Mental Health

TORONTO — Be suspicious if a child with a severe dermatologic condition is unresponsive to treatment, especially if their parent or caregiver exhibits deceptive behavior.

These could be red flags for Munchausen syndrome by proxy (MSBP), also known as factitious disorder.

“The No. 1 thing dermatologists can do in situations like this is be open to thinking outside the box and ask themselves the difficult question: Could this be something the parent is inflicting on the child,” Kelly Frasier, DO, a dermatology clinical trials and epidemiology research fellow at Northwell Health, Poughkeepsie, New York, said in an interview.

courtesy Pauline Anderson

She provided a review on advancing the understanding of the dermatologic manifestations of MSBP during a poster session at the annual meeting of the Society for Pediatric Dermatology (SPD). Dr. Frasier has a particular interest in psychodermatology — she was a mental health therapist before going to medical school.

MSBP is a type of abuse intentionally inflicted by a caregiver typically on their child “for some ulterior motive,” usually to seek attention or sympathy and not for material or financial gain, explained Dr. Frasier. People with MSBP seek medical help for exaggerated or fabricated symptoms in their child. They may alter medical tests, falsify medical records, or induce symptoms in their child.

To do this, these abusers may apply any number of caustic household products, including glue, directly to the child’s skin or even in formula. Dr. Frasier shared a picture of a baby whose formula had been doctored with a caustic substance that had dripped onto his neck and face, causing a rash with blisters.

In addition to blistering, cutaneous manifestations of MSBP can include severe bruising. Or the child may present with signs similar to those of granuloma annulare (a benign condition characterized by small, raised bumps) or cicatricial pemphigoid (a rare, chronic autoimmune blistering disorder) or may have recurrent nail avulsion, purpura, or coagulopathy, said Dr. Frasier.

In almost all cases of MSBP (an estimated 96%), the abuse is inflicted by the mother, who may have a preexisting mental illness. “Usually, a psychological disorder is at play, such as depression or anxiety,” said Dr. Frasier.

Some evidence suggests that, in cases of MSBP, the caregiver may have a personality disorder such as borderline or histrionic personality disorder — or may have suffered abuse or neglect as a child or is experiencing major stress, which some evidence suggests can trigger MSPB, she added.

This type of abuse is rarely seen in children older than 6 years, likely because they get wise to what’s going on and are better able to fight back or resist as they get older, Dr. Fraser noted.

High Mortality Rate

It’s critical that cases of MSBP are identified early. While a small proportion of child abuse cases involve MSBP, the mortality rate is extremely high, about 10%, research suggests, said Dr. Frasier.

Dermatologists should be skeptical if the child’s condition hasn’t improved despite trying numerous treatments that normally would have some effect. “If you’re doing everything you can to treat something that’s usually pretty simple in terms of what you normally see clinically and how you treat it, and you’re not seeing any improvement or things continue to get worse, that’s definitely a sign something else may be going on,” Dr. Frasier said.

Another suspicious sign is inflammation that continues “for weeks or months” and “doesn’t match up with actual lab markers and lab values,” said Dr. Frasier.

Other signs of possible MSBP include evidence of chemicals in the child’s blood, stool, or urine, or the child’s condition improves while in the hospital, but symptoms return after returning home.

Also be aware of the interaction between the parent and child, said Dr. Frasier. “See if you can pick up that something else might be going on, especially if the symptoms aren’t lining up very well with what you’re physically seeing and what your clinical impression is.”

And be suspicious of a parent’s inappropriate behavior; for example, they seem to be deliberately making symptoms worse or appear overly distraught. The seemingly caring parent could be overcompensating for what she’s doing at home, “and she wants to make sure it doesn’t appear that way,” said Dr. Frasier.

To help determine if some sort of trauma is occurring at home, the child would ideally be separated from the caregiver, perhaps with a nurse or other member of the interdisciplinary medical team, Dr. Frasier said.

It appears that pediatric dermatologists are already aware of the importance of protecting children from abuse. During a presentation at the meeting on child abuse and maltreatment in dermatology, not specifically on MSBP, Romy Cho, MD, assistant professor, Department of Pediatrics, University of Toronto, who is involved with the SCAN Program at The Hospital for Sick Children, Toronto, Canada, polled the audience on whether they had ever contacted child protective services (CPS). Almost 80% said they had.

That’s good news for Dr. Frasier. “We have to be willing to contact CPS if we think there’s something going on, and be more open to that because it’s better to be safe than sorry, especially in cases involving children.”

Dr. Frasier and Dr. Cho had no relevant disclosures.

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

TORONTO — Be suspicious if a child with a severe dermatologic condition is unresponsive to treatment, especially if their parent or caregiver exhibits deceptive behavior.

These could be red flags for Munchausen syndrome by proxy (MSBP), also known as factitious disorder.

“The No. 1 thing dermatologists can do in situations like this is be open to thinking outside the box and ask themselves the difficult question: Could this be something the parent is inflicting on the child,” Kelly Frasier, DO, a dermatology clinical trials and epidemiology research fellow at Northwell Health, Poughkeepsie, New York, said in an interview.

courtesy Pauline Anderson

She provided a review on advancing the understanding of the dermatologic manifestations of MSBP during a poster session at the annual meeting of the Society for Pediatric Dermatology (SPD). Dr. Frasier has a particular interest in psychodermatology — she was a mental health therapist before going to medical school.

MSBP is a type of abuse intentionally inflicted by a caregiver typically on their child “for some ulterior motive,” usually to seek attention or sympathy and not for material or financial gain, explained Dr. Frasier. People with MSBP seek medical help for exaggerated or fabricated symptoms in their child. They may alter medical tests, falsify medical records, or induce symptoms in their child.

To do this, these abusers may apply any number of caustic household products, including glue, directly to the child’s skin or even in formula. Dr. Frasier shared a picture of a baby whose formula had been doctored with a caustic substance that had dripped onto his neck and face, causing a rash with blisters.

In addition to blistering, cutaneous manifestations of MSBP can include severe bruising. Or the child may present with signs similar to those of granuloma annulare (a benign condition characterized by small, raised bumps) or cicatricial pemphigoid (a rare, chronic autoimmune blistering disorder) or may have recurrent nail avulsion, purpura, or coagulopathy, said Dr. Frasier.

In almost all cases of MSBP (an estimated 96%), the abuse is inflicted by the mother, who may have a preexisting mental illness. “Usually, a psychological disorder is at play, such as depression or anxiety,” said Dr. Frasier.

Some evidence suggests that, in cases of MSBP, the caregiver may have a personality disorder such as borderline or histrionic personality disorder — or may have suffered abuse or neglect as a child or is experiencing major stress, which some evidence suggests can trigger MSPB, she added.

This type of abuse is rarely seen in children older than 6 years, likely because they get wise to what’s going on and are better able to fight back or resist as they get older, Dr. Fraser noted.

High Mortality Rate

It’s critical that cases of MSBP are identified early. While a small proportion of child abuse cases involve MSBP, the mortality rate is extremely high, about 10%, research suggests, said Dr. Frasier.

Dermatologists should be skeptical if the child’s condition hasn’t improved despite trying numerous treatments that normally would have some effect. “If you’re doing everything you can to treat something that’s usually pretty simple in terms of what you normally see clinically and how you treat it, and you’re not seeing any improvement or things continue to get worse, that’s definitely a sign something else may be going on,” Dr. Frasier said.

Another suspicious sign is inflammation that continues “for weeks or months” and “doesn’t match up with actual lab markers and lab values,” said Dr. Frasier.

Other signs of possible MSBP include evidence of chemicals in the child’s blood, stool, or urine, or the child’s condition improves while in the hospital, but symptoms return after returning home.

Also be aware of the interaction between the parent and child, said Dr. Frasier. “See if you can pick up that something else might be going on, especially if the symptoms aren’t lining up very well with what you’re physically seeing and what your clinical impression is.”

And be suspicious of a parent’s inappropriate behavior; for example, they seem to be deliberately making symptoms worse or appear overly distraught. The seemingly caring parent could be overcompensating for what she’s doing at home, “and she wants to make sure it doesn’t appear that way,” said Dr. Frasier.

To help determine if some sort of trauma is occurring at home, the child would ideally be separated from the caregiver, perhaps with a nurse or other member of the interdisciplinary medical team, Dr. Frasier said.

It appears that pediatric dermatologists are already aware of the importance of protecting children from abuse. During a presentation at the meeting on child abuse and maltreatment in dermatology, not specifically on MSBP, Romy Cho, MD, assistant professor, Department of Pediatrics, University of Toronto, who is involved with the SCAN Program at The Hospital for Sick Children, Toronto, Canada, polled the audience on whether they had ever contacted child protective services (CPS). Almost 80% said they had.

That’s good news for Dr. Frasier. “We have to be willing to contact CPS if we think there’s something going on, and be more open to that because it’s better to be safe than sorry, especially in cases involving children.”

Dr. Frasier and Dr. Cho had no relevant disclosures.

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

TORONTO — Be suspicious if a child with a severe dermatologic condition is unresponsive to treatment, especially if their parent or caregiver exhibits deceptive behavior.

These could be red flags for Munchausen syndrome by proxy (MSBP), also known as factitious disorder.

“The No. 1 thing dermatologists can do in situations like this is be open to thinking outside the box and ask themselves the difficult question: Could this be something the parent is inflicting on the child,” Kelly Frasier, DO, a dermatology clinical trials and epidemiology research fellow at Northwell Health, Poughkeepsie, New York, said in an interview.

courtesy Pauline Anderson

She provided a review on advancing the understanding of the dermatologic manifestations of MSBP during a poster session at the annual meeting of the Society for Pediatric Dermatology (SPD). Dr. Frasier has a particular interest in psychodermatology — she was a mental health therapist before going to medical school.

MSBP is a type of abuse intentionally inflicted by a caregiver typically on their child “for some ulterior motive,” usually to seek attention or sympathy and not for material or financial gain, explained Dr. Frasier. People with MSBP seek medical help for exaggerated or fabricated symptoms in their child. They may alter medical tests, falsify medical records, or induce symptoms in their child.

To do this, these abusers may apply any number of caustic household products, including glue, directly to the child’s skin or even in formula. Dr. Frasier shared a picture of a baby whose formula had been doctored with a caustic substance that had dripped onto his neck and face, causing a rash with blisters.

In addition to blistering, cutaneous manifestations of MSBP can include severe bruising. Or the child may present with signs similar to those of granuloma annulare (a benign condition characterized by small, raised bumps) or cicatricial pemphigoid (a rare, chronic autoimmune blistering disorder) or may have recurrent nail avulsion, purpura, or coagulopathy, said Dr. Frasier.

In almost all cases of MSBP (an estimated 96%), the abuse is inflicted by the mother, who may have a preexisting mental illness. “Usually, a psychological disorder is at play, such as depression or anxiety,” said Dr. Frasier.

Some evidence suggests that, in cases of MSBP, the caregiver may have a personality disorder such as borderline or histrionic personality disorder — or may have suffered abuse or neglect as a child or is experiencing major stress, which some evidence suggests can trigger MSPB, she added.

This type of abuse is rarely seen in children older than 6 years, likely because they get wise to what’s going on and are better able to fight back or resist as they get older, Dr. Fraser noted.

High Mortality Rate

It’s critical that cases of MSBP are identified early. While a small proportion of child abuse cases involve MSBP, the mortality rate is extremely high, about 10%, research suggests, said Dr. Frasier.

Dermatologists should be skeptical if the child’s condition hasn’t improved despite trying numerous treatments that normally would have some effect. “If you’re doing everything you can to treat something that’s usually pretty simple in terms of what you normally see clinically and how you treat it, and you’re not seeing any improvement or things continue to get worse, that’s definitely a sign something else may be going on,” Dr. Frasier said.

Another suspicious sign is inflammation that continues “for weeks or months” and “doesn’t match up with actual lab markers and lab values,” said Dr. Frasier.

Other signs of possible MSBP include evidence of chemicals in the child’s blood, stool, or urine, or the child’s condition improves while in the hospital, but symptoms return after returning home.

Also be aware of the interaction between the parent and child, said Dr. Frasier. “See if you can pick up that something else might be going on, especially if the symptoms aren’t lining up very well with what you’re physically seeing and what your clinical impression is.”

And be suspicious of a parent’s inappropriate behavior; for example, they seem to be deliberately making symptoms worse or appear overly distraught. The seemingly caring parent could be overcompensating for what she’s doing at home, “and she wants to make sure it doesn’t appear that way,” said Dr. Frasier.

To help determine if some sort of trauma is occurring at home, the child would ideally be separated from the caregiver, perhaps with a nurse or other member of the interdisciplinary medical team, Dr. Frasier said.

It appears that pediatric dermatologists are already aware of the importance of protecting children from abuse. During a presentation at the meeting on child abuse and maltreatment in dermatology, not specifically on MSBP, Romy Cho, MD, assistant professor, Department of Pediatrics, University of Toronto, who is involved with the SCAN Program at The Hospital for Sick Children, Toronto, Canada, polled the audience on whether they had ever contacted child protective services (CPS). Almost 80% said they had.

That’s good news for Dr. Frasier. “We have to be willing to contact CPS if we think there’s something going on, and be more open to that because it’s better to be safe than sorry, especially in cases involving children.”

Dr. Frasier and Dr. Cho had no relevant disclosures.

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

One in five children (20.2%) who have an older sibling with autism spectrum disorder (ASD) are likely to be diagnosed with the disorder as well, according to a study published in Pediatrics.

When a baby had more than one older sibling with autism, the family recurrence rate rose to 36.9%, the study found.

The researchers, led by Sally Ozonoff, PhD, Department of Psychiatry and Behavioral Sciences at University of California Davis Health in Sacramento, analyzed data from 1,605 infants who had an older sibling with ASD using data from the global Baby Siblings Research Consortium.

They calculated that the rate of autism recurrence is seven times higher in families who already have one autistic child than in the general population, which points to the importance of close developmental observance in infants born in families with autistic children, particularly male infants in those families. This study replicated a 2011 study, also led by Dr. Ozonoff, which found a similar rate of familial recurrence.
 

Differences by Sex and Race

Dr. Ozonoff’s team found that sex and race played a part in likelihood of recurrence. Younger siblings of females with ASD were much more likely to develop the disorder (34.7%) than siblings of boys (22.5%). And male younger siblings were more likely to have ASD than girls (25.3% vs. 13.1%).

Additionally, ASD recurrence in White families was 17.8% while across other races collectively the recurrence rate was 25%.
 

Links with Maternal Education

Differences by maternal education were also striking. Recurrence was 32.6% when mothers had a high school or less education; 25.5% with some college; 19.7 with a college degree; and 16.9% with a graduate degree. The parental education revealed a significant effect only for mothers (P < .01); paternal education was not significant (P = .09).

Suzanne Rybczynski, MD, chief medical officer at East Tennessee Children’s Hospital in Knoxville, who was not part of the study, praised the study for following babies over time, “doing serial evaluation using two very standard tools in diagnosing autism and developmental delay.”

The babies were evaluated as early as 6 months of age, for up to seven visits. A final assessment was made at 36 months.

Dr. Rybczynski said it was interesting to see that, although ASD prevalence has increased substantially from the 2011 study (0.9%-2.8%), the findings regarding the sibling link have been consistent (18.7% in the 2011 study to 20.2% now).
 

Eliminating Biases

Dr. Rybczynski noted the current study also used diagnoses only from autism experts, which strengthened the findings, noting the potential for overdiagnosis when interviews are with the parents. “This really eliminates those biases.”

The authors explained the factors driving the need to update recurrence rate studies, including the growth in the prevalence of ASD in the last decade to 1 in 36. That may be caused partly by “greater awareness and identification of autistic females and cognitively able, verbal children.”

Also, new diagnostic criteria have been published, with different diagnostic thresholds since the last study. This study, they noted, had a sample size twice as large and more diverse than the 2011 sample.

The size and the diversity are particularly important, Dr. Rybczynski said, as it helps support more recent findings that ASD is not as heavily centered in White males as previously thought.

“We need to make sure we’re monitoring all children, especially from groups where there’s at least one older sibling or multiple siblings with autism or a sister with autism,” she said. The findings of this study are important not just for pediatricians but for families and all who have professional interactions with children.

Dr. Ozonoff reports travel reimbursements and honoraria from Autism Speaks and the Autism Science Foundation and book royalties from Guilford Press. One coauthor has served as a paid consultant to F. Hoffmann–La Roche and Servier and has received royalties from Sage Publications and Guilford Publications. Another is supported by the Stollery Children’s Hospital Foundation Chair in Autism. One coauthor reported a consulting agreement with EarliTec Diagnostics and book royalties from Wiley. A fourth coauthor has received funding from the Simons Foundation and consults for the Beasley Law Firm and Linus Technology. Dr. Rybczynski reported no relevant financial relationships.

One in five children (20.2%) who have an older sibling with autism spectrum disorder (ASD) are likely to be diagnosed with the disorder as well, according to a study published in Pediatrics.

When a baby had more than one older sibling with autism, the family recurrence rate rose to 36.9%, the study found.

The researchers, led by Sally Ozonoff, PhD, Department of Psychiatry and Behavioral Sciences at University of California Davis Health in Sacramento, analyzed data from 1,605 infants who had an older sibling with ASD using data from the global Baby Siblings Research Consortium.

They calculated that the rate of autism recurrence is seven times higher in families who already have one autistic child than in the general population, which points to the importance of close developmental observance in infants born in families with autistic children, particularly male infants in those families. This study replicated a 2011 study, also led by Dr. Ozonoff, which found a similar rate of familial recurrence.
 

Differences by Sex and Race

Dr. Ozonoff’s team found that sex and race played a part in likelihood of recurrence. Younger siblings of females with ASD were much more likely to develop the disorder (34.7%) than siblings of boys (22.5%). And male younger siblings were more likely to have ASD than girls (25.3% vs. 13.1%).

Additionally, ASD recurrence in White families was 17.8% while across other races collectively the recurrence rate was 25%.
 

Links with Maternal Education

Differences by maternal education were also striking. Recurrence was 32.6% when mothers had a high school or less education; 25.5% with some college; 19.7 with a college degree; and 16.9% with a graduate degree. The parental education revealed a significant effect only for mothers (P < .01); paternal education was not significant (P = .09).

Suzanne Rybczynski, MD, chief medical officer at East Tennessee Children’s Hospital in Knoxville, who was not part of the study, praised the study for following babies over time, “doing serial evaluation using two very standard tools in diagnosing autism and developmental delay.”

The babies were evaluated as early as 6 months of age, for up to seven visits. A final assessment was made at 36 months.

Dr. Rybczynski said it was interesting to see that, although ASD prevalence has increased substantially from the 2011 study (0.9%-2.8%), the findings regarding the sibling link have been consistent (18.7% in the 2011 study to 20.2% now).
 

Eliminating Biases

Dr. Rybczynski noted the current study also used diagnoses only from autism experts, which strengthened the findings, noting the potential for overdiagnosis when interviews are with the parents. “This really eliminates those biases.”

The authors explained the factors driving the need to update recurrence rate studies, including the growth in the prevalence of ASD in the last decade to 1 in 36. That may be caused partly by “greater awareness and identification of autistic females and cognitively able, verbal children.”

Also, new diagnostic criteria have been published, with different diagnostic thresholds since the last study. This study, they noted, had a sample size twice as large and more diverse than the 2011 sample.

The size and the diversity are particularly important, Dr. Rybczynski said, as it helps support more recent findings that ASD is not as heavily centered in White males as previously thought.

“We need to make sure we’re monitoring all children, especially from groups where there’s at least one older sibling or multiple siblings with autism or a sister with autism,” she said. The findings of this study are important not just for pediatricians but for families and all who have professional interactions with children.

Dr. Ozonoff reports travel reimbursements and honoraria from Autism Speaks and the Autism Science Foundation and book royalties from Guilford Press. One coauthor has served as a paid consultant to F. Hoffmann–La Roche and Servier and has received royalties from Sage Publications and Guilford Publications. Another is supported by the Stollery Children’s Hospital Foundation Chair in Autism. One coauthor reported a consulting agreement with EarliTec Diagnostics and book royalties from Wiley. A fourth coauthor has received funding from the Simons Foundation and consults for the Beasley Law Firm and Linus Technology. Dr. Rybczynski reported no relevant financial relationships.

One in five children (20.2%) who have an older sibling with autism spectrum disorder (ASD) are likely to be diagnosed with the disorder as well, according to a study published in Pediatrics.

When a baby had more than one older sibling with autism, the family recurrence rate rose to 36.9%, the study found.

The researchers, led by Sally Ozonoff, PhD, Department of Psychiatry and Behavioral Sciences at University of California Davis Health in Sacramento, analyzed data from 1,605 infants who had an older sibling with ASD using data from the global Baby Siblings Research Consortium.

They calculated that the rate of autism recurrence is seven times higher in families who already have one autistic child than in the general population, which points to the importance of close developmental observance in infants born in families with autistic children, particularly male infants in those families. This study replicated a 2011 study, also led by Dr. Ozonoff, which found a similar rate of familial recurrence.
 

Differences by Sex and Race

Dr. Ozonoff’s team found that sex and race played a part in likelihood of recurrence. Younger siblings of females with ASD were much more likely to develop the disorder (34.7%) than siblings of boys (22.5%). And male younger siblings were more likely to have ASD than girls (25.3% vs. 13.1%).

Additionally, ASD recurrence in White families was 17.8% while across other races collectively the recurrence rate was 25%.
 

Links with Maternal Education

Differences by maternal education were also striking. Recurrence was 32.6% when mothers had a high school or less education; 25.5% with some college; 19.7 with a college degree; and 16.9% with a graduate degree. The parental education revealed a significant effect only for mothers (P < .01); paternal education was not significant (P = .09).

Suzanne Rybczynski, MD, chief medical officer at East Tennessee Children’s Hospital in Knoxville, who was not part of the study, praised the study for following babies over time, “doing serial evaluation using two very standard tools in diagnosing autism and developmental delay.”

The babies were evaluated as early as 6 months of age, for up to seven visits. A final assessment was made at 36 months.

Dr. Rybczynski said it was interesting to see that, although ASD prevalence has increased substantially from the 2011 study (0.9%-2.8%), the findings regarding the sibling link have been consistent (18.7% in the 2011 study to 20.2% now).
 

Eliminating Biases

Dr. Rybczynski noted the current study also used diagnoses only from autism experts, which strengthened the findings, noting the potential for overdiagnosis when interviews are with the parents. “This really eliminates those biases.”

The authors explained the factors driving the need to update recurrence rate studies, including the growth in the prevalence of ASD in the last decade to 1 in 36. That may be caused partly by “greater awareness and identification of autistic females and cognitively able, verbal children.”

Also, new diagnostic criteria have been published, with different diagnostic thresholds since the last study. This study, they noted, had a sample size twice as large and more diverse than the 2011 sample.

The size and the diversity are particularly important, Dr. Rybczynski said, as it helps support more recent findings that ASD is not as heavily centered in White males as previously thought.

“We need to make sure we’re monitoring all children, especially from groups where there’s at least one older sibling or multiple siblings with autism or a sister with autism,” she said. The findings of this study are important not just for pediatricians but for families and all who have professional interactions with children.

Dr. Ozonoff reports travel reimbursements and honoraria from Autism Speaks and the Autism Science Foundation and book royalties from Guilford Press. One coauthor has served as a paid consultant to F. Hoffmann–La Roche and Servier and has received royalties from Sage Publications and Guilford Publications. Another is supported by the Stollery Children’s Hospital Foundation Chair in Autism. One coauthor reported a consulting agreement with EarliTec Diagnostics and book royalties from Wiley. A fourth coauthor has received funding from the Simons Foundation and consults for the Beasley Law Firm and Linus Technology. Dr. Rybczynski reported no relevant financial relationships.

The start of the school year is a time that is always full of anticipation and even anxiety. Who will my teachers be? Will I be in classes with friends? Have some of my friends changed over the summer? Will the work be too hard? For some children this anxiety will be so intense that they will resist going back to school. School avoidance is very important to identify and address quickly, as it can intensify and threaten development. Each day of school missed due to accommodating to a child’s anxiety makes a return to school more difficult and less likely. Days can easily become weeks and even months of missed school. A child who misses a substantial amount of school is inevitably going to face developmental delays: academic, social, behavioral and emotional. The pediatrician is often brought into these situations early, as when a child complains of vague physical symptoms that are keeping him or her from school or when a previously calm child becomes inconsolable about going to school in the mornings. With a thoughtful assessment of the potential causes of school avoidance, you can help almost all children return to school successfully.

School Refusal

Sustained school avoidance is now called “school refusal,” a term coined in the late 1990s to describe a school attendance problem driven by emotional distress, as opposed to truancy. It affects up to 15% of children (depending on the operational definition) and seems to peak in the earliest years of elementary school and again in early high school. These are not occasional absences, but missing over 80% of classroom time in a 2-week period. It is also marked by the presence of an anxiety disorder and the absence of conduct disorder. Often in such cases the parents are aware of their child’s whereabouts and motivated to return them to school. Youth with school refusal experience social and academic consequences in the short term and, over the long term, have shown problems with social, family, and professional performance, along with higher rates of major depressive disorder than is seen in the general population. Early identification of these children can make addressing the underlying distress and return to school much easier than attempts to treat after weeks or months out of school.

Identifying the Problem

With younger children, school avoidance is most commonly associated with an anxious temperament or an underlying anxiety disorder, such as separation anxiety disorder or social phobia. A family history of anxiety may contribute or impact a parent’s approach to the issue. Children often present with vague somatic concerns that are genuine symptoms of anxiety (upset stomach, headache). A screening instrument such as the Screen for Child Anxiety Related Disorders (SCARED) can be helpful, but so is inquiring about sleep and other anxiety symptoms. Do the symptoms remit on weekends or in after-school hours? Are there other environmental factors that may be stressing younger children: Are they being teased or bullied at school? Are they struggling to find friends in a new classroom? Might they be having trouble with reading or other new tasks? Perhaps they are afraid of walking to school alone. Has there been a recent change or stress at home, such as a move or parental illness? Younger children may feel more anxious about separating from parents in the face of stress. But when parents accommodate a child’s wish to avoid school, the child’s anxiety, briefly relieved, grows more persistent, gets rewarded by parental attention, and reinforces their reluctance to try new things.

Adolescents may be facing more complex challenges that lead to school avoidance. They may have an undiagnosed anxiety or mood disorder, perhaps complicated by substance abuse that is presenting as an inability to perform at school or to manage the challenge of keeping up with higher workloads. They may be facing complex situations with friends, bullying, or rejection. Those adolescents who are prone to procrastination may avoid school to manage their workload and their distress, which can then become tangled up with symptoms of anxiety and dysphoria. Missing school compounds this problem rather than solving it. Adolescents outside of the structure of school, hungry for socializing and new experiences, often turn to social media for entertainment. Days without exercise and nights without adequate sleep can make mood, attention, and anxiety symptoms worse while overdue work grows. Parents often fear that setting limits or “pushing” their stuck and miserable child may make them more depressed or even suicidal.
 

Accommodating the Problem Will Likely Make It Worse

It is worth noting that children with a genuine medical illness can also experience school avoidance. Temperamentally anxious children who stay home for several days with a febrile illness may find it overwhelming to return to school as they have become so comfortable at home. Adolescents may have fallen behind with work and find themselves unable to set a schedule and return to more structure. Youth who are managing a known mood or anxiety disorder often have low motivation or high anxiety and want to wait to feel entirely better before returning to school. Youth with a chronic condition such as severe allergies or a sustained viral infection may be anxious about managing symptoms at school. Their parents may have kept them home to be safe or until they feel better, unwittingly making the school avoidance worse.

Formulating a Management Plan

When you suspect school avoidance is present, the critical first step is to engage the parents alongside their child. Without their understanding of the nature of this behavior, it will continue. Start by acknowledging the real physical and emotional symptoms their child is experiencing; it is important that parents and patients not feel that they are being told this is “just” a psychological problem. Children rarely feign illness or manipulate; they genuinely feel bad enough to stay home. It is important that they understand this is a common problem that will get worse unless it is addressed directly. If you believe they are suffering from a mood or anxiety disorder, talk about treatment options and consider getting started with treatment while finding a therapist to participate in their care. Help everyone listen to the child or teenager to understand any realistic basis for anxiety and attempt to address it (e.g. address bullying, provide a tutor, support a parent dependent on the child, etc.)

You can partner with parents and the school to provide the child with structure and support to make the return to school manageable. Frame the challenge of “demagnetizing” home and “remagnetizing” school. When they are at home, there should be no screen time except to catch up or keep up with homework. The child should not be in bed all day unless he or she has a fever. There needs to be close attention paid to maintaining a regular routine, with bedtime and wake time, meals with family, and regular exercise. This may mean turning off the Wi-Fi while a child is at home and parents are at work and providing them with books.

Work with the school to make getting into school and staying there as easy as possible. If a child has very high distress or has been out of school for a long time, he or she may need to return gradually; perhaps aim for the child to spend an hour at school for the first few days and then gradually work up to half and full days. Younger children may benefit from having a “buddy” who meets them outside and enters school with them. This can help avoid intense emotional scenes with parents that heighten distress and lead to accommodation. The child can identify a preferred teacher (or librarian, coach, or school nurse). When they feel overwhelmed, they can have a “break” with that teacher to avoid leaving school altogether. If they enjoy sports, music, or art, emphasize these classes or practices as part of their return to school.

Remind parents and your patients that it is not a matter of making the distress better first and then returning to school. They can be in treatment for an illness and manage returning to school at the same time. Indeed, the distress around school will only get better by getting back to school. This is hard! Ask about previous challenges they have managed or mastered and remind them that this is no different. Providing parents with knowledge and support will help them to be validating of their children without accommodating their wish to avoid discomfort. This support of your patient and the parents is the first step in helping them manage a difficult period and stay on their healthiest developmental trajectory.

Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@mdedge.com.

The start of the school year is a time that is always full of anticipation and even anxiety. Who will my teachers be? Will I be in classes with friends? Have some of my friends changed over the summer? Will the work be too hard? For some children this anxiety will be so intense that they will resist going back to school. School avoidance is very important to identify and address quickly, as it can intensify and threaten development. Each day of school missed due to accommodating to a child’s anxiety makes a return to school more difficult and less likely. Days can easily become weeks and even months of missed school. A child who misses a substantial amount of school is inevitably going to face developmental delays: academic, social, behavioral and emotional. The pediatrician is often brought into these situations early, as when a child complains of vague physical symptoms that are keeping him or her from school or when a previously calm child becomes inconsolable about going to school in the mornings. With a thoughtful assessment of the potential causes of school avoidance, you can help almost all children return to school successfully.

School Refusal

Sustained school avoidance is now called “school refusal,” a term coined in the late 1990s to describe a school attendance problem driven by emotional distress, as opposed to truancy. It affects up to 15% of children (depending on the operational definition) and seems to peak in the earliest years of elementary school and again in early high school. These are not occasional absences, but missing over 80% of classroom time in a 2-week period. It is also marked by the presence of an anxiety disorder and the absence of conduct disorder. Often in such cases the parents are aware of their child’s whereabouts and motivated to return them to school. Youth with school refusal experience social and academic consequences in the short term and, over the long term, have shown problems with social, family, and professional performance, along with higher rates of major depressive disorder than is seen in the general population. Early identification of these children can make addressing the underlying distress and return to school much easier than attempts to treat after weeks or months out of school.

Identifying the Problem

With younger children, school avoidance is most commonly associated with an anxious temperament or an underlying anxiety disorder, such as separation anxiety disorder or social phobia. A family history of anxiety may contribute or impact a parent’s approach to the issue. Children often present with vague somatic concerns that are genuine symptoms of anxiety (upset stomach, headache). A screening instrument such as the Screen for Child Anxiety Related Disorders (SCARED) can be helpful, but so is inquiring about sleep and other anxiety symptoms. Do the symptoms remit on weekends or in after-school hours? Are there other environmental factors that may be stressing younger children: Are they being teased or bullied at school? Are they struggling to find friends in a new classroom? Might they be having trouble with reading or other new tasks? Perhaps they are afraid of walking to school alone. Has there been a recent change or stress at home, such as a move or parental illness? Younger children may feel more anxious about separating from parents in the face of stress. But when parents accommodate a child’s wish to avoid school, the child’s anxiety, briefly relieved, grows more persistent, gets rewarded by parental attention, and reinforces their reluctance to try new things.

Adolescents may be facing more complex challenges that lead to school avoidance. They may have an undiagnosed anxiety or mood disorder, perhaps complicated by substance abuse that is presenting as an inability to perform at school or to manage the challenge of keeping up with higher workloads. They may be facing complex situations with friends, bullying, or rejection. Those adolescents who are prone to procrastination may avoid school to manage their workload and their distress, which can then become tangled up with symptoms of anxiety and dysphoria. Missing school compounds this problem rather than solving it. Adolescents outside of the structure of school, hungry for socializing and new experiences, often turn to social media for entertainment. Days without exercise and nights without adequate sleep can make mood, attention, and anxiety symptoms worse while overdue work grows. Parents often fear that setting limits or “pushing” their stuck and miserable child may make them more depressed or even suicidal.
 

Accommodating the Problem Will Likely Make It Worse

It is worth noting that children with a genuine medical illness can also experience school avoidance. Temperamentally anxious children who stay home for several days with a febrile illness may find it overwhelming to return to school as they have become so comfortable at home. Adolescents may have fallen behind with work and find themselves unable to set a schedule and return to more structure. Youth who are managing a known mood or anxiety disorder often have low motivation or high anxiety and want to wait to feel entirely better before returning to school. Youth with a chronic condition such as severe allergies or a sustained viral infection may be anxious about managing symptoms at school. Their parents may have kept them home to be safe or until they feel better, unwittingly making the school avoidance worse.

Formulating a Management Plan

When you suspect school avoidance is present, the critical first step is to engage the parents alongside their child. Without their understanding of the nature of this behavior, it will continue. Start by acknowledging the real physical and emotional symptoms their child is experiencing; it is important that parents and patients not feel that they are being told this is “just” a psychological problem. Children rarely feign illness or manipulate; they genuinely feel bad enough to stay home. It is important that they understand this is a common problem that will get worse unless it is addressed directly. If you believe they are suffering from a mood or anxiety disorder, talk about treatment options and consider getting started with treatment while finding a therapist to participate in their care. Help everyone listen to the child or teenager to understand any realistic basis for anxiety and attempt to address it (e.g. address bullying, provide a tutor, support a parent dependent on the child, etc.)

You can partner with parents and the school to provide the child with structure and support to make the return to school manageable. Frame the challenge of “demagnetizing” home and “remagnetizing” school. When they are at home, there should be no screen time except to catch up or keep up with homework. The child should not be in bed all day unless he or she has a fever. There needs to be close attention paid to maintaining a regular routine, with bedtime and wake time, meals with family, and regular exercise. This may mean turning off the Wi-Fi while a child is at home and parents are at work and providing them with books.

Work with the school to make getting into school and staying there as easy as possible. If a child has very high distress or has been out of school for a long time, he or she may need to return gradually; perhaps aim for the child to spend an hour at school for the first few days and then gradually work up to half and full days. Younger children may benefit from having a “buddy” who meets them outside and enters school with them. This can help avoid intense emotional scenes with parents that heighten distress and lead to accommodation. The child can identify a preferred teacher (or librarian, coach, or school nurse). When they feel overwhelmed, they can have a “break” with that teacher to avoid leaving school altogether. If they enjoy sports, music, or art, emphasize these classes or practices as part of their return to school.

Remind parents and your patients that it is not a matter of making the distress better first and then returning to school. They can be in treatment for an illness and manage returning to school at the same time. Indeed, the distress around school will only get better by getting back to school. This is hard! Ask about previous challenges they have managed or mastered and remind them that this is no different. Providing parents with knowledge and support will help them to be validating of their children without accommodating their wish to avoid discomfort. This support of your patient and the parents is the first step in helping them manage a difficult period and stay on their healthiest developmental trajectory.

Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@mdedge.com.

The start of the school year is a time that is always full of anticipation and even anxiety. Who will my teachers be? Will I be in classes with friends? Have some of my friends changed over the summer? Will the work be too hard? For some children this anxiety will be so intense that they will resist going back to school. School avoidance is very important to identify and address quickly, as it can intensify and threaten development. Each day of school missed due to accommodating to a child’s anxiety makes a return to school more difficult and less likely. Days can easily become weeks and even months of missed school. A child who misses a substantial amount of school is inevitably going to face developmental delays: academic, social, behavioral and emotional. The pediatrician is often brought into these situations early, as when a child complains of vague physical symptoms that are keeping him or her from school or when a previously calm child becomes inconsolable about going to school in the mornings. With a thoughtful assessment of the potential causes of school avoidance, you can help almost all children return to school successfully.

School Refusal

Sustained school avoidance is now called “school refusal,” a term coined in the late 1990s to describe a school attendance problem driven by emotional distress, as opposed to truancy. It affects up to 15% of children (depending on the operational definition) and seems to peak in the earliest years of elementary school and again in early high school. These are not occasional absences, but missing over 80% of classroom time in a 2-week period. It is also marked by the presence of an anxiety disorder and the absence of conduct disorder. Often in such cases the parents are aware of their child’s whereabouts and motivated to return them to school. Youth with school refusal experience social and academic consequences in the short term and, over the long term, have shown problems with social, family, and professional performance, along with higher rates of major depressive disorder than is seen in the general population. Early identification of these children can make addressing the underlying distress and return to school much easier than attempts to treat after weeks or months out of school.

Identifying the Problem

With younger children, school avoidance is most commonly associated with an anxious temperament or an underlying anxiety disorder, such as separation anxiety disorder or social phobia. A family history of anxiety may contribute or impact a parent’s approach to the issue. Children often present with vague somatic concerns that are genuine symptoms of anxiety (upset stomach, headache). A screening instrument such as the Screen for Child Anxiety Related Disorders (SCARED) can be helpful, but so is inquiring about sleep and other anxiety symptoms. Do the symptoms remit on weekends or in after-school hours? Are there other environmental factors that may be stressing younger children: Are they being teased or bullied at school? Are they struggling to find friends in a new classroom? Might they be having trouble with reading or other new tasks? Perhaps they are afraid of walking to school alone. Has there been a recent change or stress at home, such as a move or parental illness? Younger children may feel more anxious about separating from parents in the face of stress. But when parents accommodate a child’s wish to avoid school, the child’s anxiety, briefly relieved, grows more persistent, gets rewarded by parental attention, and reinforces their reluctance to try new things.

Adolescents may be facing more complex challenges that lead to school avoidance. They may have an undiagnosed anxiety or mood disorder, perhaps complicated by substance abuse that is presenting as an inability to perform at school or to manage the challenge of keeping up with higher workloads. They may be facing complex situations with friends, bullying, or rejection. Those adolescents who are prone to procrastination may avoid school to manage their workload and their distress, which can then become tangled up with symptoms of anxiety and dysphoria. Missing school compounds this problem rather than solving it. Adolescents outside of the structure of school, hungry for socializing and new experiences, often turn to social media for entertainment. Days without exercise and nights without adequate sleep can make mood, attention, and anxiety symptoms worse while overdue work grows. Parents often fear that setting limits or “pushing” their stuck and miserable child may make them more depressed or even suicidal.
 

Accommodating the Problem Will Likely Make It Worse

It is worth noting that children with a genuine medical illness can also experience school avoidance. Temperamentally anxious children who stay home for several days with a febrile illness may find it overwhelming to return to school as they have become so comfortable at home. Adolescents may have fallen behind with work and find themselves unable to set a schedule and return to more structure. Youth who are managing a known mood or anxiety disorder often have low motivation or high anxiety and want to wait to feel entirely better before returning to school. Youth with a chronic condition such as severe allergies or a sustained viral infection may be anxious about managing symptoms at school. Their parents may have kept them home to be safe or until they feel better, unwittingly making the school avoidance worse.

Formulating a Management Plan

When you suspect school avoidance is present, the critical first step is to engage the parents alongside their child. Without their understanding of the nature of this behavior, it will continue. Start by acknowledging the real physical and emotional symptoms their child is experiencing; it is important that parents and patients not feel that they are being told this is “just” a psychological problem. Children rarely feign illness or manipulate; they genuinely feel bad enough to stay home. It is important that they understand this is a common problem that will get worse unless it is addressed directly. If you believe they are suffering from a mood or anxiety disorder, talk about treatment options and consider getting started with treatment while finding a therapist to participate in their care. Help everyone listen to the child or teenager to understand any realistic basis for anxiety and attempt to address it (e.g. address bullying, provide a tutor, support a parent dependent on the child, etc.)

You can partner with parents and the school to provide the child with structure and support to make the return to school manageable. Frame the challenge of “demagnetizing” home and “remagnetizing” school. When they are at home, there should be no screen time except to catch up or keep up with homework. The child should not be in bed all day unless he or she has a fever. There needs to be close attention paid to maintaining a regular routine, with bedtime and wake time, meals with family, and regular exercise. This may mean turning off the Wi-Fi while a child is at home and parents are at work and providing them with books.

Work with the school to make getting into school and staying there as easy as possible. If a child has very high distress or has been out of school for a long time, he or she may need to return gradually; perhaps aim for the child to spend an hour at school for the first few days and then gradually work up to half and full days. Younger children may benefit from having a “buddy” who meets them outside and enters school with them. This can help avoid intense emotional scenes with parents that heighten distress and lead to accommodation. The child can identify a preferred teacher (or librarian, coach, or school nurse). When they feel overwhelmed, they can have a “break” with that teacher to avoid leaving school altogether. If they enjoy sports, music, or art, emphasize these classes or practices as part of their return to school.

Remind parents and your patients that it is not a matter of making the distress better first and then returning to school. They can be in treatment for an illness and manage returning to school at the same time. Indeed, the distress around school will only get better by getting back to school. This is hard! Ask about previous challenges they have managed or mastered and remind them that this is no different. Providing parents with knowledge and support will help them to be validating of their children without accommodating their wish to avoid discomfort. This support of your patient and the parents is the first step in helping them manage a difficult period and stay on their healthiest developmental trajectory.

Dr. Swick is physician in chief at Ohana, Center for Child and Adolescent Behavioral Health, Community Hospital of the Monterey (Calif.) Peninsula. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@mdedge.com.

Individuals who are more active in the evening performed better on cognitive tests than did those who are typically more active in the morning hours, new research suggests. 

“Rather than just being personal preferences, these chronotypes could impact our cognitive function,” said study investigator, Raha West, MBChB, with Imperial College London, London, England, in a statement.

But the researchers also urged caution when interpreting the findings.

“It’s important to note that this doesn’t mean all morning people have worse cognitive performance. The findings reflect an overall trend where the majority might lean toward better cognition in the evening types,” Dr. West added. 

In addition, across the board, getting the recommended 7-9 hours of nightly sleep was best for cognitive function, and sleeping for less than 7 or more than 9 hours had detrimental effects on brain function regardless of whether an individual was a night owl or lark. 

The study was published online in BMJ Public Health. 
 

A UK Biobank Cohort Study 

The findings are based on a cross-sectional analysis of 26,820 adults aged 53-86 years from the UK Biobank database, who were categorized into two cohorts. 

Cohort 1 had 10,067 participants (56% women) who completed four cognitive tests measuring fluid intelligence/reasoning, pairs matching, reaction time, and prospective memory. Cohort 2 had 16,753 participants (56% women) who completed two cognitive assessments (pairs matching and reaction time).

Participants self-reported sleep duration, chronotype, and quality. Cognitive test scores were evaluated against sleep parameters and health and lifestyle factors including sex, age, vascular and cardiac conditions, diabetes,alcohol use, smoking habits, and body mass index.

The results revealed a positive association between normal sleep duration (7-9 hours) and cognitive scores in Cohort 1 (beta, 0.0567), while extended sleep duration negatively impacted scores across in Cohort 1 and 2 (beta, –0.188 and beta, –0.2619, respectively). 

An individual’s preference for evening or morning activity correlated strongly with their test scores. In particular, night owls consistently performed better on cognitive tests than early birds. 

“While understanding and working with your natural sleep tendencies is essential, it’s equally important to remember to get just enough sleep, not too long or too short,” Dr. West noted. “This is crucial for keeping your brain healthy and functioning at its best.”

Contrary to some previous findings, the study did not find a significant relationship between sleep, sleepiness/insomnia, and cognitive performance. This may be because specific aspects of insomnia, such as severity and chronicity, as well as comorbid conditions need to be considered, the investigators wrote. 

They added that age and diabetes consistently emerged as negative predictors of cognitive functioning across both cohorts, in line with previous research. 

Limitations of the study include the cross-sectional design, which limits causal inferences; the possibility of residual confounding; and reliance on self-reported sleep data.

Also, the study did not adjust for educational attainment, a factor potentially influential on cognitive performance and sleep patterns, because of incomplete data. The study also did not factor in depression and social isolation, which have been shown to increase the risk for cognitive decline.
 

No Real-World Implications

Several outside experts offered their perspective on the study in a statement from the UK nonprofit Science Media Centre. 

The study provides “interesting insights” into the difference in memory and thinking in people who identify themselves as a “morning” or “evening” person, Jacqui Hanley, PhD, with Alzheimer’s Research UK, said in the statement. 

However, without a detailed picture of what is going on in the brain, it’s not clear whether being a morning or evening person affects memory and thinking or whether a decline in cognition is causing changes to sleeping patterns, Dr. Hanley added. 

Roi Cohen Kadosh, PhD, CPsychol, professor of cognitive neuroscience, University of Surrey, Guildford, England, cautioned that there are “multiple potential reasons” for these associations. 

“Therefore, there are no implications in my view for the real world. I fear that the general public will not be able to understand that and will change their sleep pattern, while this study does not give any evidence that this will lead to any benefit,” Dr. Cohen Kadosh said. 

Jessica Chelekis, PhD, MBA, a sleep expert from Brunel University London, Uxbridge, England, said that the “main takeaway should be that the cultural belief that early risers are more productive than ‘night owls’ does not hold up to scientific scrutiny.” 

“While everyone should aim to get good-quality sleep each night, we should also try to be aware of what time of day we are at our (cognitive) best and work in ways that suit us. Night owls, in particular, should not be shamed into fitting a stereotype that favors an ‘early to bed, early to rise’ practice,” Dr. Chelekis said. 

Funding for the study was provided by the Korea Institute of Oriental Medicine in collaboration with Imperial College London. Dr. Hanley, Dr. Cohen Kadosh, and Dr. Chelekis have no relevant disclosures.

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

Individuals who are more active in the evening performed better on cognitive tests than did those who are typically more active in the morning hours, new research suggests. 

“Rather than just being personal preferences, these chronotypes could impact our cognitive function,” said study investigator, Raha West, MBChB, with Imperial College London, London, England, in a statement.

But the researchers also urged caution when interpreting the findings.

“It’s important to note that this doesn’t mean all morning people have worse cognitive performance. The findings reflect an overall trend where the majority might lean toward better cognition in the evening types,” Dr. West added. 

In addition, across the board, getting the recommended 7-9 hours of nightly sleep was best for cognitive function, and sleeping for less than 7 or more than 9 hours had detrimental effects on brain function regardless of whether an individual was a night owl or lark. 

The study was published online in BMJ Public Health. 
 

A UK Biobank Cohort Study 

The findings are based on a cross-sectional analysis of 26,820 adults aged 53-86 years from the UK Biobank database, who were categorized into two cohorts. 

Cohort 1 had 10,067 participants (56% women) who completed four cognitive tests measuring fluid intelligence/reasoning, pairs matching, reaction time, and prospective memory. Cohort 2 had 16,753 participants (56% women) who completed two cognitive assessments (pairs matching and reaction time).

Participants self-reported sleep duration, chronotype, and quality. Cognitive test scores were evaluated against sleep parameters and health and lifestyle factors including sex, age, vascular and cardiac conditions, diabetes,alcohol use, smoking habits, and body mass index.

The results revealed a positive association between normal sleep duration (7-9 hours) and cognitive scores in Cohort 1 (beta, 0.0567), while extended sleep duration negatively impacted scores across in Cohort 1 and 2 (beta, –0.188 and beta, –0.2619, respectively). 

An individual’s preference for evening or morning activity correlated strongly with their test scores. In particular, night owls consistently performed better on cognitive tests than early birds. 

“While understanding and working with your natural sleep tendencies is essential, it’s equally important to remember to get just enough sleep, not too long or too short,” Dr. West noted. “This is crucial for keeping your brain healthy and functioning at its best.”

Contrary to some previous findings, the study did not find a significant relationship between sleep, sleepiness/insomnia, and cognitive performance. This may be because specific aspects of insomnia, such as severity and chronicity, as well as comorbid conditions need to be considered, the investigators wrote. 

They added that age and diabetes consistently emerged as negative predictors of cognitive functioning across both cohorts, in line with previous research. 

Limitations of the study include the cross-sectional design, which limits causal inferences; the possibility of residual confounding; and reliance on self-reported sleep data.

Also, the study did not adjust for educational attainment, a factor potentially influential on cognitive performance and sleep patterns, because of incomplete data. The study also did not factor in depression and social isolation, which have been shown to increase the risk for cognitive decline.
 

No Real-World Implications

Several outside experts offered their perspective on the study in a statement from the UK nonprofit Science Media Centre. 

The study provides “interesting insights” into the difference in memory and thinking in people who identify themselves as a “morning” or “evening” person, Jacqui Hanley, PhD, with Alzheimer’s Research UK, said in the statement. 

However, without a detailed picture of what is going on in the brain, it’s not clear whether being a morning or evening person affects memory and thinking or whether a decline in cognition is causing changes to sleeping patterns, Dr. Hanley added. 

Roi Cohen Kadosh, PhD, CPsychol, professor of cognitive neuroscience, University of Surrey, Guildford, England, cautioned that there are “multiple potential reasons” for these associations. 

“Therefore, there are no implications in my view for the real world. I fear that the general public will not be able to understand that and will change their sleep pattern, while this study does not give any evidence that this will lead to any benefit,” Dr. Cohen Kadosh said. 

Jessica Chelekis, PhD, MBA, a sleep expert from Brunel University London, Uxbridge, England, said that the “main takeaway should be that the cultural belief that early risers are more productive than ‘night owls’ does not hold up to scientific scrutiny.” 

“While everyone should aim to get good-quality sleep each night, we should also try to be aware of what time of day we are at our (cognitive) best and work in ways that suit us. Night owls, in particular, should not be shamed into fitting a stereotype that favors an ‘early to bed, early to rise’ practice,” Dr. Chelekis said. 

Funding for the study was provided by the Korea Institute of Oriental Medicine in collaboration with Imperial College London. Dr. Hanley, Dr. Cohen Kadosh, and Dr. Chelekis have no relevant disclosures.

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

Individuals who are more active in the evening performed better on cognitive tests than did those who are typically more active in the morning hours, new research suggests. 

“Rather than just being personal preferences, these chronotypes could impact our cognitive function,” said study investigator, Raha West, MBChB, with Imperial College London, London, England, in a statement.

But the researchers also urged caution when interpreting the findings.

“It’s important to note that this doesn’t mean all morning people have worse cognitive performance. The findings reflect an overall trend where the majority might lean toward better cognition in the evening types,” Dr. West added. 

In addition, across the board, getting the recommended 7-9 hours of nightly sleep was best for cognitive function, and sleeping for less than 7 or more than 9 hours had detrimental effects on brain function regardless of whether an individual was a night owl or lark. 

The study was published online in BMJ Public Health. 
 

A UK Biobank Cohort Study 

The findings are based on a cross-sectional analysis of 26,820 adults aged 53-86 years from the UK Biobank database, who were categorized into two cohorts. 

Cohort 1 had 10,067 participants (56% women) who completed four cognitive tests measuring fluid intelligence/reasoning, pairs matching, reaction time, and prospective memory. Cohort 2 had 16,753 participants (56% women) who completed two cognitive assessments (pairs matching and reaction time).

Participants self-reported sleep duration, chronotype, and quality. Cognitive test scores were evaluated against sleep parameters and health and lifestyle factors including sex, age, vascular and cardiac conditions, diabetes,alcohol use, smoking habits, and body mass index.

The results revealed a positive association between normal sleep duration (7-9 hours) and cognitive scores in Cohort 1 (beta, 0.0567), while extended sleep duration negatively impacted scores across in Cohort 1 and 2 (beta, –0.188 and beta, –0.2619, respectively). 

An individual’s preference for evening or morning activity correlated strongly with their test scores. In particular, night owls consistently performed better on cognitive tests than early birds. 

“While understanding and working with your natural sleep tendencies is essential, it’s equally important to remember to get just enough sleep, not too long or too short,” Dr. West noted. “This is crucial for keeping your brain healthy and functioning at its best.”

Contrary to some previous findings, the study did not find a significant relationship between sleep, sleepiness/insomnia, and cognitive performance. This may be because specific aspects of insomnia, such as severity and chronicity, as well as comorbid conditions need to be considered, the investigators wrote. 

They added that age and diabetes consistently emerged as negative predictors of cognitive functioning across both cohorts, in line with previous research. 

Limitations of the study include the cross-sectional design, which limits causal inferences; the possibility of residual confounding; and reliance on self-reported sleep data.

Also, the study did not adjust for educational attainment, a factor potentially influential on cognitive performance and sleep patterns, because of incomplete data. The study also did not factor in depression and social isolation, which have been shown to increase the risk for cognitive decline.
 

No Real-World Implications

Several outside experts offered their perspective on the study in a statement from the UK nonprofit Science Media Centre. 

The study provides “interesting insights” into the difference in memory and thinking in people who identify themselves as a “morning” or “evening” person, Jacqui Hanley, PhD, with Alzheimer’s Research UK, said in the statement. 

However, without a detailed picture of what is going on in the brain, it’s not clear whether being a morning or evening person affects memory and thinking or whether a decline in cognition is causing changes to sleeping patterns, Dr. Hanley added. 

Roi Cohen Kadosh, PhD, CPsychol, professor of cognitive neuroscience, University of Surrey, Guildford, England, cautioned that there are “multiple potential reasons” for these associations. 

“Therefore, there are no implications in my view for the real world. I fear that the general public will not be able to understand that and will change their sleep pattern, while this study does not give any evidence that this will lead to any benefit,” Dr. Cohen Kadosh said. 

Jessica Chelekis, PhD, MBA, a sleep expert from Brunel University London, Uxbridge, England, said that the “main takeaway should be that the cultural belief that early risers are more productive than ‘night owls’ does not hold up to scientific scrutiny.” 

“While everyone should aim to get good-quality sleep each night, we should also try to be aware of what time of day we are at our (cognitive) best and work in ways that suit us. Night owls, in particular, should not be shamed into fitting a stereotype that favors an ‘early to bed, early to rise’ practice,” Dr. Chelekis said. 

Funding for the study was provided by the Korea Institute of Oriental Medicine in collaboration with Imperial College London. Dr. Hanley, Dr. Cohen Kadosh, and Dr. Chelekis have no relevant disclosures.

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

Every doctor encounters patients who complain of symptoms without identifiable physical causes. According to a recent review in The Lancet, one third of all symptoms lack somatic explanations.

How can these patients be helped, and what crucial question should always be asked? This news organization discussed this topic with Professor Peter Henningsen, a coauthor of the review, at the German Congress for Psychosomatic Medicine and Psychotherapy. Dr. Henningsen is the director of the Clinic and Polyclinic for Psychosomatic Medicine and Psychotherapy at the University Hospital Rechts der Isar of the Technical University of Munich, Munich, Germany.
 

One Common Factor

Patients often experience a wide range of symptoms that appear without any obvious cause. These symptoms include persistent pain, dizziness, cardiovascular complaints, digestive disorders, gait disturbances, exhaustion, and fatigue. There’s often a notable gap between perceived distress and the impairment of a patient’s physical functions and examination findings.

In recent years, a descriptive umbrella term has emerged for these health challenges: persistent physical symptoms. This term includes functional physical complaints lasting for months or longer without a clearly identifiable organic cause, such as chronic fatigue syndrome, irritable bowel syndrome, fibromyalgia, or multiple chemical sensitivity. It also encompasses persistent complaints in patients with an underlying condition.

According to the review, 70% of people with chronic kidney disease experience fatigue; 63% of patients with coronary artery disease have persistent pain in their arms, legs, or joints; and 31% of patients with ulcerative colitis in remission report persistent gastrointestinal symptoms.

In International Classification of Diseases (ICD), 10th Revision, the term “somatoform disorders” is used when no organic causes are identifiable. However, ICD-11 has replaced this term with the category of “somatic symptom disorders.”

“For this diagnosis, it is no longer necessary to rule out physical causes entirely,” explained Dr. Henningsen. “Instead, the focus is on psychologic and behavioral abnormalities, anxiety, increased attention to symptoms, frequent doctor consultations, and the conviction of having a serious physical illness.”

This new diagnostic approach is considered sensible because it focuses on the patient’s experience of their illness. However, it has also been criticized for potentially “psychiatrizing” patients with genuine physical ailments.
 

The ‘Prediction Machine’

Understanding the new model is crucial. “It’s about grasping what is happening with a person who persistently complains of physical symptoms,” said Dr. Henningsen.

Previously, the bottom-up model of perception, which started from the pain stimulus, was widely accepted. It was believed that pain could secondarily cause psychological symptoms. However, the role of the brain has now come to the forefront. Terms like “predictive processing” or “predictive coding” are key: The brain constantly makes predictions about the most likely interpretation of sensory impressions.

These predictions incorporate expectations, beliefs, and past experiences with symptoms, which unconsciously influence these predictions. Therefore, expectations play a role in perception for all patients regardless of whether they have an organic precondition. This phenomenon can result in patients experiencing symptoms despite minimal or no sensory input.

“Perception is always biopsychosocial,” Dr. Henningsen emphasized, and diseases are not strictly physical or psychological but rather a combination of both. The proportions of these components vary, especially in chronic illnesses, where expectations play a more significant role in pain perception than they do in fresh injuries. Because predictive processing is a general mechanism of perception, it can be involved in various diseases.

The good news is that many factors contributing to persistent physical symptoms, such as increased attention to symptoms, dysfunctional expectations, or avoidance behavior, can be positively influenced.
 

What Can Doctors Do?

Dr. Henningsen recommended that doctors treating patients with functional physical complaints focus on the following three key aspects:

• Consider the subjective experience. “The psychologic aspect is relevant in every illness. Always ask, ‘How are you coping with your symptoms? What are your expectations for the future?’ ” Dr. Henningsen explained. For instance, if a patient has been experiencing back pain for weeks, feels it’s getting worse, and believes that they will no longer be able to work, this is a significant prognostic factor. Such a patient is less likely to return to work compared with someone who is confident in their recovery.
• Communicate mindfully. The way doctors communicate with patients about their symptoms is crucial. Dr. Henningsen illustrated this with a patient with tension headaches. “An MRI might show a slight increase in signal intensity. If the doctor casually says, ‘It could be MS, but I don’t think so,’ the patient will fixate on the mention of MS.”
• Treat body and mind. There is no either-or in therapy. For example, medications can help with irritable bowel syndrome but so can psychotherapeutic measures — without implying that the condition is purely psychological. Exercise therapy can demonstrate that pain does not increase with movement, thus positively changing a patient’s expectations and reducing symptoms.

A Doctor’s ‘Toolbox’

A Norwegian study published last year in eClinicalMedicine, a Lancet journal, demonstrated the effectiveness of such an approach for treating medically unexplained physical symptoms (MUPS) in general practice.

In this study, 541 patients with MUPS participated in a two-arm, cluster-randomized trial. In total, 10 clusters of 103 general practitioners were each divided into two groups. One group used the Individual Challenge Inventory Tool (ICIT) for 11 weeks, while the other received usual treatment.

The ICIT, a structured communication tool based on cognitive-behavioral therapy, was developed by the study’s lead author, a general practitioner. Participating general practitioners were trained in using the ICIT.

Patients in the study received two or more sessions with their general practitioners. Outcomes were assessed individually, and the primary outcome was patient-reported change in function, symptoms, and quality of life as measured by the Patient Global Impression of Change. Secondary end points included work capability.

In the intervention group, 76% (n = 223) experienced significant overall improvement in function, symptoms, and the quality of life compared with 38% (n = 236) in the control group receiving usual care (mean difference, −0.8; 95% confidence interval [CI], −1.0 to −0.6; P < .0001).

After 11 weeks, sick leave decreased by 27 percentage points in the intervention group (from 52.0 to 25.2), while it dropped by only four percentage points in the usual care group (from 49.7 to 45.7).

“ICIT in primary care led to significant improvements in treatment outcomes and a reduction in sickness absence for patients with MUPS,” the authors concluded.
 

Guideline Under Revision

Medications alone often fail to adequately alleviate persistent physical symptoms. The S3 guideline “Functional Physical Complaints” lists various alternative therapies such as yoga and psychological interventions.

Dr. Henningsen and his team are revising this guideline, and publication is expected later this year. While no major changes in therapy recommendations are anticipated, the focus will be on making the guideline more user-friendly.

“It is crucial for doctors to consider psychosocial factors,” said Dr. Henningsen. “ ‘Both-and’ instead of ‘either-or’ is our motto.”

Dr. Henningsen declared no conflicts of interest.

This story was translated from the Medscape German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article appeared on Medscape.com.

Every doctor encounters patients who complain of symptoms without identifiable physical causes. According to a recent review in The Lancet, one third of all symptoms lack somatic explanations.

How can these patients be helped, and what crucial question should always be asked? This news organization discussed this topic with Professor Peter Henningsen, a coauthor of the review, at the German Congress for Psychosomatic Medicine and Psychotherapy. Dr. Henningsen is the director of the Clinic and Polyclinic for Psychosomatic Medicine and Psychotherapy at the University Hospital Rechts der Isar of the Technical University of Munich, Munich, Germany.
 

One Common Factor

Patients often experience a wide range of symptoms that appear without any obvious cause. These symptoms include persistent pain, dizziness, cardiovascular complaints, digestive disorders, gait disturbances, exhaustion, and fatigue. There’s often a notable gap between perceived distress and the impairment of a patient’s physical functions and examination findings.

In recent years, a descriptive umbrella term has emerged for these health challenges: persistent physical symptoms. This term includes functional physical complaints lasting for months or longer without a clearly identifiable organic cause, such as chronic fatigue syndrome, irritable bowel syndrome, fibromyalgia, or multiple chemical sensitivity. It also encompasses persistent complaints in patients with an underlying condition.

According to the review, 70% of people with chronic kidney disease experience fatigue; 63% of patients with coronary artery disease have persistent pain in their arms, legs, or joints; and 31% of patients with ulcerative colitis in remission report persistent gastrointestinal symptoms.

In International Classification of Diseases (ICD), 10th Revision, the term “somatoform disorders” is used when no organic causes are identifiable. However, ICD-11 has replaced this term with the category of “somatic symptom disorders.”

“For this diagnosis, it is no longer necessary to rule out physical causes entirely,” explained Dr. Henningsen. “Instead, the focus is on psychologic and behavioral abnormalities, anxiety, increased attention to symptoms, frequent doctor consultations, and the conviction of having a serious physical illness.”

This new diagnostic approach is considered sensible because it focuses on the patient’s experience of their illness. However, it has also been criticized for potentially “psychiatrizing” patients with genuine physical ailments.
 

The ‘Prediction Machine’

Understanding the new model is crucial. “It’s about grasping what is happening with a person who persistently complains of physical symptoms,” said Dr. Henningsen.

Previously, the bottom-up model of perception, which started from the pain stimulus, was widely accepted. It was believed that pain could secondarily cause psychological symptoms. However, the role of the brain has now come to the forefront. Terms like “predictive processing” or “predictive coding” are key: The brain constantly makes predictions about the most likely interpretation of sensory impressions.

These predictions incorporate expectations, beliefs, and past experiences with symptoms, which unconsciously influence these predictions. Therefore, expectations play a role in perception for all patients regardless of whether they have an organic precondition. This phenomenon can result in patients experiencing symptoms despite minimal or no sensory input.

“Perception is always biopsychosocial,” Dr. Henningsen emphasized, and diseases are not strictly physical or psychological but rather a combination of both. The proportions of these components vary, especially in chronic illnesses, where expectations play a more significant role in pain perception than they do in fresh injuries. Because predictive processing is a general mechanism of perception, it can be involved in various diseases.

The good news is that many factors contributing to persistent physical symptoms, such as increased attention to symptoms, dysfunctional expectations, or avoidance behavior, can be positively influenced.
 

What Can Doctors Do?

Dr. Henningsen recommended that doctors treating patients with functional physical complaints focus on the following three key aspects:

• Consider the subjective experience. “The psychologic aspect is relevant in every illness. Always ask, ‘How are you coping with your symptoms? What are your expectations for the future?’ ” Dr. Henningsen explained. For instance, if a patient has been experiencing back pain for weeks, feels it’s getting worse, and believes that they will no longer be able to work, this is a significant prognostic factor. Such a patient is less likely to return to work compared with someone who is confident in their recovery.
• Communicate mindfully. The way doctors communicate with patients about their symptoms is crucial. Dr. Henningsen illustrated this with a patient with tension headaches. “An MRI might show a slight increase in signal intensity. If the doctor casually says, ‘It could be MS, but I don’t think so,’ the patient will fixate on the mention of MS.”
• Treat body and mind. There is no either-or in therapy. For example, medications can help with irritable bowel syndrome but so can psychotherapeutic measures — without implying that the condition is purely psychological. Exercise therapy can demonstrate that pain does not increase with movement, thus positively changing a patient’s expectations and reducing symptoms.

A Doctor’s ‘Toolbox’

A Norwegian study published last year in eClinicalMedicine, a Lancet journal, demonstrated the effectiveness of such an approach for treating medically unexplained physical symptoms (MUPS) in general practice.

In this study, 541 patients with MUPS participated in a two-arm, cluster-randomized trial. In total, 10 clusters of 103 general practitioners were each divided into two groups. One group used the Individual Challenge Inventory Tool (ICIT) for 11 weeks, while the other received usual treatment.

The ICIT, a structured communication tool based on cognitive-behavioral therapy, was developed by the study’s lead author, a general practitioner. Participating general practitioners were trained in using the ICIT.

Patients in the study received two or more sessions with their general practitioners. Outcomes were assessed individually, and the primary outcome was patient-reported change in function, symptoms, and quality of life as measured by the Patient Global Impression of Change. Secondary end points included work capability.

In the intervention group, 76% (n = 223) experienced significant overall improvement in function, symptoms, and the quality of life compared with 38% (n = 236) in the control group receiving usual care (mean difference, −0.8; 95% confidence interval [CI], −1.0 to −0.6; P < .0001).

After 11 weeks, sick leave decreased by 27 percentage points in the intervention group (from 52.0 to 25.2), while it dropped by only four percentage points in the usual care group (from 49.7 to 45.7).

“ICIT in primary care led to significant improvements in treatment outcomes and a reduction in sickness absence for patients with MUPS,” the authors concluded.
 

Guideline Under Revision

Medications alone often fail to adequately alleviate persistent physical symptoms. The S3 guideline “Functional Physical Complaints” lists various alternative therapies such as yoga and psychological interventions.

Dr. Henningsen and his team are revising this guideline, and publication is expected later this year. While no major changes in therapy recommendations are anticipated, the focus will be on making the guideline more user-friendly.

“It is crucial for doctors to consider psychosocial factors,” said Dr. Henningsen. “ ‘Both-and’ instead of ‘either-or’ is our motto.”

Dr. Henningsen declared no conflicts of interest.

This story was translated from the Medscape German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article appeared on Medscape.com.

Every doctor encounters patients who complain of symptoms without identifiable physical causes. According to a recent review in The Lancet, one third of all symptoms lack somatic explanations.

How can these patients be helped, and what crucial question should always be asked? This news organization discussed this topic with Professor Peter Henningsen, a coauthor of the review, at the German Congress for Psychosomatic Medicine and Psychotherapy. Dr. Henningsen is the director of the Clinic and Polyclinic for Psychosomatic Medicine and Psychotherapy at the University Hospital Rechts der Isar of the Technical University of Munich, Munich, Germany.
 

One Common Factor

Patients often experience a wide range of symptoms that appear without any obvious cause. These symptoms include persistent pain, dizziness, cardiovascular complaints, digestive disorders, gait disturbances, exhaustion, and fatigue. There’s often a notable gap between perceived distress and the impairment of a patient’s physical functions and examination findings.

In recent years, a descriptive umbrella term has emerged for these health challenges: persistent physical symptoms. This term includes functional physical complaints lasting for months or longer without a clearly identifiable organic cause, such as chronic fatigue syndrome, irritable bowel syndrome, fibromyalgia, or multiple chemical sensitivity. It also encompasses persistent complaints in patients with an underlying condition.

According to the review, 70% of people with chronic kidney disease experience fatigue; 63% of patients with coronary artery disease have persistent pain in their arms, legs, or joints; and 31% of patients with ulcerative colitis in remission report persistent gastrointestinal symptoms.

In International Classification of Diseases (ICD), 10th Revision, the term “somatoform disorders” is used when no organic causes are identifiable. However, ICD-11 has replaced this term with the category of “somatic symptom disorders.”

“For this diagnosis, it is no longer necessary to rule out physical causes entirely,” explained Dr. Henningsen. “Instead, the focus is on psychologic and behavioral abnormalities, anxiety, increased attention to symptoms, frequent doctor consultations, and the conviction of having a serious physical illness.”

This new diagnostic approach is considered sensible because it focuses on the patient’s experience of their illness. However, it has also been criticized for potentially “psychiatrizing” patients with genuine physical ailments.
 

The ‘Prediction Machine’

Understanding the new model is crucial. “It’s about grasping what is happening with a person who persistently complains of physical symptoms,” said Dr. Henningsen.

Previously, the bottom-up model of perception, which started from the pain stimulus, was widely accepted. It was believed that pain could secondarily cause psychological symptoms. However, the role of the brain has now come to the forefront. Terms like “predictive processing” or “predictive coding” are key: The brain constantly makes predictions about the most likely interpretation of sensory impressions.

These predictions incorporate expectations, beliefs, and past experiences with symptoms, which unconsciously influence these predictions. Therefore, expectations play a role in perception for all patients regardless of whether they have an organic precondition. This phenomenon can result in patients experiencing symptoms despite minimal or no sensory input.

“Perception is always biopsychosocial,” Dr. Henningsen emphasized, and diseases are not strictly physical or psychological but rather a combination of both. The proportions of these components vary, especially in chronic illnesses, where expectations play a more significant role in pain perception than they do in fresh injuries. Because predictive processing is a general mechanism of perception, it can be involved in various diseases.

The good news is that many factors contributing to persistent physical symptoms, such as increased attention to symptoms, dysfunctional expectations, or avoidance behavior, can be positively influenced.
 

What Can Doctors Do?

Dr. Henningsen recommended that doctors treating patients with functional physical complaints focus on the following three key aspects:

• Consider the subjective experience. “The psychologic aspect is relevant in every illness. Always ask, ‘How are you coping with your symptoms? What are your expectations for the future?’ ” Dr. Henningsen explained. For instance, if a patient has been experiencing back pain for weeks, feels it’s getting worse, and believes that they will no longer be able to work, this is a significant prognostic factor. Such a patient is less likely to return to work compared with someone who is confident in their recovery.
• Communicate mindfully. The way doctors communicate with patients about their symptoms is crucial. Dr. Henningsen illustrated this with a patient with tension headaches. “An MRI might show a slight increase in signal intensity. If the doctor casually says, ‘It could be MS, but I don’t think so,’ the patient will fixate on the mention of MS.”
• Treat body and mind. There is no either-or in therapy. For example, medications can help with irritable bowel syndrome but so can psychotherapeutic measures — without implying that the condition is purely psychological. Exercise therapy can demonstrate that pain does not increase with movement, thus positively changing a patient’s expectations and reducing symptoms.

A Doctor’s ‘Toolbox’

A Norwegian study published last year in eClinicalMedicine, a Lancet journal, demonstrated the effectiveness of such an approach for treating medically unexplained physical symptoms (MUPS) in general practice.

In this study, 541 patients with MUPS participated in a two-arm, cluster-randomized trial. In total, 10 clusters of 103 general practitioners were each divided into two groups. One group used the Individual Challenge Inventory Tool (ICIT) for 11 weeks, while the other received usual treatment.

The ICIT, a structured communication tool based on cognitive-behavioral therapy, was developed by the study’s lead author, a general practitioner. Participating general practitioners were trained in using the ICIT.

Patients in the study received two or more sessions with their general practitioners. Outcomes were assessed individually, and the primary outcome was patient-reported change in function, symptoms, and quality of life as measured by the Patient Global Impression of Change. Secondary end points included work capability.

In the intervention group, 76% (n = 223) experienced significant overall improvement in function, symptoms, and the quality of life compared with 38% (n = 236) in the control group receiving usual care (mean difference, −0.8; 95% confidence interval [CI], −1.0 to −0.6; P < .0001).

After 11 weeks, sick leave decreased by 27 percentage points in the intervention group (from 52.0 to 25.2), while it dropped by only four percentage points in the usual care group (from 49.7 to 45.7).

“ICIT in primary care led to significant improvements in treatment outcomes and a reduction in sickness absence for patients with MUPS,” the authors concluded.
 

Guideline Under Revision

Medications alone often fail to adequately alleviate persistent physical symptoms. The S3 guideline “Functional Physical Complaints” lists various alternative therapies such as yoga and psychological interventions.

Dr. Henningsen and his team are revising this guideline, and publication is expected later this year. While no major changes in therapy recommendations are anticipated, the focus will be on making the guideline more user-friendly.

“It is crucial for doctors to consider psychosocial factors,” said Dr. Henningsen. “ ‘Both-and’ instead of ‘either-or’ is our motto.”

Dr. Henningsen declared no conflicts of interest.

This story was translated from the Medscape German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article appeared on Medscape.com.

Agitation is a neuropsychiatric symptom in patients with Alzheimer’s disease (AD), the most common form of dementia. The prevalence of this symptom is about 40%-65%, with the higher end of the range applying to patients who have moderate to severe dementia. Agitation often begins early in the course of the disease and is persistent, which contributes to increased healthcare costs and significantly increases both caregiver burden and patient distress. The DICE approach is a collaborative process for managing behavioral symptoms in dementia, wherein the caregiver describes the behaviors, the provider investigates the etiology, the provider and caregiver create a treatment plan, and the provider evaluates the outcome of the interventions. We use this widely adopted approach as the framework for discussing recent advances in the management of agitation.

Here are five things to know about managing agitation in AD.
 

1. There is a new operational definition for agitation in dementia.

Agitation in dementia is a syndrome that encompasses specific behaviors across all dementia types. The 2023 operational definition of agitation in dementia by the International Psychogeriatric Association (IPA) includes three domains: excessive motor activity (including pacing, rocking, restlessness, and performing repetitious mannerisms), verbal aggression (including using profanity, screaming, and shouting), and physical aggression (including interpersonal aggression and mishandling or destruction of property). These behaviors must be persistent or recurrent for at least 2 weeks or represent a dramatic change from the person’s baseline behavior, must be associated with excessive distress or disability beyond what is caused by the cognitive impairment itself, and result in significant impairment in at least one of the three specified functional domains. Behavioral symptoms in dementia frequently co-occur, which affects treatment and prognosis. For instance, the risk for stroke associated with antipsychotic treatments appears to be higher in dementia-related psychosis without agitation than in agitation alone or in psychosis with agitation. Therefore, the use of a rating scale such as the Neuropsychiatric Inventory–Questionnaire (NPI-Q), which takes 5 minutes or less to administer, is recommended to identify and track behavioral symptoms and caregiver distress.

2. The etiology of agitation in dementia may be multifactorial.

It is important in every case to identify all underlying etiologies so that presumed causal and/or exacerbating factors are not inadvertently missed. Agitation may be a means of communicating distress owing to unmet needs or a patient-environment mismatch (function-focused approach) or may be a direct consequence of the dementia itself (behavioral-symptom approach). These approaches are not mutually exclusive. A patient can present with agitation as a direct consequence of dementia and inadequately treated pain concurrently. 

The new IPA definition specifies several exclusion criteria for agitation in dementia, including underlying medical conditions, delirium, substance use, and suboptimal care conditions. It is especially crucial to accurately identify delirium because dementia is an independent risk factor for delirium, which in turn may accelerate the progression of cognitive and functional decline. Even subsyndromal delirium in older adults leads to a higher 3-year mortality rate that is comparable to that seen in delirium. Older adults with acute-onset agitation in the context of dementia should undergo a comprehensive assessment for delirium, as agitation may be the only indication of a serious underlying medical condition. 
 

3. Nonpharmacologic interventions should be used whenever possible. 

The wider adoption of nonpharmacologic interventions in clinical practice has been greatly limited by the heterogeneity in study protocols, including in selection of participants, in the types of dementias included, and in defining and applying the intervention strategies. Nevertheless, there is general consensus that individualized behavioral strategies that build on the patients’ interests and preserved abilities are more effective, at least in the short term. Patients best suited for these interventions are those with less cognitive decline, better communication skills, less impairment in activities of daily living, and higher responsiveness. A systematic review of systematic reviews found music therapy to be the most effective intervention for reducing agitation and aggression in dementia, along with behavioral management techniques when supervised by healthcare professionals. On the other hand, physical restraints are best avoided, as their use in hospitalized patients has been associated with longer stays, higher costs, lower odds of being discharged to home, and in long-term care patients with longer stays, with increased risk for medical complications and functional decline. 

4. Antidepressants are not all equally safe or efficacious in managing agitation.

In a network meta-analysis that looked at the effects of several antidepressants on agitation in dementia, citalopram had just under 95% probability of efficacy and was the only antidepressant that was significantly more efficacious than placebo. In the multicenter CitAD trial, citalopram was efficacious and well tolerated for the treatment of agitation in AD, but the mean dose of citalopram used, 30 mg/d, was higher than the maximum dose of 20 mg/d recommended by the US Food and Drug Administration (FDA) in those aged 60 years or above. The optimal candidates for citalopram were those under the age of 85 with mild to moderate AD and mild to moderate nonpsychotic agitation, and it took up to 9 weeks for it to be fully effective. Due to the risk for dose-dependent QTc prolongation with citalopram, a baseline ECG must be done, and a second ECG is recommended if a clinical decision is made to exceed the recommended maximum daily dose. In the CitAD trial, 66% of patients in the citalopram arm received cholinesterase inhibitors concurrently while 44% received memantine, so these symptomatic treatments for AD should not be stopped solely for initiating a citalopram trial. 

The antiagitation effect of citalopram may well be a class effect of all selective serotonin reuptake inhibitors (SSRIs), given that there is also evidence favoring the use of sertraline and escitalopram. The S-CitAD trial, the first large, randomized controlled study of escitalopram for the treatment of agitation in dementia, is expected to announce its top-line results sometime this year. However, not all antidepressant classes appear to be equally efficacious or safe. In the large, 12-week randomized placebo-controlled trial SYMBAD, mirtazapine was not only ineffective in treating nonpsychotic agitation in AD but was also associated with a higher mortality rate that just missed statistical significance. Trazodone is also often used for treating agitation, but there is insufficient evidence regarding efficacy and a high probability of adverse effects, even at low doses.
 

5. Antipsychotics may be effective drugs for treating severe dementia-related agitation.

The CATIE-AD study found that the small beneficial effects of antipsychotics for treating agitation and psychosis in AD were offset by their adverse effects and high discontinuation rates, and the FDA-imposed boxed warnings in 2005 and 2008 cautioned against the use of both first- and second-generation antipsychotics to manage dementia-related psychosis owing to an increased risk for death. Subsequently, the quest for safer and more effective alternatives culminated in the FDA approval of brexpiprazole in 2023 for the treatment of agitation in AD, but the black box warning was left in place. Three randomized controlled trials found brexpiprazole to be relatively safe, with statistically significant improvement in agitation. It was especially efficacious for severe agitation, but there is controversy about whether such improvement is clinically meaningful and whether brexpiprazole is truly superior to other antipsychotics for treating dementia-related agitation. As in the previously mentioned citalopram studies, most patients in the brexpiprazole studies received the drug as an add-on to memantine and/or a cholinesterase inhibitor, and it was proven effective over a period of up to 12 weeks across the three trials. Regarding other antipsychotics, aripiprazole and risperidone have been shown to be effective in treating agitation in patients with mixed dementia, but risperidone has also been associated with the highest risk for strokes (about 80% probability). Unfortunately, an unintended consequence of the boxed warnings on antipsychotics has been an increase in off-label substitution of psychotropic drugs with unproven efficacy and a questionable safety profile, such as valproic acid preparations, that have been linked to an increased short-term risk for accelerated brain volume loss and rapid cognitive decline, as well as a higher risk for mortality.

Lisa M. Wise, assistant professor, Psychiatry, at Oregon Health & Science University, and staff psychiatrist, Department of Psychiatry, Portland VA Medical Center, Portland, Oregon, and Vimal M. Aga, adjunct assistant professor, Department of Neurology, Oregon Health & Science University, and geriatric psychiatrist, Layton Aging and Alzheimer’s Disease Center, Portland, Oregon, have disclosed no relevant financial relationships.

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

Agitation is a neuropsychiatric symptom in patients with Alzheimer’s disease (AD), the most common form of dementia. The prevalence of this symptom is about 40%-65%, with the higher end of the range applying to patients who have moderate to severe dementia. Agitation often begins early in the course of the disease and is persistent, which contributes to increased healthcare costs and significantly increases both caregiver burden and patient distress. The DICE approach is a collaborative process for managing behavioral symptoms in dementia, wherein the caregiver describes the behaviors, the provider investigates the etiology, the provider and caregiver create a treatment plan, and the provider evaluates the outcome of the interventions. We use this widely adopted approach as the framework for discussing recent advances in the management of agitation.

Here are five things to know about managing agitation in AD.
 

1. There is a new operational definition for agitation in dementia.

Agitation in dementia is a syndrome that encompasses specific behaviors across all dementia types. The 2023 operational definition of agitation in dementia by the International Psychogeriatric Association (IPA) includes three domains: excessive motor activity (including pacing, rocking, restlessness, and performing repetitious mannerisms), verbal aggression (including using profanity, screaming, and shouting), and physical aggression (including interpersonal aggression and mishandling or destruction of property). These behaviors must be persistent or recurrent for at least 2 weeks or represent a dramatic change from the person’s baseline behavior, must be associated with excessive distress or disability beyond what is caused by the cognitive impairment itself, and result in significant impairment in at least one of the three specified functional domains. Behavioral symptoms in dementia frequently co-occur, which affects treatment and prognosis. For instance, the risk for stroke associated with antipsychotic treatments appears to be higher in dementia-related psychosis without agitation than in agitation alone or in psychosis with agitation. Therefore, the use of a rating scale such as the Neuropsychiatric Inventory–Questionnaire (NPI-Q), which takes 5 minutes or less to administer, is recommended to identify and track behavioral symptoms and caregiver distress.

2. The etiology of agitation in dementia may be multifactorial.

It is important in every case to identify all underlying etiologies so that presumed causal and/or exacerbating factors are not inadvertently missed. Agitation may be a means of communicating distress owing to unmet needs or a patient-environment mismatch (function-focused approach) or may be a direct consequence of the dementia itself (behavioral-symptom approach). These approaches are not mutually exclusive. A patient can present with agitation as a direct consequence of dementia and inadequately treated pain concurrently. 

The new IPA definition specifies several exclusion criteria for agitation in dementia, including underlying medical conditions, delirium, substance use, and suboptimal care conditions. It is especially crucial to accurately identify delirium because dementia is an independent risk factor for delirium, which in turn may accelerate the progression of cognitive and functional decline. Even subsyndromal delirium in older adults leads to a higher 3-year mortality rate that is comparable to that seen in delirium. Older adults with acute-onset agitation in the context of dementia should undergo a comprehensive assessment for delirium, as agitation may be the only indication of a serious underlying medical condition. 
 

3. Nonpharmacologic interventions should be used whenever possible. 

The wider adoption of nonpharmacologic interventions in clinical practice has been greatly limited by the heterogeneity in study protocols, including in selection of participants, in the types of dementias included, and in defining and applying the intervention strategies. Nevertheless, there is general consensus that individualized behavioral strategies that build on the patients’ interests and preserved abilities are more effective, at least in the short term. Patients best suited for these interventions are those with less cognitive decline, better communication skills, less impairment in activities of daily living, and higher responsiveness. A systematic review of systematic reviews found music therapy to be the most effective intervention for reducing agitation and aggression in dementia, along with behavioral management techniques when supervised by healthcare professionals. On the other hand, physical restraints are best avoided, as their use in hospitalized patients has been associated with longer stays, higher costs, lower odds of being discharged to home, and in long-term care patients with longer stays, with increased risk for medical complications and functional decline. 

4. Antidepressants are not all equally safe or efficacious in managing agitation.

In a network meta-analysis that looked at the effects of several antidepressants on agitation in dementia, citalopram had just under 95% probability of efficacy and was the only antidepressant that was significantly more efficacious than placebo. In the multicenter CitAD trial, citalopram was efficacious and well tolerated for the treatment of agitation in AD, but the mean dose of citalopram used, 30 mg/d, was higher than the maximum dose of 20 mg/d recommended by the US Food and Drug Administration (FDA) in those aged 60 years or above. The optimal candidates for citalopram were those under the age of 85 with mild to moderate AD and mild to moderate nonpsychotic agitation, and it took up to 9 weeks for it to be fully effective. Due to the risk for dose-dependent QTc prolongation with citalopram, a baseline ECG must be done, and a second ECG is recommended if a clinical decision is made to exceed the recommended maximum daily dose. In the CitAD trial, 66% of patients in the citalopram arm received cholinesterase inhibitors concurrently while 44% received memantine, so these symptomatic treatments for AD should not be stopped solely for initiating a citalopram trial. 

The antiagitation effect of citalopram may well be a class effect of all selective serotonin reuptake inhibitors (SSRIs), given that there is also evidence favoring the use of sertraline and escitalopram. The S-CitAD trial, the first large, randomized controlled study of escitalopram for the treatment of agitation in dementia, is expected to announce its top-line results sometime this year. However, not all antidepressant classes appear to be equally efficacious or safe. In the large, 12-week randomized placebo-controlled trial SYMBAD, mirtazapine was not only ineffective in treating nonpsychotic agitation in AD but was also associated with a higher mortality rate that just missed statistical significance. Trazodone is also often used for treating agitation, but there is insufficient evidence regarding efficacy and a high probability of adverse effects, even at low doses.
 

5. Antipsychotics may be effective drugs for treating severe dementia-related agitation.

The CATIE-AD study found that the small beneficial effects of antipsychotics for treating agitation and psychosis in AD were offset by their adverse effects and high discontinuation rates, and the FDA-imposed boxed warnings in 2005 and 2008 cautioned against the use of both first- and second-generation antipsychotics to manage dementia-related psychosis owing to an increased risk for death. Subsequently, the quest for safer and more effective alternatives culminated in the FDA approval of brexpiprazole in 2023 for the treatment of agitation in AD, but the black box warning was left in place. Three randomized controlled trials found brexpiprazole to be relatively safe, with statistically significant improvement in agitation. It was especially efficacious for severe agitation, but there is controversy about whether such improvement is clinically meaningful and whether brexpiprazole is truly superior to other antipsychotics for treating dementia-related agitation. As in the previously mentioned citalopram studies, most patients in the brexpiprazole studies received the drug as an add-on to memantine and/or a cholinesterase inhibitor, and it was proven effective over a period of up to 12 weeks across the three trials. Regarding other antipsychotics, aripiprazole and risperidone have been shown to be effective in treating agitation in patients with mixed dementia, but risperidone has also been associated with the highest risk for strokes (about 80% probability). Unfortunately, an unintended consequence of the boxed warnings on antipsychotics has been an increase in off-label substitution of psychotropic drugs with unproven efficacy and a questionable safety profile, such as valproic acid preparations, that have been linked to an increased short-term risk for accelerated brain volume loss and rapid cognitive decline, as well as a higher risk for mortality.

Lisa M. Wise, assistant professor, Psychiatry, at Oregon Health & Science University, and staff psychiatrist, Department of Psychiatry, Portland VA Medical Center, Portland, Oregon, and Vimal M. Aga, adjunct assistant professor, Department of Neurology, Oregon Health & Science University, and geriatric psychiatrist, Layton Aging and Alzheimer’s Disease Center, Portland, Oregon, have disclosed no relevant financial relationships.

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

Agitation is a neuropsychiatric symptom in patients with Alzheimer’s disease (AD), the most common form of dementia. The prevalence of this symptom is about 40%-65%, with the higher end of the range applying to patients who have moderate to severe dementia. Agitation often begins early in the course of the disease and is persistent, which contributes to increased healthcare costs and significantly increases both caregiver burden and patient distress. The DICE approach is a collaborative process for managing behavioral symptoms in dementia, wherein the caregiver describes the behaviors, the provider investigates the etiology, the provider and caregiver create a treatment plan, and the provider evaluates the outcome of the interventions. We use this widely adopted approach as the framework for discussing recent advances in the management of agitation.

Here are five things to know about managing agitation in AD.
 

1. There is a new operational definition for agitation in dementia.

Agitation in dementia is a syndrome that encompasses specific behaviors across all dementia types. The 2023 operational definition of agitation in dementia by the International Psychogeriatric Association (IPA) includes three domains: excessive motor activity (including pacing, rocking, restlessness, and performing repetitious mannerisms), verbal aggression (including using profanity, screaming, and shouting), and physical aggression (including interpersonal aggression and mishandling or destruction of property). These behaviors must be persistent or recurrent for at least 2 weeks or represent a dramatic change from the person’s baseline behavior, must be associated with excessive distress or disability beyond what is caused by the cognitive impairment itself, and result in significant impairment in at least one of the three specified functional domains. Behavioral symptoms in dementia frequently co-occur, which affects treatment and prognosis. For instance, the risk for stroke associated with antipsychotic treatments appears to be higher in dementia-related psychosis without agitation than in agitation alone or in psychosis with agitation. Therefore, the use of a rating scale such as the Neuropsychiatric Inventory–Questionnaire (NPI-Q), which takes 5 minutes or less to administer, is recommended to identify and track behavioral symptoms and caregiver distress.

2. The etiology of agitation in dementia may be multifactorial.

It is important in every case to identify all underlying etiologies so that presumed causal and/or exacerbating factors are not inadvertently missed. Agitation may be a means of communicating distress owing to unmet needs or a patient-environment mismatch (function-focused approach) or may be a direct consequence of the dementia itself (behavioral-symptom approach). These approaches are not mutually exclusive. A patient can present with agitation as a direct consequence of dementia and inadequately treated pain concurrently. 

The new IPA definition specifies several exclusion criteria for agitation in dementia, including underlying medical conditions, delirium, substance use, and suboptimal care conditions. It is especially crucial to accurately identify delirium because dementia is an independent risk factor for delirium, which in turn may accelerate the progression of cognitive and functional decline. Even subsyndromal delirium in older adults leads to a higher 3-year mortality rate that is comparable to that seen in delirium. Older adults with acute-onset agitation in the context of dementia should undergo a comprehensive assessment for delirium, as agitation may be the only indication of a serious underlying medical condition. 
 

3. Nonpharmacologic interventions should be used whenever possible. 

The wider adoption of nonpharmacologic interventions in clinical practice has been greatly limited by the heterogeneity in study protocols, including in selection of participants, in the types of dementias included, and in defining and applying the intervention strategies. Nevertheless, there is general consensus that individualized behavioral strategies that build on the patients’ interests and preserved abilities are more effective, at least in the short term. Patients best suited for these interventions are those with less cognitive decline, better communication skills, less impairment in activities of daily living, and higher responsiveness. A systematic review of systematic reviews found music therapy to be the most effective intervention for reducing agitation and aggression in dementia, along with behavioral management techniques when supervised by healthcare professionals. On the other hand, physical restraints are best avoided, as their use in hospitalized patients has been associated with longer stays, higher costs, lower odds of being discharged to home, and in long-term care patients with longer stays, with increased risk for medical complications and functional decline. 

4. Antidepressants are not all equally safe or efficacious in managing agitation.

In a network meta-analysis that looked at the effects of several antidepressants on agitation in dementia, citalopram had just under 95% probability of efficacy and was the only antidepressant that was significantly more efficacious than placebo. In the multicenter CitAD trial, citalopram was efficacious and well tolerated for the treatment of agitation in AD, but the mean dose of citalopram used, 30 mg/d, was higher than the maximum dose of 20 mg/d recommended by the US Food and Drug Administration (FDA) in those aged 60 years or above. The optimal candidates for citalopram were those under the age of 85 with mild to moderate AD and mild to moderate nonpsychotic agitation, and it took up to 9 weeks for it to be fully effective. Due to the risk for dose-dependent QTc prolongation with citalopram, a baseline ECG must be done, and a second ECG is recommended if a clinical decision is made to exceed the recommended maximum daily dose. In the CitAD trial, 66% of patients in the citalopram arm received cholinesterase inhibitors concurrently while 44% received memantine, so these symptomatic treatments for AD should not be stopped solely for initiating a citalopram trial. 

The antiagitation effect of citalopram may well be a class effect of all selective serotonin reuptake inhibitors (SSRIs), given that there is also evidence favoring the use of sertraline and escitalopram. The S-CitAD trial, the first large, randomized controlled study of escitalopram for the treatment of agitation in dementia, is expected to announce its top-line results sometime this year. However, not all antidepressant classes appear to be equally efficacious or safe. In the large, 12-week randomized placebo-controlled trial SYMBAD, mirtazapine was not only ineffective in treating nonpsychotic agitation in AD but was also associated with a higher mortality rate that just missed statistical significance. Trazodone is also often used for treating agitation, but there is insufficient evidence regarding efficacy and a high probability of adverse effects, even at low doses.
 

5. Antipsychotics may be effective drugs for treating severe dementia-related agitation.

The CATIE-AD study found that the small beneficial effects of antipsychotics for treating agitation and psychosis in AD were offset by their adverse effects and high discontinuation rates, and the FDA-imposed boxed warnings in 2005 and 2008 cautioned against the use of both first- and second-generation antipsychotics to manage dementia-related psychosis owing to an increased risk for death. Subsequently, the quest for safer and more effective alternatives culminated in the FDA approval of brexpiprazole in 2023 for the treatment of agitation in AD, but the black box warning was left in place. Three randomized controlled trials found brexpiprazole to be relatively safe, with statistically significant improvement in agitation. It was especially efficacious for severe agitation, but there is controversy about whether such improvement is clinically meaningful and whether brexpiprazole is truly superior to other antipsychotics for treating dementia-related agitation. As in the previously mentioned citalopram studies, most patients in the brexpiprazole studies received the drug as an add-on to memantine and/or a cholinesterase inhibitor, and it was proven effective over a period of up to 12 weeks across the three trials. Regarding other antipsychotics, aripiprazole and risperidone have been shown to be effective in treating agitation in patients with mixed dementia, but risperidone has also been associated with the highest risk for strokes (about 80% probability). Unfortunately, an unintended consequence of the boxed warnings on antipsychotics has been an increase in off-label substitution of psychotropic drugs with unproven efficacy and a questionable safety profile, such as valproic acid preparations, that have been linked to an increased short-term risk for accelerated brain volume loss and rapid cognitive decline, as well as a higher risk for mortality.

Lisa M. Wise, assistant professor, Psychiatry, at Oregon Health & Science University, and staff psychiatrist, Department of Psychiatry, Portland VA Medical Center, Portland, Oregon, and Vimal M. Aga, adjunct assistant professor, Department of Neurology, Oregon Health & Science University, and geriatric psychiatrist, Layton Aging and Alzheimer’s Disease Center, Portland, Oregon, have disclosed no relevant financial relationships.

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

Bacterial and nonbacterial components of the gut microbiome and their function can accurately differentiate children with autism spectrum disorder (ASD) from neurotypical children, new research shows. 

The findings could form the basis for development of a noninvasive diagnostic test for ASD and also provide novel therapeutic targets, wrote investigators, led by Siew C. Ng, MBBS, PhD, with the Microbiota I-Center (MagIC), the Chinese University of Hong Kong.

Their study was published online in Nature Microbiology. 
 

Beyond Bacteria

The gut microbiome has been shown to play a central role in modulating the gut-brain axis, potentially influencing the development of ASD. 

However, most studies in ASD have focused on the bacterial component of the microbiome. Whether nonbacterial microorganisms (such as gut archaea, fungi, and viruses) or function of the gut microbiome are altered in ASD remains unclear. 

To investigate, the researchers performed metagenomic sequencing on fecal samples from 1627 boys and girls aged 1-13 years with and without ASD from five cohorts in China. 

After controlling for diet, medication, and comorbidity, they identified 14 archaea, 51 bacteria, 7 fungi, 18 viruses, 27 microbial genes, and 12 metabolic pathways that were altered in children with ASD. 

Machine-learning models using single-kingdom panels (archaea, bacteria, fungi, viruses) achieved area under the curve (AUC) values ranging from 0.68 to 0.87 in differentiating children with ASD from neurotypical control children. 

A model based on a panel of 31 multikingdom and functional markers achieved “high predictive value” for ASD, achieving an AUC of 0.91, with comparable performance among boys and girls. 

“The reproducible performance of the models across ages, sexes, and cohorts highlights their potential as promising diagnostic tools for ASD,” the investigators wrote. 

They also noted that the accuracy of the model was largely driven by the biosynthesis pathways of ubiquinol-7 and thiamine diphosphate, which were less abundant in children with ASD, and may serve as therapeutic targets. 
 

‘Exciting’ Possibilities 

“This study broadens our understanding by including fungi, archaea, and viruses, where previous studies have largely focused on the role of gut bacteria in autism,” Bhismadev Chakrabarti, PhD, research director of the Centre for Autism at the University of Reading, United Kingdom, said in a statement from the nonprofit UK Science Media Centre. 

“The results are broadly in line with previous studies that show reduced microbial diversity in autistic individuals. It also examines one of the largest samples seen in a study like this, which further strengthens the results,” Dr. Chakrabarti added. 

He said this research may provide “new ways of detecting autism, if microbial markers turn out to strengthen the ability of genetic and behavioral tests to detect autism. A future platform that can combine genetic, microbial, and simple behavioral assessments could help address the detection gap.

“One limitation of this data is that it cannot assess any causal role for the microbiota in the development of autism,” Dr. Chakrabarti noted. 

This study was supported by InnoHK, the Government of Hong Kong, Special Administrative Region of the People’s Republic of China, The D. H. Chen Foundation, and the New Cornerstone Science Foundation through the New Cornerstone Investigator Program. Dr. Ng has served as an advisory board member for Pfizer, Ferring, Janssen, and AbbVie; has received honoraria as a speaker for Ferring, Tillotts, Menarini, Janssen, AbbVie, and Takeda; is a scientific cofounder and shareholder of GenieBiome; receives patent royalties through her affiliated institutions; and is named as a co-inventor of patent applications that cover the therapeutic and diagnostic use of microbiome. Dr. Chakrabarti has no relevant conflicts of interest.
 

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

Bacterial and nonbacterial components of the gut microbiome and their function can accurately differentiate children with autism spectrum disorder (ASD) from neurotypical children, new research shows. 

The findings could form the basis for development of a noninvasive diagnostic test for ASD and also provide novel therapeutic targets, wrote investigators, led by Siew C. Ng, MBBS, PhD, with the Microbiota I-Center (MagIC), the Chinese University of Hong Kong.

Their study was published online in Nature Microbiology. 
 

Beyond Bacteria

The gut microbiome has been shown to play a central role in modulating the gut-brain axis, potentially influencing the development of ASD. 

However, most studies in ASD have focused on the bacterial component of the microbiome. Whether nonbacterial microorganisms (such as gut archaea, fungi, and viruses) or function of the gut microbiome are altered in ASD remains unclear. 

To investigate, the researchers performed metagenomic sequencing on fecal samples from 1627 boys and girls aged 1-13 years with and without ASD from five cohorts in China. 

After controlling for diet, medication, and comorbidity, they identified 14 archaea, 51 bacteria, 7 fungi, 18 viruses, 27 microbial genes, and 12 metabolic pathways that were altered in children with ASD. 

Machine-learning models using single-kingdom panels (archaea, bacteria, fungi, viruses) achieved area under the curve (AUC) values ranging from 0.68 to 0.87 in differentiating children with ASD from neurotypical control children. 

A model based on a panel of 31 multikingdom and functional markers achieved “high predictive value” for ASD, achieving an AUC of 0.91, with comparable performance among boys and girls. 

“The reproducible performance of the models across ages, sexes, and cohorts highlights their potential as promising diagnostic tools for ASD,” the investigators wrote. 

They also noted that the accuracy of the model was largely driven by the biosynthesis pathways of ubiquinol-7 and thiamine diphosphate, which were less abundant in children with ASD, and may serve as therapeutic targets. 
 

‘Exciting’ Possibilities 

“This study broadens our understanding by including fungi, archaea, and viruses, where previous studies have largely focused on the role of gut bacteria in autism,” Bhismadev Chakrabarti, PhD, research director of the Centre for Autism at the University of Reading, United Kingdom, said in a statement from the nonprofit UK Science Media Centre. 

“The results are broadly in line with previous studies that show reduced microbial diversity in autistic individuals. It also examines one of the largest samples seen in a study like this, which further strengthens the results,” Dr. Chakrabarti added. 

He said this research may provide “new ways of detecting autism, if microbial markers turn out to strengthen the ability of genetic and behavioral tests to detect autism. A future platform that can combine genetic, microbial, and simple behavioral assessments could help address the detection gap.

“One limitation of this data is that it cannot assess any causal role for the microbiota in the development of autism,” Dr. Chakrabarti noted. 

This study was supported by InnoHK, the Government of Hong Kong, Special Administrative Region of the People’s Republic of China, The D. H. Chen Foundation, and the New Cornerstone Science Foundation through the New Cornerstone Investigator Program. Dr. Ng has served as an advisory board member for Pfizer, Ferring, Janssen, and AbbVie; has received honoraria as a speaker for Ferring, Tillotts, Menarini, Janssen, AbbVie, and Takeda; is a scientific cofounder and shareholder of GenieBiome; receives patent royalties through her affiliated institutions; and is named as a co-inventor of patent applications that cover the therapeutic and diagnostic use of microbiome. Dr. Chakrabarti has no relevant conflicts of interest.
 

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

Bacterial and nonbacterial components of the gut microbiome and their function can accurately differentiate children with autism spectrum disorder (ASD) from neurotypical children, new research shows. 

The findings could form the basis for development of a noninvasive diagnostic test for ASD and also provide novel therapeutic targets, wrote investigators, led by Siew C. Ng, MBBS, PhD, with the Microbiota I-Center (MagIC), the Chinese University of Hong Kong.

Their study was published online in Nature Microbiology. 
 

Beyond Bacteria

The gut microbiome has been shown to play a central role in modulating the gut-brain axis, potentially influencing the development of ASD. 

However, most studies in ASD have focused on the bacterial component of the microbiome. Whether nonbacterial microorganisms (such as gut archaea, fungi, and viruses) or function of the gut microbiome are altered in ASD remains unclear. 

To investigate, the researchers performed metagenomic sequencing on fecal samples from 1627 boys and girls aged 1-13 years with and without ASD from five cohorts in China. 

After controlling for diet, medication, and comorbidity, they identified 14 archaea, 51 bacteria, 7 fungi, 18 viruses, 27 microbial genes, and 12 metabolic pathways that were altered in children with ASD. 

Machine-learning models using single-kingdom panels (archaea, bacteria, fungi, viruses) achieved area under the curve (AUC) values ranging from 0.68 to 0.87 in differentiating children with ASD from neurotypical control children. 

A model based on a panel of 31 multikingdom and functional markers achieved “high predictive value” for ASD, achieving an AUC of 0.91, with comparable performance among boys and girls. 

“The reproducible performance of the models across ages, sexes, and cohorts highlights their potential as promising diagnostic tools for ASD,” the investigators wrote. 

They also noted that the accuracy of the model was largely driven by the biosynthesis pathways of ubiquinol-7 and thiamine diphosphate, which were less abundant in children with ASD, and may serve as therapeutic targets. 
 

‘Exciting’ Possibilities 

“This study broadens our understanding by including fungi, archaea, and viruses, where previous studies have largely focused on the role of gut bacteria in autism,” Bhismadev Chakrabarti, PhD, research director of the Centre for Autism at the University of Reading, United Kingdom, said in a statement from the nonprofit UK Science Media Centre. 

“The results are broadly in line with previous studies that show reduced microbial diversity in autistic individuals. It also examines one of the largest samples seen in a study like this, which further strengthens the results,” Dr. Chakrabarti added. 

He said this research may provide “new ways of detecting autism, if microbial markers turn out to strengthen the ability of genetic and behavioral tests to detect autism. A future platform that can combine genetic, microbial, and simple behavioral assessments could help address the detection gap.

“One limitation of this data is that it cannot assess any causal role for the microbiota in the development of autism,” Dr. Chakrabarti noted. 

This study was supported by InnoHK, the Government of Hong Kong, Special Administrative Region of the People’s Republic of China, The D. H. Chen Foundation, and the New Cornerstone Science Foundation through the New Cornerstone Investigator Program. Dr. Ng has served as an advisory board member for Pfizer, Ferring, Janssen, and AbbVie; has received honoraria as a speaker for Ferring, Tillotts, Menarini, Janssen, AbbVie, and Takeda; is a scientific cofounder and shareholder of GenieBiome; receives patent royalties through her affiliated institutions; and is named as a co-inventor of patent applications that cover the therapeutic and diagnostic use of microbiome. Dr. Chakrabarti has no relevant conflicts of interest.
 

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

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Eight commonly used antidepressants have been ranked by their weight gain potential. 

Results of a large observational study showed small differences in short- and long-term weight change in patients prescribed one of eight antidepressants, with bupropion associated with the lowest weight gain and escitalopram, paroxetine, and duloxetine associated with the greatest. 

Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with those taking sertraline, which was used as a comparator. 

Investigators noted that the more clinicians and patients know about how a particular antidepressant may affect patients’ weight, the better informed they can be about which antidepressants to prescribe. 

“Patients and their clinicians often have several options when starting an antidepressant for the first time. This study provides important real-world evidence regarding the amount of weight gain that should be expected after starting some of the most common antidepressants,” lead author Joshua Petimar, ScD, assistant professor of population medicine in the Harvard Pilgrim Health Care Institute at Harvard Medical School, Boston, said in a press release. 

The findings were published online in Annals of Internal Medicine. 


 

Real-World Data

Though weight gain is a commonly reported side effect of antidepressant use and may lead to medication nonadherence and worse outcomes, there is a lack of real-world data about weight change across specific medications. 

Investigators used electronic health records from eight health care systems across the United States spanning from 2010 to 2019. The analysis included information on 183,118 adults aged 20-80 years who were new users of one of eight common first-line antidepressants. Investigators measured their weight at baseline and at 6, 12, and 24 months after initiation to estimate intention-to-treat (ITT) effects of weight change.

At baseline, participants were randomly assigned to begin sertraline, citalopram, escitalopram, fluoxetine, paroxetine, bupropion, duloxetine, or venlafaxine. 

The most common antidepressants prescribed were sertraline, citalopram, and bupropion. Approximately 36% of participants had a diagnosis of depression, and 39% were diagnosed with anxiety.

Among selective serotonin reuptake inhibitors (SSRIs), escitalopram and paroxetine were associated with the greatest 6-month weight gain, whereas bupropion was associated with the least weight gain across all analyses.

Using sertraline as a comparator, 6-month weight change was lower for bupropion (difference, 0.22 kg) and higher for escitalopram (difference, 0.41 kg), duloxetine (difference, 0.34 kg), paroxetine (difference, 0.37 kg), and venlafaxine (difference, 0.17 kg).

Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with sertraline users.

Investigators noted little difference in adherence levels between medications during the study except at 6 months, when it was higher for those who took bupropion (41%) than for those taking other antidepressants (28%-36%).

The study included data only on prescriptions and investigators could not verify whether the medications were dispensed or taken as prescribed. Other limitations included missing weight information because most patients did not encounter the health system at exactly 6, 12, and 24 months; only 15%-30% had weight measurements in those months. 

Finally, the low adherence rates made it difficult to attribute relative weight change at the 12- and 24-month time points to the specific medications of interest.

“Clinicians and patients could consider these differences when making decisions about specific antidepressants, especially given the complex relationships of obesity and depression with health, quality of life, and stigma,” the authors wrote. 

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Disclosures are noted in the original article. 

A version of this article appeared on Medscape.com.

Eight commonly used antidepressants have been ranked by their weight gain potential. 

Results of a large observational study showed small differences in short- and long-term weight change in patients prescribed one of eight antidepressants, with bupropion associated with the lowest weight gain and escitalopram, paroxetine, and duloxetine associated with the greatest. 

Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with those taking sertraline, which was used as a comparator. 

Investigators noted that the more clinicians and patients know about how a particular antidepressant may affect patients’ weight, the better informed they can be about which antidepressants to prescribe. 

“Patients and their clinicians often have several options when starting an antidepressant for the first time. This study provides important real-world evidence regarding the amount of weight gain that should be expected after starting some of the most common antidepressants,” lead author Joshua Petimar, ScD, assistant professor of population medicine in the Harvard Pilgrim Health Care Institute at Harvard Medical School, Boston, said in a press release. 

The findings were published online in Annals of Internal Medicine. 


 

Real-World Data

Though weight gain is a commonly reported side effect of antidepressant use and may lead to medication nonadherence and worse outcomes, there is a lack of real-world data about weight change across specific medications. 

Investigators used electronic health records from eight health care systems across the United States spanning from 2010 to 2019. The analysis included information on 183,118 adults aged 20-80 years who were new users of one of eight common first-line antidepressants. Investigators measured their weight at baseline and at 6, 12, and 24 months after initiation to estimate intention-to-treat (ITT) effects of weight change.

At baseline, participants were randomly assigned to begin sertraline, citalopram, escitalopram, fluoxetine, paroxetine, bupropion, duloxetine, or venlafaxine. 

The most common antidepressants prescribed were sertraline, citalopram, and bupropion. Approximately 36% of participants had a diagnosis of depression, and 39% were diagnosed with anxiety.

Among selective serotonin reuptake inhibitors (SSRIs), escitalopram and paroxetine were associated with the greatest 6-month weight gain, whereas bupropion was associated with the least weight gain across all analyses.

Using sertraline as a comparator, 6-month weight change was lower for bupropion (difference, 0.22 kg) and higher for escitalopram (difference, 0.41 kg), duloxetine (difference, 0.34 kg), paroxetine (difference, 0.37 kg), and venlafaxine (difference, 0.17 kg).

Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with sertraline users.

Investigators noted little difference in adherence levels between medications during the study except at 6 months, when it was higher for those who took bupropion (41%) than for those taking other antidepressants (28%-36%).

The study included data only on prescriptions and investigators could not verify whether the medications were dispensed or taken as prescribed. Other limitations included missing weight information because most patients did not encounter the health system at exactly 6, 12, and 24 months; only 15%-30% had weight measurements in those months. 

Finally, the low adherence rates made it difficult to attribute relative weight change at the 12- and 24-month time points to the specific medications of interest.

“Clinicians and patients could consider these differences when making decisions about specific antidepressants, especially given the complex relationships of obesity and depression with health, quality of life, and stigma,” the authors wrote. 

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Disclosures are noted in the original article. 

A version of this article appeared on Medscape.com.

Eight commonly used antidepressants have been ranked by their weight gain potential. 

Results of a large observational study showed small differences in short- and long-term weight change in patients prescribed one of eight antidepressants, with bupropion associated with the lowest weight gain and escitalopram, paroxetine, and duloxetine associated with the greatest. 

Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with those taking sertraline, which was used as a comparator. 

Investigators noted that the more clinicians and patients know about how a particular antidepressant may affect patients’ weight, the better informed they can be about which antidepressants to prescribe. 

“Patients and their clinicians often have several options when starting an antidepressant for the first time. This study provides important real-world evidence regarding the amount of weight gain that should be expected after starting some of the most common antidepressants,” lead author Joshua Petimar, ScD, assistant professor of population medicine in the Harvard Pilgrim Health Care Institute at Harvard Medical School, Boston, said in a press release. 

The findings were published online in Annals of Internal Medicine. 


 

Real-World Data

Though weight gain is a commonly reported side effect of antidepressant use and may lead to medication nonadherence and worse outcomes, there is a lack of real-world data about weight change across specific medications. 

Investigators used electronic health records from eight health care systems across the United States spanning from 2010 to 2019. The analysis included information on 183,118 adults aged 20-80 years who were new users of one of eight common first-line antidepressants. Investigators measured their weight at baseline and at 6, 12, and 24 months after initiation to estimate intention-to-treat (ITT) effects of weight change.

At baseline, participants were randomly assigned to begin sertraline, citalopram, escitalopram, fluoxetine, paroxetine, bupropion, duloxetine, or venlafaxine. 

The most common antidepressants prescribed were sertraline, citalopram, and bupropion. Approximately 36% of participants had a diagnosis of depression, and 39% were diagnosed with anxiety.

Among selective serotonin reuptake inhibitors (SSRIs), escitalopram and paroxetine were associated with the greatest 6-month weight gain, whereas bupropion was associated with the least weight gain across all analyses.

Using sertraline as a comparator, 6-month weight change was lower for bupropion (difference, 0.22 kg) and higher for escitalopram (difference, 0.41 kg), duloxetine (difference, 0.34 kg), paroxetine (difference, 0.37 kg), and venlafaxine (difference, 0.17 kg).

Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with sertraline users.

Investigators noted little difference in adherence levels between medications during the study except at 6 months, when it was higher for those who took bupropion (41%) than for those taking other antidepressants (28%-36%).

The study included data only on prescriptions and investigators could not verify whether the medications were dispensed or taken as prescribed. Other limitations included missing weight information because most patients did not encounter the health system at exactly 6, 12, and 24 months; only 15%-30% had weight measurements in those months. 

Finally, the low adherence rates made it difficult to attribute relative weight change at the 12- and 24-month time points to the specific medications of interest.

“Clinicians and patients could consider these differences when making decisions about specific antidepressants, especially given the complex relationships of obesity and depression with health, quality of life, and stigma,” the authors wrote. 

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Disclosures are noted in the original article. 

A version of this article appeared on Medscape.com.

TOPLINE:

High-dose antipsychotics, particularly quetiapine, clozapine, and olanzapine, are linked to increased pneumonia risk in patients with schizophrenia, new data show. Monotherapy with high anticholinergic burden also raises pneumonia risk.

METHODOLOGY: 

• Using several nationwide data registers, investigators pulled data on individuals who received inpatient care for schizophrenia or schizoaffective disorder (n = 61,889) between 1972 and 2014.
• Data on drug use were gathered from a prescription register and included dispensing dates, cost, dose, package size, and drug formulation. Data on dates and causes of death were obtained from the Causes of Death register.
• After entering the cohort, follow-up started in January 1996 or after the first diagnosis of schizophrenia for those diagnosed between 1996 and 2014.
• The primary outcome was hospitalization caused by pneumonia as the main diagnosis for hospital admission.

TAKEAWAY: 

• During 22 years of follow-up, 8917 patients (14.4%) had one or more hospitalizations for pneumonia, and 1137 (12.8%) died within 30 days of admission.
• Pneumonia risk was the highest with the use of high-dose (> 440 mg/d) quetiapine (P = .003), followed by high- (≥ 330 mg/d) and medium-dose (180 to < 330 mg/d) clozapine (both P < .001) and high-dose (≥ 11 mg/d) olanzapine (P = .02).
• Compared with no antipsychotic use, antipsychotic monotherapy was associated with an increased pneumonia risk (P = .03), whereas antipsychotic polytherapy was not.
• Only the use of antipsychotics with high anticholinergic potency was associated with pneumonia risk (P < .001).

IN PRACTICE:

“Identification of antipsychotic drugs that are associated with pneumonia risk may better inform prevention programs (eg, vaccinations),” the researchers noted. “Second, the availability of pneumonia risk estimates for individual antipsychotics and for groups of antipsychotics may foster personalized prescribing guidelines.”

SOURCE:

The study was led by Jurjen Luykx, MD, Amsterdam University Medical Center, Amsterdam, the Netherlands. It was published online in JAMA Psychiatry.

LIMITATIONS:

The investigators could not correct for all possible risk factors that may increase pneumonia risk in individuals with schizophrenia, such as smoking and lifestyle habits. Also, cases of pneumonia that didn’t require hospital admission couldn’t be included in the analysis, so the findings may generalize only to cases of severe pneumonia.

DISCLOSURES:

The study was funded by the Finnish Ministry of Social Affairs and Health.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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

TOPLINE:

High-dose antipsychotics, particularly quetiapine, clozapine, and olanzapine, are linked to increased pneumonia risk in patients with schizophrenia, new data show. Monotherapy with high anticholinergic burden also raises pneumonia risk.

METHODOLOGY: 

• Using several nationwide data registers, investigators pulled data on individuals who received inpatient care for schizophrenia or schizoaffective disorder (n = 61,889) between 1972 and 2014.
• Data on drug use were gathered from a prescription register and included dispensing dates, cost, dose, package size, and drug formulation. Data on dates and causes of death were obtained from the Causes of Death register.
• After entering the cohort, follow-up started in January 1996 or after the first diagnosis of schizophrenia for those diagnosed between 1996 and 2014.
• The primary outcome was hospitalization caused by pneumonia as the main diagnosis for hospital admission.

TAKEAWAY: 

• During 22 years of follow-up, 8917 patients (14.4%) had one or more hospitalizations for pneumonia, and 1137 (12.8%) died within 30 days of admission.
• Pneumonia risk was the highest with the use of high-dose (> 440 mg/d) quetiapine (P = .003), followed by high- (≥ 330 mg/d) and medium-dose (180 to < 330 mg/d) clozapine (both P < .001) and high-dose (≥ 11 mg/d) olanzapine (P = .02).
• Compared with no antipsychotic use, antipsychotic monotherapy was associated with an increased pneumonia risk (P = .03), whereas antipsychotic polytherapy was not.
• Only the use of antipsychotics with high anticholinergic potency was associated with pneumonia risk (P < .001).

IN PRACTICE:

“Identification of antipsychotic drugs that are associated with pneumonia risk may better inform prevention programs (eg, vaccinations),” the researchers noted. “Second, the availability of pneumonia risk estimates for individual antipsychotics and for groups of antipsychotics may foster personalized prescribing guidelines.”

SOURCE:

The study was led by Jurjen Luykx, MD, Amsterdam University Medical Center, Amsterdam, the Netherlands. It was published online in JAMA Psychiatry.

LIMITATIONS:

The investigators could not correct for all possible risk factors that may increase pneumonia risk in individuals with schizophrenia, such as smoking and lifestyle habits. Also, cases of pneumonia that didn’t require hospital admission couldn’t be included in the analysis, so the findings may generalize only to cases of severe pneumonia.

DISCLOSURES:

The study was funded by the Finnish Ministry of Social Affairs and Health.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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

TOPLINE:

High-dose antipsychotics, particularly quetiapine, clozapine, and olanzapine, are linked to increased pneumonia risk in patients with schizophrenia, new data show. Monotherapy with high anticholinergic burden also raises pneumonia risk.

METHODOLOGY: 

• Using several nationwide data registers, investigators pulled data on individuals who received inpatient care for schizophrenia or schizoaffective disorder (n = 61,889) between 1972 and 2014.
• Data on drug use were gathered from a prescription register and included dispensing dates, cost, dose, package size, and drug formulation. Data on dates and causes of death were obtained from the Causes of Death register.
• After entering the cohort, follow-up started in January 1996 or after the first diagnosis of schizophrenia for those diagnosed between 1996 and 2014.
• The primary outcome was hospitalization caused by pneumonia as the main diagnosis for hospital admission.

TAKEAWAY: 

• During 22 years of follow-up, 8917 patients (14.4%) had one or more hospitalizations for pneumonia, and 1137 (12.8%) died within 30 days of admission.
• Pneumonia risk was the highest with the use of high-dose (> 440 mg/d) quetiapine (P = .003), followed by high- (≥ 330 mg/d) and medium-dose (180 to < 330 mg/d) clozapine (both P < .001) and high-dose (≥ 11 mg/d) olanzapine (P = .02).
• Compared with no antipsychotic use, antipsychotic monotherapy was associated with an increased pneumonia risk (P = .03), whereas antipsychotic polytherapy was not.
• Only the use of antipsychotics with high anticholinergic potency was associated with pneumonia risk (P < .001).

IN PRACTICE:

“Identification of antipsychotic drugs that are associated with pneumonia risk may better inform prevention programs (eg, vaccinations),” the researchers noted. “Second, the availability of pneumonia risk estimates for individual antipsychotics and for groups of antipsychotics may foster personalized prescribing guidelines.”

SOURCE:

The study was led by Jurjen Luykx, MD, Amsterdam University Medical Center, Amsterdam, the Netherlands. It was published online in JAMA Psychiatry.

LIMITATIONS:

The investigators could not correct for all possible risk factors that may increase pneumonia risk in individuals with schizophrenia, such as smoking and lifestyle habits. Also, cases of pneumonia that didn’t require hospital admission couldn’t be included in the analysis, so the findings may generalize only to cases of severe pneumonia.

DISCLOSURES:

The study was funded by the Finnish Ministry of Social Affairs and Health.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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