneficial, she said. For people who complain of boredom with an exercise routine, Dr. Kanaley encourages mixing it up, with activities such as different exercise classes, running, or walking on a different day of any given week.

Although the current study was conducted in China, the findings may translate to a U.S. population, Dr. Kanaley said in an interview. However, “frequently our Western diet is less healthy than the traditional Chinese diet. This may have provided an immeasurable benefit to these subjects,” although study participants did not make specific adjustments to their diets, she said.  

Additional research is needed to confirm the findings, said Dr. Kanaley. “Ideally, the study should be repeated in a population with a Western diet,” she noted.

Next steps for research include maintenance of activity

Evidence on the long-term benefits of exercise programs is limited, said Amanda Paluch, PhD, a physical activity epidemiologist at the University of Massachusetts, Amherst, in an interview.

“Chronic diseases such as diabetes can take years to develop, so understanding these important health outcomes requires years of follow-up. This study followed their study participants for 10 years, which gives us a nice glimpse of the long-term benefits of exercise training on diabetes prevention,” she said.

Data from previous observational studies of individuals’ current activity levels (without an intervention) suggest that adults who are more physically active have a lower risk of diabetes over time, said Dr. Paluch. However, the current study is one of the few with rigorous exercise interventions with extensive follow-up on diabetes risk, and it provides important evidence that a 12-month structured exercise program in inactive adults with obesity can result in meaningful long-term health benefits by lowering the risk of diabetes, she said.

“The individuals in the current study participated in a structured exercise program where their exercise sessions were supervised and coached,” Dr. Paluch noted. “Having a personalized coach may not be within the budget or time constraints for many people,” she said. Her message to clinicians for their patients: “When looking to start an exercise routine, identify an activity you enjoy and find feasible to fit into your existing life and schedule,” she said.

“Although this study was conducted in China, the results are meaningful for the U.S. population, as we would expect the physiological benefit of exercise to be consistent across various populations,” Dr. Paluch said. “However, there are certainly differences across countries at the individual level to the larger community-wide level that may influence a person’s ability to maintain physical activity and prevent diabetes, so replicating similar studies in other countries, including the U.S., would be of value.” 

“Additionally, we need more research on how to encourage maintenance of physical activity in the long-term, after the initial exercise program is over,” she said.

“From this current study, we cannot tease out whether diabetes risk is reduced because of the 12-month exercise intervention or the benefit is from maintaining physical activity regularly over the 10 years of follow-up, or a combination of the two,” said Dr. Paluch. Future studies should consider teasing out participants who were only active during the exercise intervention, then ceased being active vs. participants who continued with vigorous activity long-term, she said.

The study was supported by the National Nature Science Foundation, the National Key Research and Development Program of China, and the Shanghai Municipal Science and Technology Major Project. The researchers, Dr. Kanaley, and Dr. Paluch had no financial conflicts to disclose.

Brain atrophy patterns are similar in individuals with obesity and those with Alzheimer’s disease (AD), a new study shows.

Comparisons of MRI scans for more than 1,000 participants indicate correlations between the two conditions, especially in areas of gray matter thinning, suggesting that managing excess weight might slow cognitive decline and lower the risk for AD, according to the researchers.

However, brain maps of obesity did not correlate with maps of amyloid or tau protein accumulation.

“The fact that obesity-related brain atrophy did not correlate with the distribution of amyloid and tau proteins in AD was not what we expected,” study author Filip Morys, PhD, a postdoctoral researcher at McGill University, Montreal, said in an interview. “But it might just show that the specific mechanisms underpinning obesity- and Alzheimer’s disease–related neurodegeneration are different. This remains to be confirmed.”

The study was published in the Journal of Alzheimer’s Disease.
 

Cortical Thinning

The current study was prompted by the team’s earlier study, which showed that obesity-related neurodegeneration patterns were visually similar to those of AD, said Dr. Morys. “It was known previously that obesity is a risk factor for AD, but we wanted to directly compare brain atrophy patterns in both, which is what we did in this new study.”

The researchers analyzed data from a pooled sample of more than 1,300 participants. From the ADNI database, the researchers selected participants with AD and age- and sex-matched cognitively healthy controls. From the UK Biobank, the researchers drew a sample of lean, overweight, and obese participants without neurologic disease.

To determine how the weight status of patients with AD affects the correspondence between AD and obesity maps, they categorized participants with AD and healthy controls from the ADNI database into lean, overweight, and obese subgroups.

Then, to investigate mechanisms that might drive the similarities between obesity-related brain atrophy and AD-related amyloid-beta accumulation, they looked for overlapping areas in PET brain maps between patients with these outcomes.

The investigations showed that obesity maps were highly correlated with AD maps, but not with amyloid-beta or tau protein maps. The researchers also found significant correlations between obesity and the lean individuals with AD.

Brain regions with the highest similarities between obesity and AD were located mainly in the left temporal and bilateral prefrontal cortices.

“Our research confirms that obesity-related gray matter atrophy resembles that of AD,” the authors concluded. “Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.”

Upcoming research “will focus on investigating how weight loss can affect the risk for AD, other dementias, and cognitive decline in general,” said Dr. Morys. “At this point, our study suggests that obesity prevention, weight loss, but also decreasing other metabolic risk factors related to obesity, such as type-2 diabetes or hypertension, might reduce the risk for AD and have beneficial effects on cognition.”
 

Lifestyle habits

Commenting on the findings, Claire Sexton, DPhil, vice president of scientific programs and outreach at the Alzheimer’s Association, cautioned that a single cross-sectional study isn’t conclusive. “Previous studies have illustrated that the relationship between obesity and dementia is complex. Growing evidence indicates that people can reduce their risk of cognitive decline by adopting key lifestyle habits, like regular exercise, a heart-healthy diet and staying socially and cognitively engaged.”

The Alzheimer’s Association is leading a 2-year clinical trial, U.S. Pointer, to study how targeting these risk factors in combination may reduce risk for cognitive decline in older adults.

The work was supported by a Foundation Scheme award from the Canadian Institutes of Health Research. Dr. Morys received a postdoctoral fellowship from Fonds de Recherche du Quebec – Santé. Data collection and sharing were funded by the Alzheimer’s Disease Neuroimaging Initiative, the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and multiple pharmaceutical companies and other private sector organizations. Dr. Morys and Dr. Sexton reported no relevant financial relationships.

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

Brain atrophy patterns are similar in individuals with obesity and those with Alzheimer’s disease (AD), a new study shows.

Comparisons of MRI scans for more than 1,000 participants indicate correlations between the two conditions, especially in areas of gray matter thinning, suggesting that managing excess weight might slow cognitive decline and lower the risk for AD, according to the researchers.

However, brain maps of obesity did not correlate with maps of amyloid or tau protein accumulation.

“The fact that obesity-related brain atrophy did not correlate with the distribution of amyloid and tau proteins in AD was not what we expected,” study author Filip Morys, PhD, a postdoctoral researcher at McGill University, Montreal, said in an interview. “But it might just show that the specific mechanisms underpinning obesity- and Alzheimer’s disease–related neurodegeneration are different. This remains to be confirmed.”

The study was published in the Journal of Alzheimer’s Disease.
 

Cortical Thinning

The current study was prompted by the team’s earlier study, which showed that obesity-related neurodegeneration patterns were visually similar to those of AD, said Dr. Morys. “It was known previously that obesity is a risk factor for AD, but we wanted to directly compare brain atrophy patterns in both, which is what we did in this new study.”

The researchers analyzed data from a pooled sample of more than 1,300 participants. From the ADNI database, the researchers selected participants with AD and age- and sex-matched cognitively healthy controls. From the UK Biobank, the researchers drew a sample of lean, overweight, and obese participants without neurologic disease.

To determine how the weight status of patients with AD affects the correspondence between AD and obesity maps, they categorized participants with AD and healthy controls from the ADNI database into lean, overweight, and obese subgroups.

Then, to investigate mechanisms that might drive the similarities between obesity-related brain atrophy and AD-related amyloid-beta accumulation, they looked for overlapping areas in PET brain maps between patients with these outcomes.

The investigations showed that obesity maps were highly correlated with AD maps, but not with amyloid-beta or tau protein maps. The researchers also found significant correlations between obesity and the lean individuals with AD.

Brain regions with the highest similarities between obesity and AD were located mainly in the left temporal and bilateral prefrontal cortices.

“Our research confirms that obesity-related gray matter atrophy resembles that of AD,” the authors concluded. “Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.”

Upcoming research “will focus on investigating how weight loss can affect the risk for AD, other dementias, and cognitive decline in general,” said Dr. Morys. “At this point, our study suggests that obesity prevention, weight loss, but also decreasing other metabolic risk factors related to obesity, such as type-2 diabetes or hypertension, might reduce the risk for AD and have beneficial effects on cognition.”
 

Lifestyle habits

Commenting on the findings, Claire Sexton, DPhil, vice president of scientific programs and outreach at the Alzheimer’s Association, cautioned that a single cross-sectional study isn’t conclusive. “Previous studies have illustrated that the relationship between obesity and dementia is complex. Growing evidence indicates that people can reduce their risk of cognitive decline by adopting key lifestyle habits, like regular exercise, a heart-healthy diet and staying socially and cognitively engaged.”

The Alzheimer’s Association is leading a 2-year clinical trial, U.S. Pointer, to study how targeting these risk factors in combination may reduce risk for cognitive decline in older adults.

The work was supported by a Foundation Scheme award from the Canadian Institutes of Health Research. Dr. Morys received a postdoctoral fellowship from Fonds de Recherche du Quebec – Santé. Data collection and sharing were funded by the Alzheimer’s Disease Neuroimaging Initiative, the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and multiple pharmaceutical companies and other private sector organizations. Dr. Morys and Dr. Sexton reported no relevant financial relationships.

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

Brain atrophy patterns are similar in individuals with obesity and those with Alzheimer’s disease (AD), a new study shows.

Comparisons of MRI scans for more than 1,000 participants indicate correlations between the two conditions, especially in areas of gray matter thinning, suggesting that managing excess weight might slow cognitive decline and lower the risk for AD, according to the researchers.

However, brain maps of obesity did not correlate with maps of amyloid or tau protein accumulation.

“The fact that obesity-related brain atrophy did not correlate with the distribution of amyloid and tau proteins in AD was not what we expected,” study author Filip Morys, PhD, a postdoctoral researcher at McGill University, Montreal, said in an interview. “But it might just show that the specific mechanisms underpinning obesity- and Alzheimer’s disease–related neurodegeneration are different. This remains to be confirmed.”

The study was published in the Journal of Alzheimer’s Disease.
 

Cortical Thinning

The current study was prompted by the team’s earlier study, which showed that obesity-related neurodegeneration patterns were visually similar to those of AD, said Dr. Morys. “It was known previously that obesity is a risk factor for AD, but we wanted to directly compare brain atrophy patterns in both, which is what we did in this new study.”

The researchers analyzed data from a pooled sample of more than 1,300 participants. From the ADNI database, the researchers selected participants with AD and age- and sex-matched cognitively healthy controls. From the UK Biobank, the researchers drew a sample of lean, overweight, and obese participants without neurologic disease.

To determine how the weight status of patients with AD affects the correspondence between AD and obesity maps, they categorized participants with AD and healthy controls from the ADNI database into lean, overweight, and obese subgroups.

Then, to investigate mechanisms that might drive the similarities between obesity-related brain atrophy and AD-related amyloid-beta accumulation, they looked for overlapping areas in PET brain maps between patients with these outcomes.

The investigations showed that obesity maps were highly correlated with AD maps, but not with amyloid-beta or tau protein maps. The researchers also found significant correlations between obesity and the lean individuals with AD.

Brain regions with the highest similarities between obesity and AD were located mainly in the left temporal and bilateral prefrontal cortices.

“Our research confirms that obesity-related gray matter atrophy resembles that of AD,” the authors concluded. “Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.”

Upcoming research “will focus on investigating how weight loss can affect the risk for AD, other dementias, and cognitive decline in general,” said Dr. Morys. “At this point, our study suggests that obesity prevention, weight loss, but also decreasing other metabolic risk factors related to obesity, such as type-2 diabetes or hypertension, might reduce the risk for AD and have beneficial effects on cognition.”
 

Lifestyle habits

Commenting on the findings, Claire Sexton, DPhil, vice president of scientific programs and outreach at the Alzheimer’s Association, cautioned that a single cross-sectional study isn’t conclusive. “Previous studies have illustrated that the relationship between obesity and dementia is complex. Growing evidence indicates that people can reduce their risk of cognitive decline by adopting key lifestyle habits, like regular exercise, a heart-healthy diet and staying socially and cognitively engaged.”

The Alzheimer’s Association is leading a 2-year clinical trial, U.S. Pointer, to study how targeting these risk factors in combination may reduce risk for cognitive decline in older adults.

The work was supported by a Foundation Scheme award from the Canadian Institutes of Health Research. Dr. Morys received a postdoctoral fellowship from Fonds de Recherche du Quebec – Santé. Data collection and sharing were funded by the Alzheimer’s Disease Neuroimaging Initiative, the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and multiple pharmaceutical companies and other private sector organizations. Dr. Morys and Dr. Sexton reported no relevant financial relationships.

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

It’s a common scenario. A patient, Agnes, with symptoms of an upper respiratory infection (URI), but what’s the cause? Is it COVID-19, flu, or even RSV? I recently described just such a patient, an obese woman with type 2 diabetes, presenting with fever, cough, myalgia, and fatigue. I asked readers whether they agreed with my management of this patient.

Thank you for your comments as we continue to react to high rates of URIs. Your comments highlight the importance of local resources and practice habits when managing patients with URI.

It was clear that readers value testing to distinguish between infections. However, access to testing is highly variable around the world and is likely to be routinely used only in high-income countries. The Kaiser Family Foundation performed a cost analysis of testing for SARS-CoV-2 in 2020 and found, not surprisingly, wide variability in the cost of testing. Medicare covers tests at rates of $36-$143 per test; a study of list prices for SARS-CoV-2 tests at 93 hospitals found a median cost of $148 per test. And this does not include collection or facility fees. About 20% of tests cost more than $300.

These costs are prohibitive for many health systems. However, more devices have been introduced since that analysis, and competition and evolving technology should drive down prices. Generally, multiplex polymerase chain reaction (PCR) testing for multiple pathogens is less expensive than ordering two or three separate molecular tests and is more convenient for patients and practices alike.

Other reader comments focused on the challenges of getting accurate data on viral epidemiology, and there is certainly a time lag between infection trends and public health reports. This is exacerbated by underreporting of symptoms and more testing at home using antigen tests.

But please do not give up on epidemiology! If a test such as PCR is 90% sensitive for identifying infection, the yield in terms of the number of individuals infected with a particular virus should be high, and that is true when infection is in broad circulation. If 20% of a population of 1,000 has an infection and the test sensitivity is 90%, the yield of testing is 180 true cases versus 20 false positives.

However, if just 2% of the population of 1,000 has the infection in this same scenario, then only 18 true cases are identified. The effect on public health is certainly less, and a lower prevalence rate means that confounding variables, such as how long an individual might shed viral particles and the method of sample collection, have an outsized effect on results. This reduces the validity of diagnostic tests.

Even trends on a national level can provide some insight regarding whom to test. Traditionally, our practice has been to not routinely test patients for influenza or RSV from late spring to early fall unless there was a compelling reason, such as recent travel to an area where these infections were more prevalent. The loss of temporality for these infections since 2020 has altered this approach and made us pay more attention to reports from public health organizations.

I also appreciate the discussion of how to treat Agnes’s symptoms as she waits to improve, and anyone who suffers with or treats a viral URI knows that there are few interventions effective for such symptoms as cough and congestion. A systematic review of 29 randomized controlled trials of over-the-counter medications for cough yielded mixed and largely negative results.

Antihistamines alone do not seem to work, and guaifenesin was successful in only one of three trials. Combinations of different drug classes appeared to be slightly more effective.

My personal favorite for the management of acute cough is something that kids generally love: honey. In a review of 14 studies, 9 of which were limited to pediatric patients, honey was associated with significant reductions in cough frequency, cough severity, and total symptom score. However, there was a moderate risk of bias in the included research, and evidence of honey’s benefit in placebo-controlled trials was limited. Honey used in this research came in a variety of forms, so the best dosage is uncertain.

Clearly, advancements are needed. Better symptom management in viral URI will almost certainly improve productivity across the population and will probably reduce the inappropriate use of antibiotics as well. I have said for years that the scientists who can solve the Gordian knot of pediatric mucus deserve three Nobel prizes. I look forward to that golden day.

Dr. Vega is a clinical professor of family medicine at the University of California, Irvine. He reported a conflict of interest with McNeil Pharmaceuticals.

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

It’s a common scenario. A patient, Agnes, with symptoms of an upper respiratory infection (URI), but what’s the cause? Is it COVID-19, flu, or even RSV? I recently described just such a patient, an obese woman with type 2 diabetes, presenting with fever, cough, myalgia, and fatigue. I asked readers whether they agreed with my management of this patient.

Thank you for your comments as we continue to react to high rates of URIs. Your comments highlight the importance of local resources and practice habits when managing patients with URI.

It was clear that readers value testing to distinguish between infections. However, access to testing is highly variable around the world and is likely to be routinely used only in high-income countries. The Kaiser Family Foundation performed a cost analysis of testing for SARS-CoV-2 in 2020 and found, not surprisingly, wide variability in the cost of testing. Medicare covers tests at rates of $36-$143 per test; a study of list prices for SARS-CoV-2 tests at 93 hospitals found a median cost of $148 per test. And this does not include collection or facility fees. About 20% of tests cost more than $300.

These costs are prohibitive for many health systems. However, more devices have been introduced since that analysis, and competition and evolving technology should drive down prices. Generally, multiplex polymerase chain reaction (PCR) testing for multiple pathogens is less expensive than ordering two or three separate molecular tests and is more convenient for patients and practices alike.

Other reader comments focused on the challenges of getting accurate data on viral epidemiology, and there is certainly a time lag between infection trends and public health reports. This is exacerbated by underreporting of symptoms and more testing at home using antigen tests.

But please do not give up on epidemiology! If a test such as PCR is 90% sensitive for identifying infection, the yield in terms of the number of individuals infected with a particular virus should be high, and that is true when infection is in broad circulation. If 20% of a population of 1,000 has an infection and the test sensitivity is 90%, the yield of testing is 180 true cases versus 20 false positives.

However, if just 2% of the population of 1,000 has the infection in this same scenario, then only 18 true cases are identified. The effect on public health is certainly less, and a lower prevalence rate means that confounding variables, such as how long an individual might shed viral particles and the method of sample collection, have an outsized effect on results. This reduces the validity of diagnostic tests.

Even trends on a national level can provide some insight regarding whom to test. Traditionally, our practice has been to not routinely test patients for influenza or RSV from late spring to early fall unless there was a compelling reason, such as recent travel to an area where these infections were more prevalent. The loss of temporality for these infections since 2020 has altered this approach and made us pay more attention to reports from public health organizations.

I also appreciate the discussion of how to treat Agnes’s symptoms as she waits to improve, and anyone who suffers with or treats a viral URI knows that there are few interventions effective for such symptoms as cough and congestion. A systematic review of 29 randomized controlled trials of over-the-counter medications for cough yielded mixed and largely negative results.

Antihistamines alone do not seem to work, and guaifenesin was successful in only one of three trials. Combinations of different drug classes appeared to be slightly more effective.

My personal favorite for the management of acute cough is something that kids generally love: honey. In a review of 14 studies, 9 of which were limited to pediatric patients, honey was associated with significant reductions in cough frequency, cough severity, and total symptom score. However, there was a moderate risk of bias in the included research, and evidence of honey’s benefit in placebo-controlled trials was limited. Honey used in this research came in a variety of forms, so the best dosage is uncertain.

Clearly, advancements are needed. Better symptom management in viral URI will almost certainly improve productivity across the population and will probably reduce the inappropriate use of antibiotics as well. I have said for years that the scientists who can solve the Gordian knot of pediatric mucus deserve three Nobel prizes. I look forward to that golden day.

Dr. Vega is a clinical professor of family medicine at the University of California, Irvine. He reported a conflict of interest with McNeil Pharmaceuticals.

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

It’s a common scenario. A patient, Agnes, with symptoms of an upper respiratory infection (URI), but what’s the cause? Is it COVID-19, flu, or even RSV? I recently described just such a patient, an obese woman with type 2 diabetes, presenting with fever, cough, myalgia, and fatigue. I asked readers whether they agreed with my management of this patient.

Thank you for your comments as we continue to react to high rates of URIs. Your comments highlight the importance of local resources and practice habits when managing patients with URI.

It was clear that readers value testing to distinguish between infections. However, access to testing is highly variable around the world and is likely to be routinely used only in high-income countries. The Kaiser Family Foundation performed a cost analysis of testing for SARS-CoV-2 in 2020 and found, not surprisingly, wide variability in the cost of testing. Medicare covers tests at rates of $36-$143 per test; a study of list prices for SARS-CoV-2 tests at 93 hospitals found a median cost of $148 per test. And this does not include collection or facility fees. About 20% of tests cost more than $300.

These costs are prohibitive for many health systems. However, more devices have been introduced since that analysis, and competition and evolving technology should drive down prices. Generally, multiplex polymerase chain reaction (PCR) testing for multiple pathogens is less expensive than ordering two or three separate molecular tests and is more convenient for patients and practices alike.

Other reader comments focused on the challenges of getting accurate data on viral epidemiology, and there is certainly a time lag between infection trends and public health reports. This is exacerbated by underreporting of symptoms and more testing at home using antigen tests.

But please do not give up on epidemiology! If a test such as PCR is 90% sensitive for identifying infection, the yield in terms of the number of individuals infected with a particular virus should be high, and that is true when infection is in broad circulation. If 20% of a population of 1,000 has an infection and the test sensitivity is 90%, the yield of testing is 180 true cases versus 20 false positives.

However, if just 2% of the population of 1,000 has the infection in this same scenario, then only 18 true cases are identified. The effect on public health is certainly less, and a lower prevalence rate means that confounding variables, such as how long an individual might shed viral particles and the method of sample collection, have an outsized effect on results. This reduces the validity of diagnostic tests.

Even trends on a national level can provide some insight regarding whom to test. Traditionally, our practice has been to not routinely test patients for influenza or RSV from late spring to early fall unless there was a compelling reason, such as recent travel to an area where these infections were more prevalent. The loss of temporality for these infections since 2020 has altered this approach and made us pay more attention to reports from public health organizations.

I also appreciate the discussion of how to treat Agnes’s symptoms as she waits to improve, and anyone who suffers with or treats a viral URI knows that there are few interventions effective for such symptoms as cough and congestion. A systematic review of 29 randomized controlled trials of over-the-counter medications for cough yielded mixed and largely negative results.

Antihistamines alone do not seem to work, and guaifenesin was successful in only one of three trials. Combinations of different drug classes appeared to be slightly more effective.

My personal favorite for the management of acute cough is something that kids generally love: honey. In a review of 14 studies, 9 of which were limited to pediatric patients, honey was associated with significant reductions in cough frequency, cough severity, and total symptom score. However, there was a moderate risk of bias in the included research, and evidence of honey’s benefit in placebo-controlled trials was limited. Honey used in this research came in a variety of forms, so the best dosage is uncertain.

Clearly, advancements are needed. Better symptom management in viral URI will almost certainly improve productivity across the population and will probably reduce the inappropriate use of antibiotics as well. I have said for years that the scientists who can solve the Gordian knot of pediatric mucus deserve three Nobel prizes. I look forward to that golden day.

Dr. Vega is a clinical professor of family medicine at the University of California, Irvine. He reported a conflict of interest with McNeil Pharmaceuticals.

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

The introduction of the soft drinks industry levy (SDIL) – dubbed the ‘sugar tax’ – in England was followed by a drop in the number of older primary school girls succumbing to obesity, according to researchers from the Universities of Cambridge, Oxford, and Bath, with colleagues at the London School of Hygiene and Tropical Medicine.

The study, published in PLOS Medicine, has led to calls to extend the levy to other unhealthy foods and drinks

Obesity has become a global public health problem, the researchers said. In England, around 10% of 4- to 5-year-old children and 20% of 10- to 11-year-olds were recorded as obese in 2020. Childhood obesity is associated with depression in children and the adults into which they maturate, as well as with serious health problems in later life including high blood pressure and type 2 diabetes.

In the United Kingdom, young people consume significantly more added sugars than are recommended – by late adolescence, typically 70 g of added sugar per day, more than double the recommended 30g. The team said that sugar-sweetened beverages (SSB) are the primary sources of dietary added sugars in children, with high consumption commonly observed in more deprived areas where obesity prevalence is also highest.
 

Protecting children from excessive sugar

The two-tier SDIL on drinks manufacturers was implemented in April 2018 and aimed to protect children from excessive sugar consumption and tackle childhood obesity by incentivizing reformulation of SSBs in the U.K. with reduced sugar content.

To assess the effects of SDIL, the researchers used data from the National Child Measurement Programme on over 1 million children at ages 4 to 5 years (reception class) and 10 to 11 years (school year 6) in state-maintained English primary schools. The surveillance program includes annual repeat cross-sectional measurements, enabling the researchers to examine trajectories in monthly prevalence of obesity from September 2013 to November 2019, 19 months after the implementation of the SDIL.

Taking account of previous trends in obesity levels, they estimated both absolute and relative changes in obesity prevalence, both overall and by sex and deprivation, and compared obesity levels after the SDIL with predicted levels had the tax not been introduced, controlling for children’s sex and the level of deprivation of their school area.

Although they found no significant association with obesity levels in reception-age children or year-6 boys, they noted an overall absolute reduction in obesity prevalence of 1.6 percentage points (PPs) (95% confidence interval, 1.1-2.1) in 10- to 11-year-old (year 6) girls. This equated to an 8% relative reduction in obesity rates compared with a counterfactual estimated from the trend prior to the SDIL announcement in March 2016, adjusted for temporal variations in obesity prevalence.

The researchers estimated that this was equivalent to preventing 5,234 cases of obesity per year in this group of year-6 girls alone.
 

Obesity reductions greatest in most deprived areas

Reductions were greatest in girls whose schools were in the most deprived areas, where children are known to consume the largest amount of sugary drinks. The greatest reductions in obesity were observed in the two most deprived quintiles – such that in the lowest quintile the absolute obesity prevalence reduction was 2.4 PP (95% CI, 1.6-3.2), equivalent to a 9% reduction in those living in the most deprived areas.

There are several reasons why the sugar tax did not lead to changes in levels of obesity among the younger children, the researchers said. Very young children consume fewer sugar-sweetened drinks than older children, so the soft drinks levy would have had a smaller effect. Also, fruit juices are not included in the levy, but contribute similar amounts of sugar in young children’s diets as do sugar-sweetened beverages.
 

Advertising may impact consumption in boys

It’s also unclear why the sugar tax might affect obesity prevalence in girls and boys differently, they said, especially since boys are higher consumers of sugar-sweetened beverages. One explanation is the possible impact of advertising – numerous studies have found that boys are often exposed to more food advertising than girls, both through higher levels of TV viewing and in how adverts are framed. Physical activity is often used to promote junk food and boys, compared with girls, have been shown to be more likely to believe that energy-dense junk foods depicted in adverts will boost physical performance, and so are more likely to choose energy-dense, nutrient-poor products following celebrity endorsements.

Tax ‘led to positive health impacts’

“Our findings suggest that the U.K. SDIL led to positive health impacts in the form of reduced obesity levels in girls aged 10-11 years,” the authors said. However: “Additional strategies beyond SSB taxation will be needed to reduce obesity prevalence overall, and particularly in older boys and younger children.”

Dr. Nina Rogers from the MRC Epidemiology Unit at Cambridge (England), who led the study, said: “We urgently need to find ways to tackle the increasing numbers of children living with obesity, otherwise we risk our children growing up to face significant health problems. That was one reason why the U.K.’s SDIL was introduced, and the evidence so far is promising. We’ve shown for the first time that it is likely to have helped prevent thousands of children each year becoming obese.

“It isn’t a straightforward picture, though, as it was mainly older girls who benefited. But the fact that we saw the biggest difference among girls from areas of high deprivation is important and is a step towards reducing the health inequalities they face.”

Although the researchers found an association rather than a causal link, this study adds to previous findings that the levy was associated with a substantial reduction in the amount of sugar in soft drinks.

Senior author Professor Jean Adams from the MRC Epidemiology Unit said: “We know that consuming too many sugary drinks contributes to obesity and that the U.K. soft drinks levy led to a drop in the amount of sugar in soft drinks available in the U.K., so it makes sense that we also see a drop in cases of obesity, although we only found this in girls. Children from more deprived backgrounds tend to consume the largest amount of sugary drinks, and it was among girls in this group that we saw the biggest change.”

Tom Sanders, professor emeritus of nutrition and dietetics at King’s College London, said: “The claim that the soft drink levy might have prevented 5,000 children from becoming obese is speculative because it is based on an association not actual measurements of consumption.”

He added that: “As well as continuing to discourage the consumption of sugar sweetened beverages and sweets, wider recognition should be given to foods such as biscuits [and] deep-fried foods (crisps, corn snacks, chips) that make [a] bigger contribution to excess calorie intake in children. Tackling poverty, however, is probably [the] best way to improve the diets of socially deprived children.”
 

Government ‘should learn from this success’

Asked to comment by this news organization, Katharine Jenner, director of the Obesity Health Alliance, said: “Government should be heartened that their soft drinks policy is already improving the health of young girls, regardless of where they live. The government should learn from this success, especially when compared with the many unsuccessful attempts to persuade industry to change their products voluntarily.  They must now press ahead with policies that make it easier for everyone to eat a healthier diet, including extending the soft drinks industry levy to include other less healthy foods and drinks and measures to take junk food out of the spotlight. 

“The research notes that numerous studies have found that boys are often exposed to more food advertising content than girls, negating the impact of the soft drinks levy [so] we need restriction on junk food marketing now, to put healthy food back in the spotlight.”

The research was supported by the National Institute of Health and Care Research and the Medical Research Council.

A version of this article originally appeared on MedscapeUK.

The introduction of the soft drinks industry levy (SDIL) – dubbed the ‘sugar tax’ – in England was followed by a drop in the number of older primary school girls succumbing to obesity, according to researchers from the Universities of Cambridge, Oxford, and Bath, with colleagues at the London School of Hygiene and Tropical Medicine.

The study, published in PLOS Medicine, has led to calls to extend the levy to other unhealthy foods and drinks

Obesity has become a global public health problem, the researchers said. In England, around 10% of 4- to 5-year-old children and 20% of 10- to 11-year-olds were recorded as obese in 2020. Childhood obesity is associated with depression in children and the adults into which they maturate, as well as with serious health problems in later life including high blood pressure and type 2 diabetes.

In the United Kingdom, young people consume significantly more added sugars than are recommended – by late adolescence, typically 70 g of added sugar per day, more than double the recommended 30g. The team said that sugar-sweetened beverages (SSB) are the primary sources of dietary added sugars in children, with high consumption commonly observed in more deprived areas where obesity prevalence is also highest.
 

Protecting children from excessive sugar

The two-tier SDIL on drinks manufacturers was implemented in April 2018 and aimed to protect children from excessive sugar consumption and tackle childhood obesity by incentivizing reformulation of SSBs in the U.K. with reduced sugar content.

To assess the effects of SDIL, the researchers used data from the National Child Measurement Programme on over 1 million children at ages 4 to 5 years (reception class) and 10 to 11 years (school year 6) in state-maintained English primary schools. The surveillance program includes annual repeat cross-sectional measurements, enabling the researchers to examine trajectories in monthly prevalence of obesity from September 2013 to November 2019, 19 months after the implementation of the SDIL.

Taking account of previous trends in obesity levels, they estimated both absolute and relative changes in obesity prevalence, both overall and by sex and deprivation, and compared obesity levels after the SDIL with predicted levels had the tax not been introduced, controlling for children’s sex and the level of deprivation of their school area.

Although they found no significant association with obesity levels in reception-age children or year-6 boys, they noted an overall absolute reduction in obesity prevalence of 1.6 percentage points (PPs) (95% confidence interval, 1.1-2.1) in 10- to 11-year-old (year 6) girls. This equated to an 8% relative reduction in obesity rates compared with a counterfactual estimated from the trend prior to the SDIL announcement in March 2016, adjusted for temporal variations in obesity prevalence.

The researchers estimated that this was equivalent to preventing 5,234 cases of obesity per year in this group of year-6 girls alone.
 

Obesity reductions greatest in most deprived areas

Reductions were greatest in girls whose schools were in the most deprived areas, where children are known to consume the largest amount of sugary drinks. The greatest reductions in obesity were observed in the two most deprived quintiles – such that in the lowest quintile the absolute obesity prevalence reduction was 2.4 PP (95% CI, 1.6-3.2), equivalent to a 9% reduction in those living in the most deprived areas.

There are several reasons why the sugar tax did not lead to changes in levels of obesity among the younger children, the researchers said. Very young children consume fewer sugar-sweetened drinks than older children, so the soft drinks levy would have had a smaller effect. Also, fruit juices are not included in the levy, but contribute similar amounts of sugar in young children’s diets as do sugar-sweetened beverages.
 

Advertising may impact consumption in boys

It’s also unclear why the sugar tax might affect obesity prevalence in girls and boys differently, they said, especially since boys are higher consumers of sugar-sweetened beverages. One explanation is the possible impact of advertising – numerous studies have found that boys are often exposed to more food advertising than girls, both through higher levels of TV viewing and in how adverts are framed. Physical activity is often used to promote junk food and boys, compared with girls, have been shown to be more likely to believe that energy-dense junk foods depicted in adverts will boost physical performance, and so are more likely to choose energy-dense, nutrient-poor products following celebrity endorsements.

Tax ‘led to positive health impacts’

“Our findings suggest that the U.K. SDIL led to positive health impacts in the form of reduced obesity levels in girls aged 10-11 years,” the authors said. However: “Additional strategies beyond SSB taxation will be needed to reduce obesity prevalence overall, and particularly in older boys and younger children.”

Dr. Nina Rogers from the MRC Epidemiology Unit at Cambridge (England), who led the study, said: “We urgently need to find ways to tackle the increasing numbers of children living with obesity, otherwise we risk our children growing up to face significant health problems. That was one reason why the U.K.’s SDIL was introduced, and the evidence so far is promising. We’ve shown for the first time that it is likely to have helped prevent thousands of children each year becoming obese.

“It isn’t a straightforward picture, though, as it was mainly older girls who benefited. But the fact that we saw the biggest difference among girls from areas of high deprivation is important and is a step towards reducing the health inequalities they face.”

Although the researchers found an association rather than a causal link, this study adds to previous findings that the levy was associated with a substantial reduction in the amount of sugar in soft drinks.

Senior author Professor Jean Adams from the MRC Epidemiology Unit said: “We know that consuming too many sugary drinks contributes to obesity and that the U.K. soft drinks levy led to a drop in the amount of sugar in soft drinks available in the U.K., so it makes sense that we also see a drop in cases of obesity, although we only found this in girls. Children from more deprived backgrounds tend to consume the largest amount of sugary drinks, and it was among girls in this group that we saw the biggest change.”

Tom Sanders, professor emeritus of nutrition and dietetics at King’s College London, said: “The claim that the soft drink levy might have prevented 5,000 children from becoming obese is speculative because it is based on an association not actual measurements of consumption.”

He added that: “As well as continuing to discourage the consumption of sugar sweetened beverages and sweets, wider recognition should be given to foods such as biscuits [and] deep-fried foods (crisps, corn snacks, chips) that make [a] bigger contribution to excess calorie intake in children. Tackling poverty, however, is probably [the] best way to improve the diets of socially deprived children.”
 

Government ‘should learn from this success’

Asked to comment by this news organization, Katharine Jenner, director of the Obesity Health Alliance, said: “Government should be heartened that their soft drinks policy is already improving the health of young girls, regardless of where they live. The government should learn from this success, especially when compared with the many unsuccessful attempts to persuade industry to change their products voluntarily.  They must now press ahead with policies that make it easier for everyone to eat a healthier diet, including extending the soft drinks industry levy to include other less healthy foods and drinks and measures to take junk food out of the spotlight. 

“The research notes that numerous studies have found that boys are often exposed to more food advertising content than girls, negating the impact of the soft drinks levy [so] we need restriction on junk food marketing now, to put healthy food back in the spotlight.”

The research was supported by the National Institute of Health and Care Research and the Medical Research Council.

A version of this article originally appeared on MedscapeUK.

The introduction of the soft drinks industry levy (SDIL) – dubbed the ‘sugar tax’ – in England was followed by a drop in the number of older primary school girls succumbing to obesity, according to researchers from the Universities of Cambridge, Oxford, and Bath, with colleagues at the London School of Hygiene and Tropical Medicine.

The study, published in PLOS Medicine, has led to calls to extend the levy to other unhealthy foods and drinks

Obesity has become a global public health problem, the researchers said. In England, around 10% of 4- to 5-year-old children and 20% of 10- to 11-year-olds were recorded as obese in 2020. Childhood obesity is associated with depression in children and the adults into which they maturate, as well as with serious health problems in later life including high blood pressure and type 2 diabetes.

In the United Kingdom, young people consume significantly more added sugars than are recommended – by late adolescence, typically 70 g of added sugar per day, more than double the recommended 30g. The team said that sugar-sweetened beverages (SSB) are the primary sources of dietary added sugars in children, with high consumption commonly observed in more deprived areas where obesity prevalence is also highest.
 

Protecting children from excessive sugar

The two-tier SDIL on drinks manufacturers was implemented in April 2018 and aimed to protect children from excessive sugar consumption and tackle childhood obesity by incentivizing reformulation of SSBs in the U.K. with reduced sugar content.

To assess the effects of SDIL, the researchers used data from the National Child Measurement Programme on over 1 million children at ages 4 to 5 years (reception class) and 10 to 11 years (school year 6) in state-maintained English primary schools. The surveillance program includes annual repeat cross-sectional measurements, enabling the researchers to examine trajectories in monthly prevalence of obesity from September 2013 to November 2019, 19 months after the implementation of the SDIL.

Taking account of previous trends in obesity levels, they estimated both absolute and relative changes in obesity prevalence, both overall and by sex and deprivation, and compared obesity levels after the SDIL with predicted levels had the tax not been introduced, controlling for children’s sex and the level of deprivation of their school area.

Although they found no significant association with obesity levels in reception-age children or year-6 boys, they noted an overall absolute reduction in obesity prevalence of 1.6 percentage points (PPs) (95% confidence interval, 1.1-2.1) in 10- to 11-year-old (year 6) girls. This equated to an 8% relative reduction in obesity rates compared with a counterfactual estimated from the trend prior to the SDIL announcement in March 2016, adjusted for temporal variations in obesity prevalence.

The researchers estimated that this was equivalent to preventing 5,234 cases of obesity per year in this group of year-6 girls alone.
 

Obesity reductions greatest in most deprived areas

Reductions were greatest in girls whose schools were in the most deprived areas, where children are known to consume the largest amount of sugary drinks. The greatest reductions in obesity were observed in the two most deprived quintiles – such that in the lowest quintile the absolute obesity prevalence reduction was 2.4 PP (95% CI, 1.6-3.2), equivalent to a 9% reduction in those living in the most deprived areas.

There are several reasons why the sugar tax did not lead to changes in levels of obesity among the younger children, the researchers said. Very young children consume fewer sugar-sweetened drinks than older children, so the soft drinks levy would have had a smaller effect. Also, fruit juices are not included in the levy, but contribute similar amounts of sugar in young children’s diets as do sugar-sweetened beverages.
 

Advertising may impact consumption in boys

It’s also unclear why the sugar tax might affect obesity prevalence in girls and boys differently, they said, especially since boys are higher consumers of sugar-sweetened beverages. One explanation is the possible impact of advertising – numerous studies have found that boys are often exposed to more food advertising than girls, both through higher levels of TV viewing and in how adverts are framed. Physical activity is often used to promote junk food and boys, compared with girls, have been shown to be more likely to believe that energy-dense junk foods depicted in adverts will boost physical performance, and so are more likely to choose energy-dense, nutrient-poor products following celebrity endorsements.

Tax ‘led to positive health impacts’

“Our findings suggest that the U.K. SDIL led to positive health impacts in the form of reduced obesity levels in girls aged 10-11 years,” the authors said. However: “Additional strategies beyond SSB taxation will be needed to reduce obesity prevalence overall, and particularly in older boys and younger children.”

Dr. Nina Rogers from the MRC Epidemiology Unit at Cambridge (England), who led the study, said: “We urgently need to find ways to tackle the increasing numbers of children living with obesity, otherwise we risk our children growing up to face significant health problems. That was one reason why the U.K.’s SDIL was introduced, and the evidence so far is promising. We’ve shown for the first time that it is likely to have helped prevent thousands of children each year becoming obese.

“It isn’t a straightforward picture, though, as it was mainly older girls who benefited. But the fact that we saw the biggest difference among girls from areas of high deprivation is important and is a step towards reducing the health inequalities they face.”

Although the researchers found an association rather than a causal link, this study adds to previous findings that the levy was associated with a substantial reduction in the amount of sugar in soft drinks.

Senior author Professor Jean Adams from the MRC Epidemiology Unit said: “We know that consuming too many sugary drinks contributes to obesity and that the U.K. soft drinks levy led to a drop in the amount of sugar in soft drinks available in the U.K., so it makes sense that we also see a drop in cases of obesity, although we only found this in girls. Children from more deprived backgrounds tend to consume the largest amount of sugary drinks, and it was among girls in this group that we saw the biggest change.”

Tom Sanders, professor emeritus of nutrition and dietetics at King’s College London, said: “The claim that the soft drink levy might have prevented 5,000 children from becoming obese is speculative because it is based on an association not actual measurements of consumption.”

He added that: “As well as continuing to discourage the consumption of sugar sweetened beverages and sweets, wider recognition should be given to foods such as biscuits [and] deep-fried foods (crisps, corn snacks, chips) that make [a] bigger contribution to excess calorie intake in children. Tackling poverty, however, is probably [the] best way to improve the diets of socially deprived children.”
 

Government ‘should learn from this success’

Asked to comment by this news organization, Katharine Jenner, director of the Obesity Health Alliance, said: “Government should be heartened that their soft drinks policy is already improving the health of young girls, regardless of where they live. The government should learn from this success, especially when compared with the many unsuccessful attempts to persuade industry to change their products voluntarily.  They must now press ahead with policies that make it easier for everyone to eat a healthier diet, including extending the soft drinks industry levy to include other less healthy foods and drinks and measures to take junk food out of the spotlight. 

“The research notes that numerous studies have found that boys are often exposed to more food advertising content than girls, negating the impact of the soft drinks levy [so] we need restriction on junk food marketing now, to put healthy food back in the spotlight.”

The research was supported by the National Institute of Health and Care Research and the Medical Research Council.

A version of this article originally appeared on MedscapeUK.

Apparently, offering children effective treatments for a chronic disease that markedly increases their risk for other chronic diseases, regularly erodes their quality of life, and is the No. 1 target of school-based bullying is wrong.

At least that’s my take watching the coverage of the recent American Academy of Pediatrics new pediatric obesity treatment guidelines that, gasp, suggest that children whose severity of obesity warrants medication or surgeries be offered medication or surgery. Because it’s wiser to not try to treat the obesity that›s contributing to a child’s type 2 diabetes, hypertension, fatty liver disease, or reduced quality of life?

The reaction isn’t surprising. Some of those who are up in arms about it have clinical or research careers dependent on championing their own favorite dietary strategies as if they are more effective and reproducible than decades of uniformly disappointing studies proving that they’re not. Others are upset because, for reasons that at times may be personal and at times may be conflicted, they believe that obesity should not be treated and/or that sustained weight loss is impossible. But overarchingly, probably the bulk of the hoopla stems from obesity being seen as a moral failing. Because the notion that those who suffer with obesity are themselves to blame has been the prevailing societal view for decades, if not centuries.

Working with families of children with obesity severe enough for them to seek help, it’s clear that if desire were sufficient to will it away, we wouldn’t need treatment guidelines let alone medications or surgery. Near uniformly, parents describe their children being bullied consequent to and being deeply self-conscious of their weight.

And what would those who think children shouldn’t be offered reproducibly effective treatment for obesity have them do about it? Many seem to think it would be preferable for kids to be placed on formal diets and, of course, that they should go out and play more. And though I’m all for encouraging the improvement of a child’s dietary quality and activity level, anyone suggesting those as panaceas for childhood obesity haven’t a clue. Not to mention the fact that, in most cases, improving overall dietary quality, something worthwhile at any weight, isn’t the dietary goal being recommended. Instead, the prescription seems to be restrictive dieting coupled with overexercising, which, unlike appropriately and thoughtfully informed and utilized medication, may increase a child’s risk of maladaptive thinking around food and fitness as well as disordered eating, not to mention challenge their self-esteem if their lifestyle results are underwhelming.

This brings us to one of the most bizarre takes on this whole business – that medications will be pushed and used when not necessary. No doubt that at times, that may occur, but the issue is that of a clinician’s overzealous prescribing and not of the treatment options or indications. Consider childhood asthma. There is no worry or uproar that children with mild asthma that isn’t having an impact on their quality of life or markedly risking their health will be placed on multiple inhaled steroids and treatments. Why? Because clinicians have been taught how to dispassionately evaluate treatment needs for asthma, monitor disease course, and not simply prescribe everything in our armamentarium.

Shocking, I know, but as is the case with every other medical condition, I think doctors are capable of learning and following an algorithm covering the indications and options for the treatment of childhood obesity.

How that looks also mirrors what’s seen with any other chronic noncommunicable disease with varied severity and impact. Doctors will evaluate each child with obesity to see whether it’s having a detrimental effect on their health or quality of life. They will monitor their patients’ obesity to see if it’s worsening and will, when necessary, undertake investigations to rule out its potential contribution to common comorbidities like type 2 diabetes, hypertension, and fatty liver disease. And, when appropriate, they will provide information on available treatment options – from lifestyle to medication to surgery and the risks, benefits, and realistic expectations associated with each – and then, without judgment, support their patients’ treatment choices because blame-free informed discussion and supportive prescription of care is, in fact, the distillation of our jobs.

If people are looking to be outraged rather than focusing their outrage on what we now need to do about childhood obesity, they should instead look to what got us here: our obesogenic environment. We and our children are swimming against a torrential current of cheap ultraprocessed calories being pushed upon us by a broken societal food culture that values convenience and simultaneously embraces the notion that knowledge is a match versus the thousands of genes and dozens of hormones that increasingly sophisticated food industry marketers and scientists prey upon. When dealing with torrential currents, we need to do more than just recommend swimming lessons.

Like asthma, which may be exacerbated by pollution in our environment both outdoors and indoors, childhood obesity is a modern-day environmentally influenced disease with varied penetrance that does not always require active treatment. Like asthma, childhood obesity is not a disease that children choose to have; it’s not a disease that can be willed away; and it’s not a disease that responds uniformly, dramatically, or enduringly to diet and exercise. Finally, literally and figuratively, like asthma, for childhood obesity, we thankfully now have a number of effective treatment options that we can offer, and it’s only our societal weight bias that leads to thinking that’s anything but great.

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

Apparently, offering children effective treatments for a chronic disease that markedly increases their risk for other chronic diseases, regularly erodes their quality of life, and is the No. 1 target of school-based bullying is wrong.

At least that’s my take watching the coverage of the recent American Academy of Pediatrics new pediatric obesity treatment guidelines that, gasp, suggest that children whose severity of obesity warrants medication or surgeries be offered medication or surgery. Because it’s wiser to not try to treat the obesity that›s contributing to a child’s type 2 diabetes, hypertension, fatty liver disease, or reduced quality of life?

The reaction isn’t surprising. Some of those who are up in arms about it have clinical or research careers dependent on championing their own favorite dietary strategies as if they are more effective and reproducible than decades of uniformly disappointing studies proving that they’re not. Others are upset because, for reasons that at times may be personal and at times may be conflicted, they believe that obesity should not be treated and/or that sustained weight loss is impossible. But overarchingly, probably the bulk of the hoopla stems from obesity being seen as a moral failing. Because the notion that those who suffer with obesity are themselves to blame has been the prevailing societal view for decades, if not centuries.

Working with families of children with obesity severe enough for them to seek help, it’s clear that if desire were sufficient to will it away, we wouldn’t need treatment guidelines let alone medications or surgery. Near uniformly, parents describe their children being bullied consequent to and being deeply self-conscious of their weight.

And what would those who think children shouldn’t be offered reproducibly effective treatment for obesity have them do about it? Many seem to think it would be preferable for kids to be placed on formal diets and, of course, that they should go out and play more. And though I’m all for encouraging the improvement of a child’s dietary quality and activity level, anyone suggesting those as panaceas for childhood obesity haven’t a clue. Not to mention the fact that, in most cases, improving overall dietary quality, something worthwhile at any weight, isn’t the dietary goal being recommended. Instead, the prescription seems to be restrictive dieting coupled with overexercising, which, unlike appropriately and thoughtfully informed and utilized medication, may increase a child’s risk of maladaptive thinking around food and fitness as well as disordered eating, not to mention challenge their self-esteem if their lifestyle results are underwhelming.

This brings us to one of the most bizarre takes on this whole business – that medications will be pushed and used when not necessary. No doubt that at times, that may occur, but the issue is that of a clinician’s overzealous prescribing and not of the treatment options or indications. Consider childhood asthma. There is no worry or uproar that children with mild asthma that isn’t having an impact on their quality of life or markedly risking their health will be placed on multiple inhaled steroids and treatments. Why? Because clinicians have been taught how to dispassionately evaluate treatment needs for asthma, monitor disease course, and not simply prescribe everything in our armamentarium.

Shocking, I know, but as is the case with every other medical condition, I think doctors are capable of learning and following an algorithm covering the indications and options for the treatment of childhood obesity.

How that looks also mirrors what’s seen with any other chronic noncommunicable disease with varied severity and impact. Doctors will evaluate each child with obesity to see whether it’s having a detrimental effect on their health or quality of life. They will monitor their patients’ obesity to see if it’s worsening and will, when necessary, undertake investigations to rule out its potential contribution to common comorbidities like type 2 diabetes, hypertension, and fatty liver disease. And, when appropriate, they will provide information on available treatment options – from lifestyle to medication to surgery and the risks, benefits, and realistic expectations associated with each – and then, without judgment, support their patients’ treatment choices because blame-free informed discussion and supportive prescription of care is, in fact, the distillation of our jobs.

If people are looking to be outraged rather than focusing their outrage on what we now need to do about childhood obesity, they should instead look to what got us here: our obesogenic environment. We and our children are swimming against a torrential current of cheap ultraprocessed calories being pushed upon us by a broken societal food culture that values convenience and simultaneously embraces the notion that knowledge is a match versus the thousands of genes and dozens of hormones that increasingly sophisticated food industry marketers and scientists prey upon. When dealing with torrential currents, we need to do more than just recommend swimming lessons.

Like asthma, which may be exacerbated by pollution in our environment both outdoors and indoors, childhood obesity is a modern-day environmentally influenced disease with varied penetrance that does not always require active treatment. Like asthma, childhood obesity is not a disease that children choose to have; it’s not a disease that can be willed away; and it’s not a disease that responds uniformly, dramatically, or enduringly to diet and exercise. Finally, literally and figuratively, like asthma, for childhood obesity, we thankfully now have a number of effective treatment options that we can offer, and it’s only our societal weight bias that leads to thinking that’s anything but great.

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

Apparently, offering children effective treatments for a chronic disease that markedly increases their risk for other chronic diseases, regularly erodes their quality of life, and is the No. 1 target of school-based bullying is wrong.

At least that’s my take watching the coverage of the recent American Academy of Pediatrics new pediatric obesity treatment guidelines that, gasp, suggest that children whose severity of obesity warrants medication or surgeries be offered medication or surgery. Because it’s wiser to not try to treat the obesity that›s contributing to a child’s type 2 diabetes, hypertension, fatty liver disease, or reduced quality of life?

The reaction isn’t surprising. Some of those who are up in arms about it have clinical or research careers dependent on championing their own favorite dietary strategies as if they are more effective and reproducible than decades of uniformly disappointing studies proving that they’re not. Others are upset because, for reasons that at times may be personal and at times may be conflicted, they believe that obesity should not be treated and/or that sustained weight loss is impossible. But overarchingly, probably the bulk of the hoopla stems from obesity being seen as a moral failing. Because the notion that those who suffer with obesity are themselves to blame has been the prevailing societal view for decades, if not centuries.

Working with families of children with obesity severe enough for them to seek help, it’s clear that if desire were sufficient to will it away, we wouldn’t need treatment guidelines let alone medications or surgery. Near uniformly, parents describe their children being bullied consequent to and being deeply self-conscious of their weight.

And what would those who think children shouldn’t be offered reproducibly effective treatment for obesity have them do about it? Many seem to think it would be preferable for kids to be placed on formal diets and, of course, that they should go out and play more. And though I’m all for encouraging the improvement of a child’s dietary quality and activity level, anyone suggesting those as panaceas for childhood obesity haven’t a clue. Not to mention the fact that, in most cases, improving overall dietary quality, something worthwhile at any weight, isn’t the dietary goal being recommended. Instead, the prescription seems to be restrictive dieting coupled with overexercising, which, unlike appropriately and thoughtfully informed and utilized medication, may increase a child’s risk of maladaptive thinking around food and fitness as well as disordered eating, not to mention challenge their self-esteem if their lifestyle results are underwhelming.

This brings us to one of the most bizarre takes on this whole business – that medications will be pushed and used when not necessary. No doubt that at times, that may occur, but the issue is that of a clinician’s overzealous prescribing and not of the treatment options or indications. Consider childhood asthma. There is no worry or uproar that children with mild asthma that isn’t having an impact on their quality of life or markedly risking their health will be placed on multiple inhaled steroids and treatments. Why? Because clinicians have been taught how to dispassionately evaluate treatment needs for asthma, monitor disease course, and not simply prescribe everything in our armamentarium.

Shocking, I know, but as is the case with every other medical condition, I think doctors are capable of learning and following an algorithm covering the indications and options for the treatment of childhood obesity.

How that looks also mirrors what’s seen with any other chronic noncommunicable disease with varied severity and impact. Doctors will evaluate each child with obesity to see whether it’s having a detrimental effect on their health or quality of life. They will monitor their patients’ obesity to see if it’s worsening and will, when necessary, undertake investigations to rule out its potential contribution to common comorbidities like type 2 diabetes, hypertension, and fatty liver disease. And, when appropriate, they will provide information on available treatment options – from lifestyle to medication to surgery and the risks, benefits, and realistic expectations associated with each – and then, without judgment, support their patients’ treatment choices because blame-free informed discussion and supportive prescription of care is, in fact, the distillation of our jobs.

If people are looking to be outraged rather than focusing their outrage on what we now need to do about childhood obesity, they should instead look to what got us here: our obesogenic environment. We and our children are swimming against a torrential current of cheap ultraprocessed calories being pushed upon us by a broken societal food culture that values convenience and simultaneously embraces the notion that knowledge is a match versus the thousands of genes and dozens of hormones that increasingly sophisticated food industry marketers and scientists prey upon. When dealing with torrential currents, we need to do more than just recommend swimming lessons.

Like asthma, which may be exacerbated by pollution in our environment both outdoors and indoors, childhood obesity is a modern-day environmentally influenced disease with varied penetrance that does not always require active treatment. Like asthma, childhood obesity is not a disease that children choose to have; it’s not a disease that can be willed away; and it’s not a disease that responds uniformly, dramatically, or enduringly to diet and exercise. Finally, literally and figuratively, like asthma, for childhood obesity, we thankfully now have a number of effective treatment options that we can offer, and it’s only our societal weight bias that leads to thinking that’s anything but great.

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