Family Practice News

A young boy with a habit of screaming when he didn’t get his way is among the patients Joannie Yeh, MD, a primary care physician at Nemours Children’s Health in Media, Pennsylvania, has helped in her practice.

Yeh taught the boy to stretch out his hands into the shape of a starfish, then trace around the edges of his fingers while breathing slowly and deeply. His parents later reported that after using the strategy at home, their son was no longer taking his rage out on his younger siblings.

Interventions like breathing exercises are just a few techniques Yeh hopes more primary care clinicians will teach young patients as mental health issues among this population soar to a national state of emergency, major medical groups say. But many children go without treatment because of shortages of mental health clinicians and long wait-lists for appointments.

“Knowledge of different types of interventions allows pediatricians to offer more options to families — more than just medication alone,” Yeh said. “There are some strategies, like cognitive behavioral therapy, that a therapist is equipped to deliver, but we can help explain them or teach simple skills that borrow from principles of higher-level techniques and can help patients and families while they wait to see a therapist.”

The use of techniques that are based on mindfulness, cognitive behavioral therapy, and psychotherapy are especially helpful to pediatricians after a child’s answers on a screener indicate they may be struggling with anxiety, depression, or attention-deficit/hyperactivity disorder (ADHD), said Theresa Nguyen, MD, chair of pediatrics at Greater Baltimore Medical Center, Baltimore.

“It kind of sucks if you come in worried and then your doctor says, ‘Okay, let me send you to a psychiatrist who you can’t see for 6 months; let me send you to a therapist who’s going to take a couple of weeks to get in with,’” Nguyen said.

Yeh said over the past few years she has cared for more youth coming in as follow-ups after an emergency department visit for a mental health episode.

“Oftentimes, this is the first time we become aware that the child is struggling,” Yeh said. “We are seeing issues like intentional medication overdose, referrals after other self-harm actions, or even the discovery of a note indicating the intention to do harm to self.”

Suicide deaths among 10- to 14-year-olds tripled between 2007 and 2018 and held steady through 2021, with rates climbing even among children as young as 8 years, according to a research in JAMA Network Open. Meanwhile, one in five high school students seriously contemplated suicide in 2023 (27% girls, 14% boys).

 

Mental Health Strategies for Kids in Primary Care

While pediatricians cannot replace a mental health professional, they have the unique advantage of maintaining a long-term relationship with patients. Experts said clinicians should take an active role in supporting the mental health of patients through a variety of evidence-based strategies.

Changing Thought Patterns 

Cognitive-behavioral therapy (CBT) involves identifying and challenging automatic negative thoughts, which can affect a child’s emotional state and lead to behaviors like withdrawal or lashing out.

Yeh recommended asking a child about what is bothering them, pointing out unhelpful and negative thoughts, and then offering a different, positive one instead.

She also often draws a picture of the CBT chart, which is a visual representation of how feelings lead to thoughts, and then behaviors.

“I draw this diagram because it helps give the patients a visual understanding of how their feelings and emotions are connected,” Yeh said.

 

Tools to Tolerate Stressful Situations

Simple tools like breathing exercises, body scanning, and physical exercise can help children better tolerate distress.

Pediatricians can also recommend families use guided meditations, which have been shown to lower anxiety and increase positive social behavior, said Mollie Grow, MD, an associate professor of pediatrics at the University of Washington Medicine and Seattle Children’s Hospital, both in Seattle.

But a child might first need to get negative energy out before they can become calm.

“So I’m like, ‘okay, let’s do actual physical exercise. Give me 10 jumping jacks.’ No one’s nervous after those jumping jacks,” Nguyen said. “When you’ve already been triggered, your nerves have gotten going, and you’re starting to spiral, you can’t slow yourself down enough to do a breathing exercise.”

Nguyen also said that cold water quickly calms the nervous system.

“I’ll run cold water in the office and have them put their hand in it until it’s almost frozen,” and the child or teen is able to think more clearly, Nguyen said. “It’s a real physiological response. It works.”

 

The Origin of a Feeling 

Explaining how symptoms of anxiety, depression, or ADHD work can help children and teens better understand that what they are experiencing is normal and better cope, Yeh said.

Clinicians might teach patients about how shallow breathing — a symptom of anxiety — is a result of the brain scanning for danger, and how slowing breathing tricks the brain into feeling safe again.

 

Barriers Abound

The use of these interventions in pediatric settings is not yet widespread, Grow said.

But starting in July 2025, the Accreditation Council for Graduate Medical Education will require pediatric residencies to include 4 weeks of mental health training. How that requirement is fulfilled will be up to residencies, said Brian Alverson, MD, pediatric program director and vice-chair of education at Nemours Children’s Hospital in Wilmington, Delaware.

Even with training, many pediatricians lack the time to address mental health issues during an office visit, said Carlos Lerner, MD, a professor of clinical pediatrics at University of California, Los Angeles Health. And despite low or sometimes no reimbursement for discussing these issues with patients, “the reality is we end up doing it anyway.”

Treating issues like anxiety and depression “is a daily, constant part of the care that I provide for my patients,” said Lerner. “Whether the pandemic or social media exacerbated it, we are absolutely seeing a rise in mental health issues.”

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

A young boy with a habit of screaming when he didn’t get his way is among the patients Joannie Yeh, MD, a primary care physician at Nemours Children’s Health in Media, Pennsylvania, has helped in her practice.

Yeh taught the boy to stretch out his hands into the shape of a starfish, then trace around the edges of his fingers while breathing slowly and deeply. His parents later reported that after using the strategy at home, their son was no longer taking his rage out on his younger siblings.

Interventions like breathing exercises are just a few techniques Yeh hopes more primary care clinicians will teach young patients as mental health issues among this population soar to a national state of emergency, major medical groups say. But many children go without treatment because of shortages of mental health clinicians and long wait-lists for appointments.

“Knowledge of different types of interventions allows pediatricians to offer more options to families — more than just medication alone,” Yeh said. “There are some strategies, like cognitive behavioral therapy, that a therapist is equipped to deliver, but we can help explain them or teach simple skills that borrow from principles of higher-level techniques and can help patients and families while they wait to see a therapist.”

The use of techniques that are based on mindfulness, cognitive behavioral therapy, and psychotherapy are especially helpful to pediatricians after a child’s answers on a screener indicate they may be struggling with anxiety, depression, or attention-deficit/hyperactivity disorder (ADHD), said Theresa Nguyen, MD, chair of pediatrics at Greater Baltimore Medical Center, Baltimore.

“It kind of sucks if you come in worried and then your doctor says, ‘Okay, let me send you to a psychiatrist who you can’t see for 6 months; let me send you to a therapist who’s going to take a couple of weeks to get in with,’” Nguyen said.

Yeh said over the past few years she has cared for more youth coming in as follow-ups after an emergency department visit for a mental health episode.

“Oftentimes, this is the first time we become aware that the child is struggling,” Yeh said. “We are seeing issues like intentional medication overdose, referrals after other self-harm actions, or even the discovery of a note indicating the intention to do harm to self.”

Suicide deaths among 10- to 14-year-olds tripled between 2007 and 2018 and held steady through 2021, with rates climbing even among children as young as 8 years, according to a research in JAMA Network Open. Meanwhile, one in five high school students seriously contemplated suicide in 2023 (27% girls, 14% boys).

 

Mental Health Strategies for Kids in Primary Care

While pediatricians cannot replace a mental health professional, they have the unique advantage of maintaining a long-term relationship with patients. Experts said clinicians should take an active role in supporting the mental health of patients through a variety of evidence-based strategies.

Changing Thought Patterns 

Cognitive-behavioral therapy (CBT) involves identifying and challenging automatic negative thoughts, which can affect a child’s emotional state and lead to behaviors like withdrawal or lashing out.

Yeh recommended asking a child about what is bothering them, pointing out unhelpful and negative thoughts, and then offering a different, positive one instead.

She also often draws a picture of the CBT chart, which is a visual representation of how feelings lead to thoughts, and then behaviors.

“I draw this diagram because it helps give the patients a visual understanding of how their feelings and emotions are connected,” Yeh said.

 

Tools to Tolerate Stressful Situations

Simple tools like breathing exercises, body scanning, and physical exercise can help children better tolerate distress.

Pediatricians can also recommend families use guided meditations, which have been shown to lower anxiety and increase positive social behavior, said Mollie Grow, MD, an associate professor of pediatrics at the University of Washington Medicine and Seattle Children’s Hospital, both in Seattle.

But a child might first need to get negative energy out before they can become calm.

“So I’m like, ‘okay, let’s do actual physical exercise. Give me 10 jumping jacks.’ No one’s nervous after those jumping jacks,” Nguyen said. “When you’ve already been triggered, your nerves have gotten going, and you’re starting to spiral, you can’t slow yourself down enough to do a breathing exercise.”

Nguyen also said that cold water quickly calms the nervous system.

“I’ll run cold water in the office and have them put their hand in it until it’s almost frozen,” and the child or teen is able to think more clearly, Nguyen said. “It’s a real physiological response. It works.”

 

The Origin of a Feeling 

Explaining how symptoms of anxiety, depression, or ADHD work can help children and teens better understand that what they are experiencing is normal and better cope, Yeh said.

Clinicians might teach patients about how shallow breathing — a symptom of anxiety — is a result of the brain scanning for danger, and how slowing breathing tricks the brain into feeling safe again.

 

Barriers Abound

The use of these interventions in pediatric settings is not yet widespread, Grow said.

But starting in July 2025, the Accreditation Council for Graduate Medical Education will require pediatric residencies to include 4 weeks of mental health training. How that requirement is fulfilled will be up to residencies, said Brian Alverson, MD, pediatric program director and vice-chair of education at Nemours Children’s Hospital in Wilmington, Delaware.

Even with training, many pediatricians lack the time to address mental health issues during an office visit, said Carlos Lerner, MD, a professor of clinical pediatrics at University of California, Los Angeles Health. And despite low or sometimes no reimbursement for discussing these issues with patients, “the reality is we end up doing it anyway.”

Treating issues like anxiety and depression “is a daily, constant part of the care that I provide for my patients,” said Lerner. “Whether the pandemic or social media exacerbated it, we are absolutely seeing a rise in mental health issues.”

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

A young boy with a habit of screaming when he didn’t get his way is among the patients Joannie Yeh, MD, a primary care physician at Nemours Children’s Health in Media, Pennsylvania, has helped in her practice.

Yeh taught the boy to stretch out his hands into the shape of a starfish, then trace around the edges of his fingers while breathing slowly and deeply. His parents later reported that after using the strategy at home, their son was no longer taking his rage out on his younger siblings.

Interventions like breathing exercises are just a few techniques Yeh hopes more primary care clinicians will teach young patients as mental health issues among this population soar to a national state of emergency, major medical groups say. But many children go without treatment because of shortages of mental health clinicians and long wait-lists for appointments.

“Knowledge of different types of interventions allows pediatricians to offer more options to families — more than just medication alone,” Yeh said. “There are some strategies, like cognitive behavioral therapy, that a therapist is equipped to deliver, but we can help explain them or teach simple skills that borrow from principles of higher-level techniques and can help patients and families while they wait to see a therapist.”

The use of techniques that are based on mindfulness, cognitive behavioral therapy, and psychotherapy are especially helpful to pediatricians after a child’s answers on a screener indicate they may be struggling with anxiety, depression, or attention-deficit/hyperactivity disorder (ADHD), said Theresa Nguyen, MD, chair of pediatrics at Greater Baltimore Medical Center, Baltimore.

“It kind of sucks if you come in worried and then your doctor says, ‘Okay, let me send you to a psychiatrist who you can’t see for 6 months; let me send you to a therapist who’s going to take a couple of weeks to get in with,’” Nguyen said.

Yeh said over the past few years she has cared for more youth coming in as follow-ups after an emergency department visit for a mental health episode.

“Oftentimes, this is the first time we become aware that the child is struggling,” Yeh said. “We are seeing issues like intentional medication overdose, referrals after other self-harm actions, or even the discovery of a note indicating the intention to do harm to self.”

Suicide deaths among 10- to 14-year-olds tripled between 2007 and 2018 and held steady through 2021, with rates climbing even among children as young as 8 years, according to a research in JAMA Network Open. Meanwhile, one in five high school students seriously contemplated suicide in 2023 (27% girls, 14% boys).

 

Mental Health Strategies for Kids in Primary Care

While pediatricians cannot replace a mental health professional, they have the unique advantage of maintaining a long-term relationship with patients. Experts said clinicians should take an active role in supporting the mental health of patients through a variety of evidence-based strategies.

Changing Thought Patterns 

Cognitive-behavioral therapy (CBT) involves identifying and challenging automatic negative thoughts, which can affect a child’s emotional state and lead to behaviors like withdrawal or lashing out.

Yeh recommended asking a child about what is bothering them, pointing out unhelpful and negative thoughts, and then offering a different, positive one instead.

She also often draws a picture of the CBT chart, which is a visual representation of how feelings lead to thoughts, and then behaviors.

“I draw this diagram because it helps give the patients a visual understanding of how their feelings and emotions are connected,” Yeh said.

 

Tools to Tolerate Stressful Situations

Simple tools like breathing exercises, body scanning, and physical exercise can help children better tolerate distress.

Pediatricians can also recommend families use guided meditations, which have been shown to lower anxiety and increase positive social behavior, said Mollie Grow, MD, an associate professor of pediatrics at the University of Washington Medicine and Seattle Children’s Hospital, both in Seattle.

But a child might first need to get negative energy out before they can become calm.

“So I’m like, ‘okay, let’s do actual physical exercise. Give me 10 jumping jacks.’ No one’s nervous after those jumping jacks,” Nguyen said. “When you’ve already been triggered, your nerves have gotten going, and you’re starting to spiral, you can’t slow yourself down enough to do a breathing exercise.”

Nguyen also said that cold water quickly calms the nervous system.

“I’ll run cold water in the office and have them put their hand in it until it’s almost frozen,” and the child or teen is able to think more clearly, Nguyen said. “It’s a real physiological response. It works.”

 

The Origin of a Feeling 

Explaining how symptoms of anxiety, depression, or ADHD work can help children and teens better understand that what they are experiencing is normal and better cope, Yeh said.

Clinicians might teach patients about how shallow breathing — a symptom of anxiety — is a result of the brain scanning for danger, and how slowing breathing tricks the brain into feeling safe again.

 

Barriers Abound

The use of these interventions in pediatric settings is not yet widespread, Grow said.

But starting in July 2025, the Accreditation Council for Graduate Medical Education will require pediatric residencies to include 4 weeks of mental health training. How that requirement is fulfilled will be up to residencies, said Brian Alverson, MD, pediatric program director and vice-chair of education at Nemours Children’s Hospital in Wilmington, Delaware.

Even with training, many pediatricians lack the time to address mental health issues during an office visit, said Carlos Lerner, MD, a professor of clinical pediatrics at University of California, Los Angeles Health. And despite low or sometimes no reimbursement for discussing these issues with patients, “the reality is we end up doing it anyway.”

Treating issues like anxiety and depression “is a daily, constant part of the care that I provide for my patients,” said Lerner. “Whether the pandemic or social media exacerbated it, we are absolutely seeing a rise in mental health issues.”

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

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

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

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

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

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

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

New evidence–based clinical practice guidelines from the Alzheimer’s Association provide updated recommendations on evaluating individuals suspected of having Alzheimer’s disease and Alzheimer’s disease–related neurodegenerative disorders in both primary and specialty care settings.

This is the first update since 2001 for specialists and the first guideline for primary care physicians. Executive summaries of the guidelines were published in three articles online on December 23 in a special issue of Alzheimer’s & Dementia.

 

What’s New? 

“With this guideline, we expand the scope of prior guidelines by providing recommendations for practicing clinicians on the process from start to finish,” coauthor Brad Dickerson, MD, director of the Massachusetts General Hospital Frontotemporal Disorders Unit and professor of neurology at Harvard Medical School, Boston, said in a statement.

“If clinicians adopt these recommendations and healthcare systems provide adequate resources, outcomes should improve in most patients in most practice settings,” Dickerson added in an interview.

Through a modified-Delphi approach and guideline-development process, an expert workgroup representing primary and specialty care reviewed 7374 publications, of which 133 met inclusion criteria.

Based on the information, the workgroup outlined a three-step patient-centered evaluation process, which includes assessing cognitive functional status, identifying the cognitive-behavioral syndrome based on specific symptoms, and determining the likely brain diseases or conditions causing the symptoms.

 

What Are the Key Recommendations?

The guidelines include 19 “practical” recommendations that are applicable to any practice setting. They capture the core elements of a high-quality evaluation and disclosure process, the author said. Here is a brief summary of the recommendations: 

Initial evaluation: Perform a multitiered evaluation for patients who self-report or whose care partner or clinician reports cognitive, behavioral, or functional changes.

Patient-centered communication: Partner with the patient and/or care partner to establish shared goals for the evaluation process; assess the patient’s capacity to engage in goal setting.

Diagnostic formulation: Use a tiered approach to assessments and tests based on individual presentation, risk factors, and profile, aiming to determine the level of impairment, cognitive-behavioral syndrome, and likely causes and contributing factors.

History taking: Gather reliable information from informants about changes in cognition, activities of daily living, mood, neuropsychiatric symptoms, and sensory/motor functions. Document individualized risk factors for cognitive decline.

Examination: Conduct a comprehensive examination of cognition, mood, behavior, and a dementia-focused neurologic evaluation using validated tools.

Laboratory tests: Perform tiered, individualized laboratory evaluations, starting with routine tests for all patients.

Structural imaging: Obtain structural brain imaging (MRI preferred, CT as an alternative) to help establish a cause.

Ongoing communication: Engage in ongoing dialogue with patient/care partner to guide them throughout the diagnostic process.

Diagnostic disclosure: Share findings honestly and compassionately, explaining the syndrome, its severity, probable cause, prognosis, treatment options and support resources.

Specialist referral: Refer patients with atypical, uncertain, early-onset, or rapidly progressing symptoms to a dementia subspecialist.

Neuropsychological testing: Use in instances of diagnostic uncertainty or patients with complex clinical profiles. At a minimum, the neuropsychological evaluation should include normed neuropsychological testing of the domains of learning and memory (in particular delayed free and cued recall/recognition), attention, executive function, visuospatial function, and language.

Advanced diagnostic testing: When diagnostic uncertainty remains, obtain additional laboratory tests tailored to individual patient profiles.

Molecular imaging: In a patient with an established cognitive-behavioral syndrome in whom there is continued diagnostic uncertainty regarding cause(s) after structural imaging, a dementia specialist can obtain molecular imaging with fluorodeoxyglucose PET to improve diagnostic accuracy.

Cerebrospinal fluid (CSF) analysis: Utilize CSF biomarkers to evaluate amyloid beta and tau profiles in cases with unresolved diagnostic uncertainty.

Amyloid PET imaging: Perform amyloid PET scans for patients with persistent diagnostic uncertainty after other assessments.

Genetic counseling and testing: Consider genetic testing for patients with strong autosomal dominant family histories and involve a genetic counselor.

 

Future Directions?

Maria C. Carrillo, PhD, chief science officer and medical affairs lead for the Alzheimer’s Association, encourages clinicians to incorporate these guidelines into their practice.

“These guidelines are important because they guide clinicians in the evaluation of memory complaints, which could have many underlying causes. That is the necessary start for an early and accurate Alzheimer’s diagnosis,” Carrillo said in a statement.

Dickerson said the new guidelines do not address blood-based biomarkers “because nobody really feels that they are ready for prime time yet, even though they’re getting rolled out as clinical products.” 

However, the recommendations will be revised as needed. “That’s one of the values of setting this up as a process; whenever any new development occurs, it will be easy to update the guidelines to show where that new test or new biomarker fits in the overall process,” he said.

 

New Appropriate Use Guidance

A separate workgroup, jointly convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging, has revised appropriate use criteria (AUC) for amyloid PET imaging and developed AUC for tau PET imaging.

They were simultaneously published online in Alzheimer’s & Dementia and The Journal of Nuclear Medicine. They are the first revision since the initial AUC for amyloid PET was introduced in 2013.

“The updated amyloid/tau appropriate use criteria will help ensure these tracers are used in a cost-effective manner and the scan results will be used appropriately to add value to the diagnosis and management of dementia,” said workgroup members Kevin Donohoe, MD, with Beth Israel Deaconess Medical Center, Boston, and Phillip Kuo, MD, with City of Hope National Medical Center, Duarte, California.

The AUC include 17 real-world scenarios in which amyloid or tau PET may be considered, with the two tests considered separately and given their own rating for each scenario.

Overall, the strongest evidence for their use includes assessment and prognosis for people with mild cognitive impairment; assessment of people with dementia when the cause is not clearly known; and determining eligibility for treatment with new disease-modifying therapies, and monitoring response to these treatments, the workgroup said.

“Whereas the prior AUC was written at a time when only the deposition of amyloid could be documented, the new therapeutic agents allow us to demonstrate the actual clearance of amyloid during therapy,” Donohoe and Kuo explained.

“These new therapeutic agents are expensive and, as with most medications, may cause unwanted side effects. The most recent version of the AUC includes information about the appropriate use of amyloid imaging for both documenting the presence of amyloid deposits in the brain, making anti-amyloid therapy an option, as well as documenting the effectiveness of the therapeutic agents as amyloid is (or is not) cleared from the brain,” Donahoe and Kuo noted.

The revised AUC also state that, in most cases, amyloid and tau PET tests should not be used for people who do not have cognitive impairment, even if they carry the APOE4 risk-related gene for Alzheimer’s disease; nonmedical use such as for legal concerns, insurance coverage, or employment screening; and in place of genetic testing in patients suspected of carrying a disease-causing genetic mutation.

In a statement, lead author Gil D. Rabinovici, MD, with University of California, San Francisco, emphasized that the AUC “should be considered guidelines for clinicians, not a substitute for careful clinical judgment that considers the full clinical context for each patient with cognitive complaints.”

This research was funded by the Alzheimer’s Association. Disclosures for guideline authors are available with the original articles.

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

New evidence–based clinical practice guidelines from the Alzheimer’s Association provide updated recommendations on evaluating individuals suspected of having Alzheimer’s disease and Alzheimer’s disease–related neurodegenerative disorders in both primary and specialty care settings.

This is the first update since 2001 for specialists and the first guideline for primary care physicians. Executive summaries of the guidelines were published in three articles online on December 23 in a special issue of Alzheimer’s & Dementia.

 

What’s New? 

“With this guideline, we expand the scope of prior guidelines by providing recommendations for practicing clinicians on the process from start to finish,” coauthor Brad Dickerson, MD, director of the Massachusetts General Hospital Frontotemporal Disorders Unit and professor of neurology at Harvard Medical School, Boston, said in a statement.

“If clinicians adopt these recommendations and healthcare systems provide adequate resources, outcomes should improve in most patients in most practice settings,” Dickerson added in an interview.

Through a modified-Delphi approach and guideline-development process, an expert workgroup representing primary and specialty care reviewed 7374 publications, of which 133 met inclusion criteria.

Based on the information, the workgroup outlined a three-step patient-centered evaluation process, which includes assessing cognitive functional status, identifying the cognitive-behavioral syndrome based on specific symptoms, and determining the likely brain diseases or conditions causing the symptoms.

 

What Are the Key Recommendations?

The guidelines include 19 “practical” recommendations that are applicable to any practice setting. They capture the core elements of a high-quality evaluation and disclosure process, the author said. Here is a brief summary of the recommendations: 

Initial evaluation: Perform a multitiered evaluation for patients who self-report or whose care partner or clinician reports cognitive, behavioral, or functional changes.

Patient-centered communication: Partner with the patient and/or care partner to establish shared goals for the evaluation process; assess the patient’s capacity to engage in goal setting.

Diagnostic formulation: Use a tiered approach to assessments and tests based on individual presentation, risk factors, and profile, aiming to determine the level of impairment, cognitive-behavioral syndrome, and likely causes and contributing factors.

History taking: Gather reliable information from informants about changes in cognition, activities of daily living, mood, neuropsychiatric symptoms, and sensory/motor functions. Document individualized risk factors for cognitive decline.

Examination: Conduct a comprehensive examination of cognition, mood, behavior, and a dementia-focused neurologic evaluation using validated tools.

Laboratory tests: Perform tiered, individualized laboratory evaluations, starting with routine tests for all patients.

Structural imaging: Obtain structural brain imaging (MRI preferred, CT as an alternative) to help establish a cause.

Ongoing communication: Engage in ongoing dialogue with patient/care partner to guide them throughout the diagnostic process.

Diagnostic disclosure: Share findings honestly and compassionately, explaining the syndrome, its severity, probable cause, prognosis, treatment options and support resources.

Specialist referral: Refer patients with atypical, uncertain, early-onset, or rapidly progressing symptoms to a dementia subspecialist.

Neuropsychological testing: Use in instances of diagnostic uncertainty or patients with complex clinical profiles. At a minimum, the neuropsychological evaluation should include normed neuropsychological testing of the domains of learning and memory (in particular delayed free and cued recall/recognition), attention, executive function, visuospatial function, and language.

Advanced diagnostic testing: When diagnostic uncertainty remains, obtain additional laboratory tests tailored to individual patient profiles.

Molecular imaging: In a patient with an established cognitive-behavioral syndrome in whom there is continued diagnostic uncertainty regarding cause(s) after structural imaging, a dementia specialist can obtain molecular imaging with fluorodeoxyglucose PET to improve diagnostic accuracy.

Cerebrospinal fluid (CSF) analysis: Utilize CSF biomarkers to evaluate amyloid beta and tau profiles in cases with unresolved diagnostic uncertainty.

Amyloid PET imaging: Perform amyloid PET scans for patients with persistent diagnostic uncertainty after other assessments.

Genetic counseling and testing: Consider genetic testing for patients with strong autosomal dominant family histories and involve a genetic counselor.

 

Future Directions?

Maria C. Carrillo, PhD, chief science officer and medical affairs lead for the Alzheimer’s Association, encourages clinicians to incorporate these guidelines into their practice.

“These guidelines are important because they guide clinicians in the evaluation of memory complaints, which could have many underlying causes. That is the necessary start for an early and accurate Alzheimer’s diagnosis,” Carrillo said in a statement.

Dickerson said the new guidelines do not address blood-based biomarkers “because nobody really feels that they are ready for prime time yet, even though they’re getting rolled out as clinical products.” 

However, the recommendations will be revised as needed. “That’s one of the values of setting this up as a process; whenever any new development occurs, it will be easy to update the guidelines to show where that new test or new biomarker fits in the overall process,” he said.

 

New Appropriate Use Guidance

A separate workgroup, jointly convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging, has revised appropriate use criteria (AUC) for amyloid PET imaging and developed AUC for tau PET imaging.

They were simultaneously published online in Alzheimer’s & Dementia and The Journal of Nuclear Medicine. They are the first revision since the initial AUC for amyloid PET was introduced in 2013.

“The updated amyloid/tau appropriate use criteria will help ensure these tracers are used in a cost-effective manner and the scan results will be used appropriately to add value to the diagnosis and management of dementia,” said workgroup members Kevin Donohoe, MD, with Beth Israel Deaconess Medical Center, Boston, and Phillip Kuo, MD, with City of Hope National Medical Center, Duarte, California.

The AUC include 17 real-world scenarios in which amyloid or tau PET may be considered, with the two tests considered separately and given their own rating for each scenario.

Overall, the strongest evidence for their use includes assessment and prognosis for people with mild cognitive impairment; assessment of people with dementia when the cause is not clearly known; and determining eligibility for treatment with new disease-modifying therapies, and monitoring response to these treatments, the workgroup said.

“Whereas the prior AUC was written at a time when only the deposition of amyloid could be documented, the new therapeutic agents allow us to demonstrate the actual clearance of amyloid during therapy,” Donohoe and Kuo explained.

“These new therapeutic agents are expensive and, as with most medications, may cause unwanted side effects. The most recent version of the AUC includes information about the appropriate use of amyloid imaging for both documenting the presence of amyloid deposits in the brain, making anti-amyloid therapy an option, as well as documenting the effectiveness of the therapeutic agents as amyloid is (or is not) cleared from the brain,” Donahoe and Kuo noted.

The revised AUC also state that, in most cases, amyloid and tau PET tests should not be used for people who do not have cognitive impairment, even if they carry the APOE4 risk-related gene for Alzheimer’s disease; nonmedical use such as for legal concerns, insurance coverage, or employment screening; and in place of genetic testing in patients suspected of carrying a disease-causing genetic mutation.

In a statement, lead author Gil D. Rabinovici, MD, with University of California, San Francisco, emphasized that the AUC “should be considered guidelines for clinicians, not a substitute for careful clinical judgment that considers the full clinical context for each patient with cognitive complaints.”

This research was funded by the Alzheimer’s Association. Disclosures for guideline authors are available with the original articles.

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

New evidence–based clinical practice guidelines from the Alzheimer’s Association provide updated recommendations on evaluating individuals suspected of having Alzheimer’s disease and Alzheimer’s disease–related neurodegenerative disorders in both primary and specialty care settings.

This is the first update since 2001 for specialists and the first guideline for primary care physicians. Executive summaries of the guidelines were published in three articles online on December 23 in a special issue of Alzheimer’s & Dementia.

 

What’s New? 

“With this guideline, we expand the scope of prior guidelines by providing recommendations for practicing clinicians on the process from start to finish,” coauthor Brad Dickerson, MD, director of the Massachusetts General Hospital Frontotemporal Disorders Unit and professor of neurology at Harvard Medical School, Boston, said in a statement.

“If clinicians adopt these recommendations and healthcare systems provide adequate resources, outcomes should improve in most patients in most practice settings,” Dickerson added in an interview.

Through a modified-Delphi approach and guideline-development process, an expert workgroup representing primary and specialty care reviewed 7374 publications, of which 133 met inclusion criteria.

Based on the information, the workgroup outlined a three-step patient-centered evaluation process, which includes assessing cognitive functional status, identifying the cognitive-behavioral syndrome based on specific symptoms, and determining the likely brain diseases or conditions causing the symptoms.

 

What Are the Key Recommendations?

The guidelines include 19 “practical” recommendations that are applicable to any practice setting. They capture the core elements of a high-quality evaluation and disclosure process, the author said. Here is a brief summary of the recommendations: 

Initial evaluation: Perform a multitiered evaluation for patients who self-report or whose care partner or clinician reports cognitive, behavioral, or functional changes.

Patient-centered communication: Partner with the patient and/or care partner to establish shared goals for the evaluation process; assess the patient’s capacity to engage in goal setting.

Diagnostic formulation: Use a tiered approach to assessments and tests based on individual presentation, risk factors, and profile, aiming to determine the level of impairment, cognitive-behavioral syndrome, and likely causes and contributing factors.

History taking: Gather reliable information from informants about changes in cognition, activities of daily living, mood, neuropsychiatric symptoms, and sensory/motor functions. Document individualized risk factors for cognitive decline.

Examination: Conduct a comprehensive examination of cognition, mood, behavior, and a dementia-focused neurologic evaluation using validated tools.

Laboratory tests: Perform tiered, individualized laboratory evaluations, starting with routine tests for all patients.

Structural imaging: Obtain structural brain imaging (MRI preferred, CT as an alternative) to help establish a cause.

Ongoing communication: Engage in ongoing dialogue with patient/care partner to guide them throughout the diagnostic process.

Diagnostic disclosure: Share findings honestly and compassionately, explaining the syndrome, its severity, probable cause, prognosis, treatment options and support resources.

Specialist referral: Refer patients with atypical, uncertain, early-onset, or rapidly progressing symptoms to a dementia subspecialist.

Neuropsychological testing: Use in instances of diagnostic uncertainty or patients with complex clinical profiles. At a minimum, the neuropsychological evaluation should include normed neuropsychological testing of the domains of learning and memory (in particular delayed free and cued recall/recognition), attention, executive function, visuospatial function, and language.

Advanced diagnostic testing: When diagnostic uncertainty remains, obtain additional laboratory tests tailored to individual patient profiles.

Molecular imaging: In a patient with an established cognitive-behavioral syndrome in whom there is continued diagnostic uncertainty regarding cause(s) after structural imaging, a dementia specialist can obtain molecular imaging with fluorodeoxyglucose PET to improve diagnostic accuracy.

Cerebrospinal fluid (CSF) analysis: Utilize CSF biomarkers to evaluate amyloid beta and tau profiles in cases with unresolved diagnostic uncertainty.

Amyloid PET imaging: Perform amyloid PET scans for patients with persistent diagnostic uncertainty after other assessments.

Genetic counseling and testing: Consider genetic testing for patients with strong autosomal dominant family histories and involve a genetic counselor.

 

Future Directions?

Maria C. Carrillo, PhD, chief science officer and medical affairs lead for the Alzheimer’s Association, encourages clinicians to incorporate these guidelines into their practice.

“These guidelines are important because they guide clinicians in the evaluation of memory complaints, which could have many underlying causes. That is the necessary start for an early and accurate Alzheimer’s diagnosis,” Carrillo said in a statement.

Dickerson said the new guidelines do not address blood-based biomarkers “because nobody really feels that they are ready for prime time yet, even though they’re getting rolled out as clinical products.” 

However, the recommendations will be revised as needed. “That’s one of the values of setting this up as a process; whenever any new development occurs, it will be easy to update the guidelines to show where that new test or new biomarker fits in the overall process,” he said.

 

New Appropriate Use Guidance

A separate workgroup, jointly convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging, has revised appropriate use criteria (AUC) for amyloid PET imaging and developed AUC for tau PET imaging.

They were simultaneously published online in Alzheimer’s & Dementia and The Journal of Nuclear Medicine. They are the first revision since the initial AUC for amyloid PET was introduced in 2013.

“The updated amyloid/tau appropriate use criteria will help ensure these tracers are used in a cost-effective manner and the scan results will be used appropriately to add value to the diagnosis and management of dementia,” said workgroup members Kevin Donohoe, MD, with Beth Israel Deaconess Medical Center, Boston, and Phillip Kuo, MD, with City of Hope National Medical Center, Duarte, California.

The AUC include 17 real-world scenarios in which amyloid or tau PET may be considered, with the two tests considered separately and given their own rating for each scenario.

Overall, the strongest evidence for their use includes assessment and prognosis for people with mild cognitive impairment; assessment of people with dementia when the cause is not clearly known; and determining eligibility for treatment with new disease-modifying therapies, and monitoring response to these treatments, the workgroup said.

“Whereas the prior AUC was written at a time when only the deposition of amyloid could be documented, the new therapeutic agents allow us to demonstrate the actual clearance of amyloid during therapy,” Donohoe and Kuo explained.

“These new therapeutic agents are expensive and, as with most medications, may cause unwanted side effects. The most recent version of the AUC includes information about the appropriate use of amyloid imaging for both documenting the presence of amyloid deposits in the brain, making anti-amyloid therapy an option, as well as documenting the effectiveness of the therapeutic agents as amyloid is (or is not) cleared from the brain,” Donahoe and Kuo noted.

The revised AUC also state that, in most cases, amyloid and tau PET tests should not be used for people who do not have cognitive impairment, even if they carry the APOE4 risk-related gene for Alzheimer’s disease; nonmedical use such as for legal concerns, insurance coverage, or employment screening; and in place of genetic testing in patients suspected of carrying a disease-causing genetic mutation.

In a statement, lead author Gil D. Rabinovici, MD, with University of California, San Francisco, emphasized that the AUC “should be considered guidelines for clinicians, not a substitute for careful clinical judgment that considers the full clinical context for each patient with cognitive complaints.”

This research was funded by the Alzheimer’s Association. Disclosures for guideline authors are available with the original articles.

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

A Lancet Commission has redefined obesity by classifying it as either “clinical obesity,” a disease, or “preclinical,” a health risk factor, with the distinction based on factors beyond body mass index (BMI).

“We propose a radical overhaul of the actual diagnosis of obesity to improve global healthcare and practices and policies. The specific aims were to facilitate individualized assessment and care of people living with obesity while preserving resources by reducing overdiagnosis and unnecessary or inadequate interventions,” Professor Louise Baur, chair of Child & Adolescent Health at the University of Sydney, Australia, said during a UK Science Media Centre (SMC) news briefing.

The report calls first for a diagnosis of obesity via confirmation of excess adiposity using measures such as waist circumference or waist-to-hip ratio in addition to BMI. Next, a clinical assessment of signs and symptoms of organ dysfunction due to obesity and/or functional limitations determines whether the individual has the disease “clinical obesity,” or “preclinical obesity,” a condition of health risk but not an illness itself.

Published on January 14, 2025, in The Lancet Diabetes & Endocrinology, the document also provides broad guidance on management for the two obesity conditions, emphasizing a personalized and stigma-free approach. The Lancet Commission on Obesity comprised 56 experts in relevant fields including endocrinology, surgery, nutrition, and public health, along with people living with obesity.

The report has been endorsed by more than 75 medical organizations, including the Association of British Clinical Diabetologists, the American Association of Clinical Endocrinologists, the American Diabetes Association, the American Heart Association, the Obesity Society, the World Obesity Federation, and obesity and endocrinology societies from countries in Europe, Latin America, Asia, and South Africa.

In recent years, many in the field have found fault with the current BMI-based definition of obesity (> 30 for people of European descent or other cutoffs for specific ethnic groups), primarily because BMI alone doesn’t reflect a person’s fat vs lean mass, fat distribution, or overall health. The new definition aims to overcome these limitations, as well as settle the debate about whether obesity is a “disease.”

“We now have a clinical diagnosis for obesity, which has been lacking. ... The traditional classification based on BMI ... reflects simply whether or not there is excess adiposity, and sometimes not even precise in that regard, either…It has never been a classification that was meant to diagnose a specific illness with its own clinical characteristics in the same way we diagnose any other illness,” Commission Chair Francesco Rubino, MD, professor and chair of Metabolic and Bariatric Surgery at King’s College London, England, said in an interview.

He added, “The fact that now we have a clinical diagnosis allows recognition of the nuance that obesity is generally a risk and for some can be an illness. There are some who have risk but don’t have the illness here and now. And it’s crucially important for clinical decision-making, but also for policies to have a distinction between those two things because the treatment strategy for one and the other are substantially different.”

Asked to comment, obesity specialist Michael A. Weintraub, MD, clinical assistant professor of endocrinology at New York University Langone Health, said in an interview, “I wholeheartedly agree with modifying the definition of obesity in this more accurate way. ... There has already been a lot of talk about the fallibility of BMI and that BMI over 30 does not equal obesity. ... So a major Commission article like this I think can really move those discussions even more into the forefront and start changing practice.” 

However, Weintraub added, “I think there needs to be another step here of more practical guidance on how to actually implement this ... including how to measure waist circumference and to put it into a patient flow.” 

Asked to comment, obesity expert Luca Busetto, MD, associate professor of internal medicine at the Department of Medicine of the University of Padova, Italy, said in an interview that he agrees with the general concept of moving beyond BMI in defining obesity. That view was expressed in a proposed “framework” from the European Association for the Study of Obesity (EASO), for which Busetto was the lead author.

Busetto also agrees with the emphasis on the need for a complete clinical evaluation of patients to define their health status. “The precise definition of the symptoms defining clinical obesity in adults and children is extremely important, emphasizing the fact that obesity is a severe and disabling disease by itself, even without or before the occurrence of obesity-related complications,” he said.

However, he takes issue with the Commission’s designation that “preclinical” obesity is not a disease. “The critical point of disagreement for me is the message that obesity is a disease only if it is clinical or only if it presents functional impairment or clinical symptoms. This remains, in my opinion, an oversimplification, not taking into account the fact that the pathophysiological mechanisms that lead to fat accumulation and ‘adipose tissue-based chronic disease’ usually start well before the occurrence of symptoms.”

Busetto pointed to examples such as type 2 diabetes and chronic kidney disease, both of which can be asymptomatic in their early phases yet are still considered diseases at those points. “I have no problem in accepting a distinction between preclinical and clinical stages of the disease, and I like the definition of clinical obesity, but why should this imply the fact that obesity is NOT a disease since its beginning?”

The Commission does state that preclinical obesity should be addressed, mostly with preventive approaches but in some cases with more intensive management. “This is highly relevant, but the risk of an undertreatment of obesity in its asymptomatic state remains in place. This could delay appropriate management for a progressive disease that certainly should not be treated only when presenting symptoms. It would be too late,” Busetto said.

And EASO framework coauthor Gijs Goossens, PhD, professor of cardiometabolic physiology of obesity at Maastricht University Medical Centre, the Netherlands, added a concern that those with excess adiposity but lower BMI might be missed entirely, noting “Since abdominal fat accumulation better predicts chronic cardiometabolic diseases and can also be accompanied by clinical manifestations in individuals with overweight as a consequence of compromised adipose tissue function, the proposed model may lead to underdiagnosis or undertreatment in individuals with BMI 25-30 who have excess abdominal fat.”

 

Diagnosis and Management Beyond BMI

The Commission advises the use of BMI solely as a marker to screen for potential obesity. Those with a BMI > 40 can be assumed to have excess body fat. For others with a BMI at or near the threshold for obesity in a specific country or ethnic group or for whom there is the clinical judgment of the potential for clinical obesity, confirmation of excess or abnormal adiposity is needed by one of the following:

• At least one measurement of body size and BMI
• At least two measures of body size, regardless of BMI
• Direct body fat measurement, such as a dual-energy x-ray absorptiometry (DEXA) scan

Measurement of body size can be assessed in three ways: 

• Waist circumference ≥ 102 cm for men and ≥ 88 cm for women
• Waist-to-hip ratio > 0.90 for men and > 0.50 for women
• Waist-to-height ratio > 0.50 for all.

Weintraub noted, “Telemedicine is a useful tool used by many patients and providers but may also make it challenging to accurately assess someone’s body size. Having technology like an iPhone app to measure body size would circumvent this challenge but this type of tool has not yet been validated.” 

If the person does not have excess adiposity, they don’t have obesity. Those with excess adiposity do have obesity. Further assessment is then needed to establish whether the person has an illness, that is, clinical obesity, indicated by signs/symptoms of organ dysfunction, and/or limitations of daily activities. If not, they have “preclinical” obesity.

The document provides a list of 18 obesity-related organ, tissue, and body system criteria for diagnosing “clinical” obesity in adults, including upper airways (eg, apneas/hypopneas), respiratory (breathlessness), cardiovascular (hypertension, heart failure), liver (fatty liver disease with hepatic fibrosis), reproductive (polycystic ovary syndrome, hypogonadism), and metabolism (hyperglycemia, hypertriglyceridemia, low high-density lipoprotein cholesterol). A list of 13 such criteria is also provided for children. “Limitations of day-to-day activities” are included on both lists.

 

Management Differs by Designation

For preclinical obesity, management should focus on risk reduction and prevention of progression to clinical obesity or other obesity-related diseases. Such approaches include health counseling for weight loss or prevention of weight gain, monitoring over time, and active weight loss interventions in people at higher risk of developing clinical obesity and other obesity-related diseases.

Management for clinical obesity focuses on improvements or reversal of the organ dysfunction. The type of evidence-based treatment and management should be informed by individual risk-benefit assessments and decided via “active discussion” with the patient. Success is determined by improvement in the signs and symptoms rather than measures of weight loss.

In response to a reporter’s question at the SMC briefing about the implications for the use of weight-loss medications, Rubino noted that this wasn’t the focus of the report, but nonetheless said that this new obesity definition could help with their targeted use. “The strategy and intent by which you use the drugs is different in clinical and preclinical obesity. ... Pharmacological interventions could be used for patients with high-risk preclinical obesity, with the intent of reducing risk, but we ... would use the same medication at a different intensity, dose, and maybe in combination therapies.”

As for clinical obesity, “It could be more or less severe and could affect more than one organ, and so clinical obesity might require drugs, might require surgery, or may require, in some cases, a combination of both of them, to achieve the best possible outcomes. ... We want to make sure that the person is restoring health ... with whatever it takes.”

Rubino believes this new definition will convince the remaining clinicians who haven’t yet accepted the concept of obesity as a disease. “When they see clinical obesity, I think it will be much harder to say that a biological process that is capable of causing a dysfunction in the heart or the lungs is less of a disease than another biological process that causes similar dysfunction in the heart of the lungs. ... It’s going to be objective. Obesity is a spectrum of different situations. ... When it’s an illness, clinical obesity, it’s not a matter of if or when. It’s a matter of fact.”

There were no industrial grants or other funding for this initiative. King’s Health Partners hosted the initiative and provided logistical and personnel support to facilitate administrative work and the Delphi-like consensus-development process. Rubino declared receiving research grants from Ethicon (Johnson & Johnson), Novo Nordisk, and Medtronic; consulting fees from Morphic Medical; speaking honoraria from Medtronic, Ethicon, Novo Nordisk, Eli Lilly, and Amgen. Rubino has served (unpaid) as a member of the scientific advisory board for Keyron and a member of the data safety and monitoring board for GI Metabolic Solutions; is president of the Metabolic Health Institute (non-profit); and is the sole director of Metabolic Health International and London Metabolic and Bariatric Surgery (private practice). Baur declared serving on the scientific advisory board for Novo Nordisk (for the ACTION Teens study) and Eli Lilly and receiving speaker fees (paid to the institution) from Novo Nordisk.

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

A Lancet Commission has redefined obesity by classifying it as either “clinical obesity,” a disease, or “preclinical,” a health risk factor, with the distinction based on factors beyond body mass index (BMI).

“We propose a radical overhaul of the actual diagnosis of obesity to improve global healthcare and practices and policies. The specific aims were to facilitate individualized assessment and care of people living with obesity while preserving resources by reducing overdiagnosis and unnecessary or inadequate interventions,” Professor Louise Baur, chair of Child & Adolescent Health at the University of Sydney, Australia, said during a UK Science Media Centre (SMC) news briefing.

The report calls first for a diagnosis of obesity via confirmation of excess adiposity using measures such as waist circumference or waist-to-hip ratio in addition to BMI. Next, a clinical assessment of signs and symptoms of organ dysfunction due to obesity and/or functional limitations determines whether the individual has the disease “clinical obesity,” or “preclinical obesity,” a condition of health risk but not an illness itself.

Published on January 14, 2025, in The Lancet Diabetes & Endocrinology, the document also provides broad guidance on management for the two obesity conditions, emphasizing a personalized and stigma-free approach. The Lancet Commission on Obesity comprised 56 experts in relevant fields including endocrinology, surgery, nutrition, and public health, along with people living with obesity.

The report has been endorsed by more than 75 medical organizations, including the Association of British Clinical Diabetologists, the American Association of Clinical Endocrinologists, the American Diabetes Association, the American Heart Association, the Obesity Society, the World Obesity Federation, and obesity and endocrinology societies from countries in Europe, Latin America, Asia, and South Africa.

In recent years, many in the field have found fault with the current BMI-based definition of obesity (> 30 for people of European descent or other cutoffs for specific ethnic groups), primarily because BMI alone doesn’t reflect a person’s fat vs lean mass, fat distribution, or overall health. The new definition aims to overcome these limitations, as well as settle the debate about whether obesity is a “disease.”

“We now have a clinical diagnosis for obesity, which has been lacking. ... The traditional classification based on BMI ... reflects simply whether or not there is excess adiposity, and sometimes not even precise in that regard, either…It has never been a classification that was meant to diagnose a specific illness with its own clinical characteristics in the same way we diagnose any other illness,” Commission Chair Francesco Rubino, MD, professor and chair of Metabolic and Bariatric Surgery at King’s College London, England, said in an interview.

He added, “The fact that now we have a clinical diagnosis allows recognition of the nuance that obesity is generally a risk and for some can be an illness. There are some who have risk but don’t have the illness here and now. And it’s crucially important for clinical decision-making, but also for policies to have a distinction between those two things because the treatment strategy for one and the other are substantially different.”

Asked to comment, obesity specialist Michael A. Weintraub, MD, clinical assistant professor of endocrinology at New York University Langone Health, said in an interview, “I wholeheartedly agree with modifying the definition of obesity in this more accurate way. ... There has already been a lot of talk about the fallibility of BMI and that BMI over 30 does not equal obesity. ... So a major Commission article like this I think can really move those discussions even more into the forefront and start changing practice.” 

However, Weintraub added, “I think there needs to be another step here of more practical guidance on how to actually implement this ... including how to measure waist circumference and to put it into a patient flow.” 

Asked to comment, obesity expert Luca Busetto, MD, associate professor of internal medicine at the Department of Medicine of the University of Padova, Italy, said in an interview that he agrees with the general concept of moving beyond BMI in defining obesity. That view was expressed in a proposed “framework” from the European Association for the Study of Obesity (EASO), for which Busetto was the lead author.

Busetto also agrees with the emphasis on the need for a complete clinical evaluation of patients to define their health status. “The precise definition of the symptoms defining clinical obesity in adults and children is extremely important, emphasizing the fact that obesity is a severe and disabling disease by itself, even without or before the occurrence of obesity-related complications,” he said.

However, he takes issue with the Commission’s designation that “preclinical” obesity is not a disease. “The critical point of disagreement for me is the message that obesity is a disease only if it is clinical or only if it presents functional impairment or clinical symptoms. This remains, in my opinion, an oversimplification, not taking into account the fact that the pathophysiological mechanisms that lead to fat accumulation and ‘adipose tissue-based chronic disease’ usually start well before the occurrence of symptoms.”

Busetto pointed to examples such as type 2 diabetes and chronic kidney disease, both of which can be asymptomatic in their early phases yet are still considered diseases at those points. “I have no problem in accepting a distinction between preclinical and clinical stages of the disease, and I like the definition of clinical obesity, but why should this imply the fact that obesity is NOT a disease since its beginning?”

The Commission does state that preclinical obesity should be addressed, mostly with preventive approaches but in some cases with more intensive management. “This is highly relevant, but the risk of an undertreatment of obesity in its asymptomatic state remains in place. This could delay appropriate management for a progressive disease that certainly should not be treated only when presenting symptoms. It would be too late,” Busetto said.

And EASO framework coauthor Gijs Goossens, PhD, professor of cardiometabolic physiology of obesity at Maastricht University Medical Centre, the Netherlands, added a concern that those with excess adiposity but lower BMI might be missed entirely, noting “Since abdominal fat accumulation better predicts chronic cardiometabolic diseases and can also be accompanied by clinical manifestations in individuals with overweight as a consequence of compromised adipose tissue function, the proposed model may lead to underdiagnosis or undertreatment in individuals with BMI 25-30 who have excess abdominal fat.”

 

Diagnosis and Management Beyond BMI

The Commission advises the use of BMI solely as a marker to screen for potential obesity. Those with a BMI > 40 can be assumed to have excess body fat. For others with a BMI at or near the threshold for obesity in a specific country or ethnic group or for whom there is the clinical judgment of the potential for clinical obesity, confirmation of excess or abnormal adiposity is needed by one of the following:

• At least one measurement of body size and BMI
• At least two measures of body size, regardless of BMI
• Direct body fat measurement, such as a dual-energy x-ray absorptiometry (DEXA) scan

Measurement of body size can be assessed in three ways: 

• Waist circumference ≥ 102 cm for men and ≥ 88 cm for women
• Waist-to-hip ratio > 0.90 for men and > 0.50 for women
• Waist-to-height ratio > 0.50 for all.

Weintraub noted, “Telemedicine is a useful tool used by many patients and providers but may also make it challenging to accurately assess someone’s body size. Having technology like an iPhone app to measure body size would circumvent this challenge but this type of tool has not yet been validated.” 

If the person does not have excess adiposity, they don’t have obesity. Those with excess adiposity do have obesity. Further assessment is then needed to establish whether the person has an illness, that is, clinical obesity, indicated by signs/symptoms of organ dysfunction, and/or limitations of daily activities. If not, they have “preclinical” obesity.

The document provides a list of 18 obesity-related organ, tissue, and body system criteria for diagnosing “clinical” obesity in adults, including upper airways (eg, apneas/hypopneas), respiratory (breathlessness), cardiovascular (hypertension, heart failure), liver (fatty liver disease with hepatic fibrosis), reproductive (polycystic ovary syndrome, hypogonadism), and metabolism (hyperglycemia, hypertriglyceridemia, low high-density lipoprotein cholesterol). A list of 13 such criteria is also provided for children. “Limitations of day-to-day activities” are included on both lists.

 

Management Differs by Designation

For preclinical obesity, management should focus on risk reduction and prevention of progression to clinical obesity or other obesity-related diseases. Such approaches include health counseling for weight loss or prevention of weight gain, monitoring over time, and active weight loss interventions in people at higher risk of developing clinical obesity and other obesity-related diseases.

Management for clinical obesity focuses on improvements or reversal of the organ dysfunction. The type of evidence-based treatment and management should be informed by individual risk-benefit assessments and decided via “active discussion” with the patient. Success is determined by improvement in the signs and symptoms rather than measures of weight loss.

In response to a reporter’s question at the SMC briefing about the implications for the use of weight-loss medications, Rubino noted that this wasn’t the focus of the report, but nonetheless said that this new obesity definition could help with their targeted use. “The strategy and intent by which you use the drugs is different in clinical and preclinical obesity. ... Pharmacological interventions could be used for patients with high-risk preclinical obesity, with the intent of reducing risk, but we ... would use the same medication at a different intensity, dose, and maybe in combination therapies.”

As for clinical obesity, “It could be more or less severe and could affect more than one organ, and so clinical obesity might require drugs, might require surgery, or may require, in some cases, a combination of both of them, to achieve the best possible outcomes. ... We want to make sure that the person is restoring health ... with whatever it takes.”

Rubino believes this new definition will convince the remaining clinicians who haven’t yet accepted the concept of obesity as a disease. “When they see clinical obesity, I think it will be much harder to say that a biological process that is capable of causing a dysfunction in the heart or the lungs is less of a disease than another biological process that causes similar dysfunction in the heart of the lungs. ... It’s going to be objective. Obesity is a spectrum of different situations. ... When it’s an illness, clinical obesity, it’s not a matter of if or when. It’s a matter of fact.”

There were no industrial grants or other funding for this initiative. King’s Health Partners hosted the initiative and provided logistical and personnel support to facilitate administrative work and the Delphi-like consensus-development process. Rubino declared receiving research grants from Ethicon (Johnson & Johnson), Novo Nordisk, and Medtronic; consulting fees from Morphic Medical; speaking honoraria from Medtronic, Ethicon, Novo Nordisk, Eli Lilly, and Amgen. Rubino has served (unpaid) as a member of the scientific advisory board for Keyron and a member of the data safety and monitoring board for GI Metabolic Solutions; is president of the Metabolic Health Institute (non-profit); and is the sole director of Metabolic Health International and London Metabolic and Bariatric Surgery (private practice). Baur declared serving on the scientific advisory board for Novo Nordisk (for the ACTION Teens study) and Eli Lilly and receiving speaker fees (paid to the institution) from Novo Nordisk.

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

A Lancet Commission has redefined obesity by classifying it as either “clinical obesity,” a disease, or “preclinical,” a health risk factor, with the distinction based on factors beyond body mass index (BMI).

“We propose a radical overhaul of the actual diagnosis of obesity to improve global healthcare and practices and policies. The specific aims were to facilitate individualized assessment and care of people living with obesity while preserving resources by reducing overdiagnosis and unnecessary or inadequate interventions,” Professor Louise Baur, chair of Child & Adolescent Health at the University of Sydney, Australia, said during a UK Science Media Centre (SMC) news briefing.

The report calls first for a diagnosis of obesity via confirmation of excess adiposity using measures such as waist circumference or waist-to-hip ratio in addition to BMI. Next, a clinical assessment of signs and symptoms of organ dysfunction due to obesity and/or functional limitations determines whether the individual has the disease “clinical obesity,” or “preclinical obesity,” a condition of health risk but not an illness itself.

Published on January 14, 2025, in The Lancet Diabetes & Endocrinology, the document also provides broad guidance on management for the two obesity conditions, emphasizing a personalized and stigma-free approach. The Lancet Commission on Obesity comprised 56 experts in relevant fields including endocrinology, surgery, nutrition, and public health, along with people living with obesity.

The report has been endorsed by more than 75 medical organizations, including the Association of British Clinical Diabetologists, the American Association of Clinical Endocrinologists, the American Diabetes Association, the American Heart Association, the Obesity Society, the World Obesity Federation, and obesity and endocrinology societies from countries in Europe, Latin America, Asia, and South Africa.

In recent years, many in the field have found fault with the current BMI-based definition of obesity (> 30 for people of European descent or other cutoffs for specific ethnic groups), primarily because BMI alone doesn’t reflect a person’s fat vs lean mass, fat distribution, or overall health. The new definition aims to overcome these limitations, as well as settle the debate about whether obesity is a “disease.”

“We now have a clinical diagnosis for obesity, which has been lacking. ... The traditional classification based on BMI ... reflects simply whether or not there is excess adiposity, and sometimes not even precise in that regard, either…It has never been a classification that was meant to diagnose a specific illness with its own clinical characteristics in the same way we diagnose any other illness,” Commission Chair Francesco Rubino, MD, professor and chair of Metabolic and Bariatric Surgery at King’s College London, England, said in an interview.

He added, “The fact that now we have a clinical diagnosis allows recognition of the nuance that obesity is generally a risk and for some can be an illness. There are some who have risk but don’t have the illness here and now. And it’s crucially important for clinical decision-making, but also for policies to have a distinction between those two things because the treatment strategy for one and the other are substantially different.”

Asked to comment, obesity specialist Michael A. Weintraub, MD, clinical assistant professor of endocrinology at New York University Langone Health, said in an interview, “I wholeheartedly agree with modifying the definition of obesity in this more accurate way. ... There has already been a lot of talk about the fallibility of BMI and that BMI over 30 does not equal obesity. ... So a major Commission article like this I think can really move those discussions even more into the forefront and start changing practice.” 

However, Weintraub added, “I think there needs to be another step here of more practical guidance on how to actually implement this ... including how to measure waist circumference and to put it into a patient flow.” 

Asked to comment, obesity expert Luca Busetto, MD, associate professor of internal medicine at the Department of Medicine of the University of Padova, Italy, said in an interview that he agrees with the general concept of moving beyond BMI in defining obesity. That view was expressed in a proposed “framework” from the European Association for the Study of Obesity (EASO), for which Busetto was the lead author.

Busetto also agrees with the emphasis on the need for a complete clinical evaluation of patients to define their health status. “The precise definition of the symptoms defining clinical obesity in adults and children is extremely important, emphasizing the fact that obesity is a severe and disabling disease by itself, even without or before the occurrence of obesity-related complications,” he said.

However, he takes issue with the Commission’s designation that “preclinical” obesity is not a disease. “The critical point of disagreement for me is the message that obesity is a disease only if it is clinical or only if it presents functional impairment or clinical symptoms. This remains, in my opinion, an oversimplification, not taking into account the fact that the pathophysiological mechanisms that lead to fat accumulation and ‘adipose tissue-based chronic disease’ usually start well before the occurrence of symptoms.”

Busetto pointed to examples such as type 2 diabetes and chronic kidney disease, both of which can be asymptomatic in their early phases yet are still considered diseases at those points. “I have no problem in accepting a distinction between preclinical and clinical stages of the disease, and I like the definition of clinical obesity, but why should this imply the fact that obesity is NOT a disease since its beginning?”

The Commission does state that preclinical obesity should be addressed, mostly with preventive approaches but in some cases with more intensive management. “This is highly relevant, but the risk of an undertreatment of obesity in its asymptomatic state remains in place. This could delay appropriate management for a progressive disease that certainly should not be treated only when presenting symptoms. It would be too late,” Busetto said.

And EASO framework coauthor Gijs Goossens, PhD, professor of cardiometabolic physiology of obesity at Maastricht University Medical Centre, the Netherlands, added a concern that those with excess adiposity but lower BMI might be missed entirely, noting “Since abdominal fat accumulation better predicts chronic cardiometabolic diseases and can also be accompanied by clinical manifestations in individuals with overweight as a consequence of compromised adipose tissue function, the proposed model may lead to underdiagnosis or undertreatment in individuals with BMI 25-30 who have excess abdominal fat.”

 

Diagnosis and Management Beyond BMI

The Commission advises the use of BMI solely as a marker to screen for potential obesity. Those with a BMI > 40 can be assumed to have excess body fat. For others with a BMI at or near the threshold for obesity in a specific country or ethnic group or for whom there is the clinical judgment of the potential for clinical obesity, confirmation of excess or abnormal adiposity is needed by one of the following:

• At least one measurement of body size and BMI
• At least two measures of body size, regardless of BMI
• Direct body fat measurement, such as a dual-energy x-ray absorptiometry (DEXA) scan

Measurement of body size can be assessed in three ways: 

• Waist circumference ≥ 102 cm for men and ≥ 88 cm for women
• Waist-to-hip ratio > 0.90 for men and > 0.50 for women
• Waist-to-height ratio > 0.50 for all.

Weintraub noted, “Telemedicine is a useful tool used by many patients and providers but may also make it challenging to accurately assess someone’s body size. Having technology like an iPhone app to measure body size would circumvent this challenge but this type of tool has not yet been validated.” 

If the person does not have excess adiposity, they don’t have obesity. Those with excess adiposity do have obesity. Further assessment is then needed to establish whether the person has an illness, that is, clinical obesity, indicated by signs/symptoms of organ dysfunction, and/or limitations of daily activities. If not, they have “preclinical” obesity.

The document provides a list of 18 obesity-related organ, tissue, and body system criteria for diagnosing “clinical” obesity in adults, including upper airways (eg, apneas/hypopneas), respiratory (breathlessness), cardiovascular (hypertension, heart failure), liver (fatty liver disease with hepatic fibrosis), reproductive (polycystic ovary syndrome, hypogonadism), and metabolism (hyperglycemia, hypertriglyceridemia, low high-density lipoprotein cholesterol). A list of 13 such criteria is also provided for children. “Limitations of day-to-day activities” are included on both lists.

 

Management Differs by Designation

For preclinical obesity, management should focus on risk reduction and prevention of progression to clinical obesity or other obesity-related diseases. Such approaches include health counseling for weight loss or prevention of weight gain, monitoring over time, and active weight loss interventions in people at higher risk of developing clinical obesity and other obesity-related diseases.

Management for clinical obesity focuses on improvements or reversal of the organ dysfunction. The type of evidence-based treatment and management should be informed by individual risk-benefit assessments and decided via “active discussion” with the patient. Success is determined by improvement in the signs and symptoms rather than measures of weight loss.

In response to a reporter’s question at the SMC briefing about the implications for the use of weight-loss medications, Rubino noted that this wasn’t the focus of the report, but nonetheless said that this new obesity definition could help with their targeted use. “The strategy and intent by which you use the drugs is different in clinical and preclinical obesity. ... Pharmacological interventions could be used for patients with high-risk preclinical obesity, with the intent of reducing risk, but we ... would use the same medication at a different intensity, dose, and maybe in combination therapies.”

As for clinical obesity, “It could be more or less severe and could affect more than one organ, and so clinical obesity might require drugs, might require surgery, or may require, in some cases, a combination of both of them, to achieve the best possible outcomes. ... We want to make sure that the person is restoring health ... with whatever it takes.”

Rubino believes this new definition will convince the remaining clinicians who haven’t yet accepted the concept of obesity as a disease. “When they see clinical obesity, I think it will be much harder to say that a biological process that is capable of causing a dysfunction in the heart or the lungs is less of a disease than another biological process that causes similar dysfunction in the heart of the lungs. ... It’s going to be objective. Obesity is a spectrum of different situations. ... When it’s an illness, clinical obesity, it’s not a matter of if or when. It’s a matter of fact.”

There were no industrial grants or other funding for this initiative. King’s Health Partners hosted the initiative and provided logistical and personnel support to facilitate administrative work and the Delphi-like consensus-development process. Rubino declared receiving research grants from Ethicon (Johnson & Johnson), Novo Nordisk, and Medtronic; consulting fees from Morphic Medical; speaking honoraria from Medtronic, Ethicon, Novo Nordisk, Eli Lilly, and Amgen. Rubino has served (unpaid) as a member of the scientific advisory board for Keyron and a member of the data safety and monitoring board for GI Metabolic Solutions; is president of the Metabolic Health Institute (non-profit); and is the sole director of Metabolic Health International and London Metabolic and Bariatric Surgery (private practice). Baur declared serving on the scientific advisory board for Novo Nordisk (for the ACTION Teens study) and Eli Lilly and receiving speaker fees (paid to the institution) from Novo Nordisk.

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

You could be forgiven if you are confused about how blood pressure (BP) affects dementia. First, you read an article extolling the benefits of BP lowering, then a study about how stopping antihypertensives slows cognitive decline in nursing home residents. It’s enough to make you lose your mind.

The Brain Benefits of BP Lowering

It should be stated unequivocally that you should absolutely treat high BP. It may have once been acceptable to state, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.” But those dark days are long behind us.

In these divided times, at least we can agree that we should treat high BP. The cardiovascular (CV) benefits, in and of themselves, justify the decision. But BP’s relationship with dementia is more complex. There are different types of dementia even though we tend to lump them all into one category. Vascular dementia is driven by the same pathophysiology and risk factors as cardiac disease. It’s intuitive that treating hypertension, diabetes, hypercholesterolemia, and smoking will decrease the risk for stroke and limit the damage to the brain that we see with repeated vascular insults. For Alzheimer’s disease, high BP and other CV risk factors seem to increase the risk even if the mechanism is not fully elucidated.

Estimates suggest that if we could lower the prevalence of hypertension by 25%, there would be 160,000 fewer cases of Alzheimer’s disease. But the data are not as robust as one might hope. A 2021 Cochrane review found that hypertension treatment slowed cognitive decline, but the quality of the evidence was low. Short duration of follow-up, dropouts, crossovers, and other problems with the data precluded any certainty. What’s more, hypertension in midlife is associated with cognitive decline and dementia, but its impact in those over age 70 is less clear. Later in life, or once cognitive impairment has already developed, it may be too late for BP lowering to have any impact.

 

Potential Harms of Lowering BP

All this needs to be weighed against the potential harms of treating hypertension. I will reiterate that hypertension should be treated and treated aggressively for the prevention of CV events. But overtreatment, especially in older patients, is associated with hypotension, falls, and syncope. Older patients are also at risk for polypharmacy and drug-drug interactions. 

When it comes to dementia, there is also a concern that overtreating high BP could make things worse. Hypotension and decreased cerebral perfusion could hasten cognitive decline by depriving the brain of that all too necessary oxygen. 

A Korean nationwide survey showed a U-shaped association between BP and Alzheimer’s disease risk in adults (mean age, 67 years), with both high and low BPs associated with a higher risk for Alzheimer’s disease. Though not all studies agree. A post hoc analysis of SPRINT MIND did not find any negative impact of intensive BP lowering on cognitive outcomes or cerebral perfusion in older adults (mean age, 68 years). But it didn’t do much good either. Given the heterogeneity of the data, doubts remain on whether aggressive BP lowering might be detrimental in older patients with comorbidities and preexisting dementia. The obvious corollary then is whether deprescribing hypertensive medications could be beneficial.

A recent publication in JAMA Internal Medicine attempted to address this very question. The cohort study used data from Veterans Affairs nursing home residents (mean age, 78 years) to emulate a randomized trial on deprescribing antihypertensives and cognitive decline. Many of the residents’ cognitive scores worsened over the course of follow-up; however, the decline was less pronounced in the deprescribing group (10% vs 12%). The same group did a similar analysis looking at CV outcomes and found no increased risk for heart attack or stroke with deprescribing BP medications. Taken together, these nursing home data suggest that deprescribing may help slow cognitive decline without the expected trade-off of increased CV events.

 

Deprescribing, Yes or No? 

However, randomized data would obviously be preferable, and these are in short supply. One such trial, the DANTE study, found no benefit to deprescribing in terms of cognition in adults aged 75 years or older with mild cognitive impairment. The study follow-up was only 16 weeks, however, which is hardly enough time to demonstrate any effect, positive or negative. The most that can be said is that it didn’t cause many short-term adverse events.

Perhaps the best conclusion to draw from this somewhat underwhelming collection of data is that lowering high BP is important, but less important the closer we get to the end of life. Hypotension is obviously bad, and overly aggressive BP lowering is going to lead to negative outcomes in older adults because gravity is an unforgiving mistress. 

Deprescribing antihypertensives in older adults is probably not going to cause major negative outcomes, but whether it will do much good in nonhypotensive patients is debatable. The bigger problem is the millions of people with undiagnosed or undertreated hypertension. We would probably have less dementia if we treated hypertension when it does the most good: as a primary-prevention strategy in midlife.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He disclosed no relevant conflicts of interest.

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