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Binge eating in ADHD may not be impulsivity-related

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The disinhibited binge eating style often seen in individuals with high ADHD symptoms is attributable to a heightened neural reward response to food rather than to the impulsivity that’s a core feature of ADHD, Elizabeth Martin, MSc, reported at the virtual congress of the European College of Neuropsychopharmacology.

 

She presented a functional MRI brain-imaging study designed to help pin down the mechanism involved in the disordered eating patterns that often accompany ADHD.

“Determining the underlying mechanism between binge eating and ADHD may be helpful in developing novel therapies for both ADHD and binge eating disorder. Our research suggests that further investigation of the role of altered reward processing in ADHD may be an avenue for this,” said Ms. Martin, a doctoral researcher in the department of psychology at the University of Birmingham (England).

She and her coinvestigators recruited 31 university student volunteers with high ADHD symptoms as evidenced by their mean score of 29.3 on the 0-54 Conners’ Adult ADHD Rating Scale, and 27 others with low ADHD symptoms and a mean Conners’ score of 6.8. The two groups didn’t differ in age or BMI. However, not surprisingly, the high-ADHD group exhibited greater impulsivity, with a mean score of 72 on the Barratt Impulsiveness Scale, versus 56.5 in the low ADHD group.

A battery of eating disorder scales was applied to assess participants in terms of binge/disinhibited or restrictive eating patterns. The high- and low–ADHD symptom groups didn’t differ in terms of prevalence of a restrictive eating style, which was low, but the high-ADHD participants scored on average roughly 50% higher on the binge/disinhibited eating style measure, compared with the low-ADHD group.

Each study participant underwent a 1-hour BOLD (blood oxygen level dependent) functional MRI scan while performing two sets of tasks. One task entailed quickly looking at 120 photos of food items and an equal number of nonfood items and rating how appealing the pictures were. The other challenge was what psychologists call a go/no-go task, a computerized cognitive test used to assess inhibitory control based upon reaction times and error rates.

On the go/no-go task, there were no between-group differences in rates of errors of omission or commission or reaction time. Moreover, the MRI results indicated there were no between-group differences in neural circuitry activation during this task. The investigators therefore concluded that the tendency toward binge eating in the high–ADHD symptoms group was not tied to greater impulsivity as reflected in less effective inhibitory processes.

The food picture rating task told a different story. The MRIs demonstrated increased responses to food versus nonfood images in the high-ADHD subjects, compared with the low-ADHD subjects in reward-related brain areas, including the ventromedial prefrontal cortex, caudate nucleus, and ventral tegmental area.

“This is the first evidence that ADHD symptoms in young adults are associated with enhanced neural activation in key reward-related brain areas in response to viewing food pictures,” according to Ms. Martin. “This suggests that enhanced responsiveness to food cues may be a mediating mechanism underlying overeating in ADHD.”

Of note, only one drug – lisdexamfetamine dimesylate (Vyvanse) is Food and Drug Administration-approved for the treatment of both ADHD and binge-eating disorder.

“Until now it’s been unclear how lisdexamfetamine dimesylate reduces binge eating, but our results suggest that one mechanism worthy of further investigation is the potential effect of the drug on food reward processes,” Ms. Martin said.

She reported having no financial conflicts regarding the study, which was supported by university funding.

SOURCE: Martin E. ECNP 2020. Abstr. P.041.

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The disinhibited binge eating style often seen in individuals with high ADHD symptoms is attributable to a heightened neural reward response to food rather than to the impulsivity that’s a core feature of ADHD, Elizabeth Martin, MSc, reported at the virtual congress of the European College of Neuropsychopharmacology.

 

She presented a functional MRI brain-imaging study designed to help pin down the mechanism involved in the disordered eating patterns that often accompany ADHD.

“Determining the underlying mechanism between binge eating and ADHD may be helpful in developing novel therapies for both ADHD and binge eating disorder. Our research suggests that further investigation of the role of altered reward processing in ADHD may be an avenue for this,” said Ms. Martin, a doctoral researcher in the department of psychology at the University of Birmingham (England).

She and her coinvestigators recruited 31 university student volunteers with high ADHD symptoms as evidenced by their mean score of 29.3 on the 0-54 Conners’ Adult ADHD Rating Scale, and 27 others with low ADHD symptoms and a mean Conners’ score of 6.8. The two groups didn’t differ in age or BMI. However, not surprisingly, the high-ADHD group exhibited greater impulsivity, with a mean score of 72 on the Barratt Impulsiveness Scale, versus 56.5 in the low ADHD group.

A battery of eating disorder scales was applied to assess participants in terms of binge/disinhibited or restrictive eating patterns. The high- and low–ADHD symptom groups didn’t differ in terms of prevalence of a restrictive eating style, which was low, but the high-ADHD participants scored on average roughly 50% higher on the binge/disinhibited eating style measure, compared with the low-ADHD group.

Each study participant underwent a 1-hour BOLD (blood oxygen level dependent) functional MRI scan while performing two sets of tasks. One task entailed quickly looking at 120 photos of food items and an equal number of nonfood items and rating how appealing the pictures were. The other challenge was what psychologists call a go/no-go task, a computerized cognitive test used to assess inhibitory control based upon reaction times and error rates.

On the go/no-go task, there were no between-group differences in rates of errors of omission or commission or reaction time. Moreover, the MRI results indicated there were no between-group differences in neural circuitry activation during this task. The investigators therefore concluded that the tendency toward binge eating in the high–ADHD symptoms group was not tied to greater impulsivity as reflected in less effective inhibitory processes.

The food picture rating task told a different story. The MRIs demonstrated increased responses to food versus nonfood images in the high-ADHD subjects, compared with the low-ADHD subjects in reward-related brain areas, including the ventromedial prefrontal cortex, caudate nucleus, and ventral tegmental area.

“This is the first evidence that ADHD symptoms in young adults are associated with enhanced neural activation in key reward-related brain areas in response to viewing food pictures,” according to Ms. Martin. “This suggests that enhanced responsiveness to food cues may be a mediating mechanism underlying overeating in ADHD.”

Of note, only one drug – lisdexamfetamine dimesylate (Vyvanse) is Food and Drug Administration-approved for the treatment of both ADHD and binge-eating disorder.

“Until now it’s been unclear how lisdexamfetamine dimesylate reduces binge eating, but our results suggest that one mechanism worthy of further investigation is the potential effect of the drug on food reward processes,” Ms. Martin said.

She reported having no financial conflicts regarding the study, which was supported by university funding.

SOURCE: Martin E. ECNP 2020. Abstr. P.041.

The disinhibited binge eating style often seen in individuals with high ADHD symptoms is attributable to a heightened neural reward response to food rather than to the impulsivity that’s a core feature of ADHD, Elizabeth Martin, MSc, reported at the virtual congress of the European College of Neuropsychopharmacology.

 

She presented a functional MRI brain-imaging study designed to help pin down the mechanism involved in the disordered eating patterns that often accompany ADHD.

“Determining the underlying mechanism between binge eating and ADHD may be helpful in developing novel therapies for both ADHD and binge eating disorder. Our research suggests that further investigation of the role of altered reward processing in ADHD may be an avenue for this,” said Ms. Martin, a doctoral researcher in the department of psychology at the University of Birmingham (England).

She and her coinvestigators recruited 31 university student volunteers with high ADHD symptoms as evidenced by their mean score of 29.3 on the 0-54 Conners’ Adult ADHD Rating Scale, and 27 others with low ADHD symptoms and a mean Conners’ score of 6.8. The two groups didn’t differ in age or BMI. However, not surprisingly, the high-ADHD group exhibited greater impulsivity, with a mean score of 72 on the Barratt Impulsiveness Scale, versus 56.5 in the low ADHD group.

A battery of eating disorder scales was applied to assess participants in terms of binge/disinhibited or restrictive eating patterns. The high- and low–ADHD symptom groups didn’t differ in terms of prevalence of a restrictive eating style, which was low, but the high-ADHD participants scored on average roughly 50% higher on the binge/disinhibited eating style measure, compared with the low-ADHD group.

Each study participant underwent a 1-hour BOLD (blood oxygen level dependent) functional MRI scan while performing two sets of tasks. One task entailed quickly looking at 120 photos of food items and an equal number of nonfood items and rating how appealing the pictures were. The other challenge was what psychologists call a go/no-go task, a computerized cognitive test used to assess inhibitory control based upon reaction times and error rates.

On the go/no-go task, there were no between-group differences in rates of errors of omission or commission or reaction time. Moreover, the MRI results indicated there were no between-group differences in neural circuitry activation during this task. The investigators therefore concluded that the tendency toward binge eating in the high–ADHD symptoms group was not tied to greater impulsivity as reflected in less effective inhibitory processes.

The food picture rating task told a different story. The MRIs demonstrated increased responses to food versus nonfood images in the high-ADHD subjects, compared with the low-ADHD subjects in reward-related brain areas, including the ventromedial prefrontal cortex, caudate nucleus, and ventral tegmental area.

“This is the first evidence that ADHD symptoms in young adults are associated with enhanced neural activation in key reward-related brain areas in response to viewing food pictures,” according to Ms. Martin. “This suggests that enhanced responsiveness to food cues may be a mediating mechanism underlying overeating in ADHD.”

Of note, only one drug – lisdexamfetamine dimesylate (Vyvanse) is Food and Drug Administration-approved for the treatment of both ADHD and binge-eating disorder.

“Until now it’s been unclear how lisdexamfetamine dimesylate reduces binge eating, but our results suggest that one mechanism worthy of further investigation is the potential effect of the drug on food reward processes,” Ms. Martin said.

She reported having no financial conflicts regarding the study, which was supported by university funding.

SOURCE: Martin E. ECNP 2020. Abstr. P.041.

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Reassuring findings on SSRIs and diabetes risk in children

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Thu, 09/17/2020 - 11:25

 

SSRIs are associated with a much lower risk of type 2 diabetes (T2D) in children and adolescents than previously reported, new research shows.

Investigators found publicly insured patients treated with SSRIs had a 13% increased risk for T2D, compared with those not treated with these agents. In addition, those taking SSRIs continuously (defined as receiving one or more prescriptions every 3 months) had a 33% increased risk of T2D.

On the other hand, privately insured youth had a much lower increased risk – a finding that may be attributable to a lower prevalence of risk factors for T2D in this group.

“We cannot exclude that children and adolescents treated with SSRIs may be at a small increased risk of developing T2D, particularly publicly insured patients, but the magnitude of association was weaker than previous thought and much smaller than other known risk factors for T2DM, such as obesity, race, and poverty,” lead investigator Jenny Sun, PhD, said in an interview.

“When weighing the known benefits and risks of SSRI treatment in children and adolescents, our findings provide reassurance that the risk of T2DM is not as substantial as initially reported,” said Dr. Sun, a postdoctoral research fellow in the department of population medicine at Harvard Medical School’s Harvard Pilgrim Health Care Institute, Boston.

The study was published online Sept. 2 in JAMA Psychiatry.

Limited evidence

Previous research suggested that SSRIs increase the risk of T2D by up to 90% in children and adolescents.

However, the investigators noted, the study reporting this finding was too small to draw conclusions about the SSRI class as a whole also did not examine specific SSRIs.

In addition, although “several studies have reported that antidepressant use may be a risk factor for T2D in adults, evidence was limited in children and adolescents,” said Dr. Sun.

“Rapid changes in growth during childhood and adolescents can alter drugs’ pharmacokinetics and pharmacodynamics, so high-quality, age-specific data are needed to inform prescribing decisions,” she said.

For the current study, the researchers analyzed claims data on almost 1.6 million patients aged 10-19 years (58.3% female; mean age, 15.1 years) from two large claims databases.

The analysis focused on those with a diagnosis warranting treatment with an SSRI, including depression, generalized or social anxiety disorder, obsessive compulsive disorder, PTSD, panic disorder, or bulimia nervosa.

The Medicaid Analytic Extract database consisted of 316,178 patients insured through Medicaid or the Children’s Health Insurance Program. The IBM MarketScan database consisted of 211,460 privately insured patients. Patients were followed up for a mean of 2.3 and 2.2 years, respectively.

Patients who initiated SSRI treatment were compared with those with a similar indication but who were not taking an SSRI. Secondary analyses compared new SSRI users with patients who recently initiated treatment with bupropion, which has no metabolic side effects, or with patients who recently initiated psychotherapy.

“In observational data, it is difficult to mimic a placebo group, often used in RCTs [randomized, controlled trials], therefore several comparator groups were explored to broaden our understanding,” said Dr. Sun.

In addition, the researchers compared the individual SSRI medications, using fluoxetine as a comparator.

A wide range of more than 100 potential confounders or “proxies of confounders,” were taken into account, including demographic characteristics, psychiatric diagnoses, metabolic conditions, concomitant medications, and use of health care services.

The researchers conducted two analyses. They included an intention-to-treat (ITT) analysis that was restricted to patients with one or more additional SSRI prescriptions during the 6 months following the index exposure assessment period.

 

 

Close monitoring required

An as-treated analysis estimated the association of continuous SSRI treatment (vs. untreated, bupropion treatment, and psychotherapy), with adherence assessed at 3-month intervals.

Initiation and continuation of SSRI treatment in publicly insured patients were both associated with a considerably higher risk of T2D, compared with untreated patients, and a steeper risk, compared with their privately insured counterparts.

For newly treated publicly insured patients initiated on SSRI treatment, the ITT adjusted hazard ratio was 1.13 (95% confidence interval, 1.04-1.22).

There was an even stronger association among continuously treated publicly insured patients, with an as-treated aHR of 1.33 (95% CI, 1.21-1.47). The authors noted that this corresponds to 6.6 additional T2D cases per 10,000 patients continuously treated for at least 2 years.

The association was weaker in privately insured patients (ITT aHR, 1.01; 95% CI, 0.84-1.23; as-treated aHR, 1.10; 95% CI, 0.88-1.36).

The secondary analyses yielded similar findings: When SSRI treatment was compared with psychotherapy, the as-treated aHR for publicly insured patients was 1.44 (95% CI, 1.25-1.65), whereas the aHR for privately insured patients was lower at 1.21 (95% CI, 0.93-1.57)

The investigators found no increased risk when SSRIs were compared with bupropion, and the within-class analysis showed that none of the SSRIs carried an increased hazard of T2D, compared with fluoxetine.

“Publicly insured patients are enrolled in Medicaid and the Children’s Health Insurance Program, whereas privately insured patients are generally covered by their parent’s employer-sponsored insurance,” said Dr. Sun.

“Publicly insured patients are of lower socioeconomic status and represent a population with greater overall medical burden, more comorbidities, and a higher prevalence of risk factors for T2D, such as obesity, at the time of treatment initiation,” she said.

She added that high-risk children and youth should be closely monitored and clinicians should also consider recommending dietary modifications and increased exercise to offset T2D risk.

Useful ‘real-world data’

William Cooper, MD, MPH, professor of pediatrics and health policy at Vanderbilt University Medical Center in Nashville, Tenn., said that the study “provides a fascinating look at risks of SSRI medications in children and adolescents.”

Dr. Cooper, who was not involved with the study, said that the authors “draw from real-world data representing two different populations and carefully consider factors which might confound the associations.”

The results, he said, “provide important benefits for patients, families, and clinicians as they weigh the risks and benefits of using SSRIs for children who need treatment for depression and anxiety disorders.

“As a pediatrician, I would find these results useful as I work with my patients, their families, and behavioral health colleagues in making important treatment decisions.”

The study was supported by a training grant from the program in pharmacoepidemiology at the Harvard School of Public Health. Dr. Sun disclosed no relevant financial relationships. Dr. Cooper disclosed no relevant financial relationships.

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

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SSRIs are associated with a much lower risk of type 2 diabetes (T2D) in children and adolescents than previously reported, new research shows.

Investigators found publicly insured patients treated with SSRIs had a 13% increased risk for T2D, compared with those not treated with these agents. In addition, those taking SSRIs continuously (defined as receiving one or more prescriptions every 3 months) had a 33% increased risk of T2D.

On the other hand, privately insured youth had a much lower increased risk – a finding that may be attributable to a lower prevalence of risk factors for T2D in this group.

“We cannot exclude that children and adolescents treated with SSRIs may be at a small increased risk of developing T2D, particularly publicly insured patients, but the magnitude of association was weaker than previous thought and much smaller than other known risk factors for T2DM, such as obesity, race, and poverty,” lead investigator Jenny Sun, PhD, said in an interview.

“When weighing the known benefits and risks of SSRI treatment in children and adolescents, our findings provide reassurance that the risk of T2DM is not as substantial as initially reported,” said Dr. Sun, a postdoctoral research fellow in the department of population medicine at Harvard Medical School’s Harvard Pilgrim Health Care Institute, Boston.

The study was published online Sept. 2 in JAMA Psychiatry.

Limited evidence

Previous research suggested that SSRIs increase the risk of T2D by up to 90% in children and adolescents.

However, the investigators noted, the study reporting this finding was too small to draw conclusions about the SSRI class as a whole also did not examine specific SSRIs.

In addition, although “several studies have reported that antidepressant use may be a risk factor for T2D in adults, evidence was limited in children and adolescents,” said Dr. Sun.

“Rapid changes in growth during childhood and adolescents can alter drugs’ pharmacokinetics and pharmacodynamics, so high-quality, age-specific data are needed to inform prescribing decisions,” she said.

For the current study, the researchers analyzed claims data on almost 1.6 million patients aged 10-19 years (58.3% female; mean age, 15.1 years) from two large claims databases.

The analysis focused on those with a diagnosis warranting treatment with an SSRI, including depression, generalized or social anxiety disorder, obsessive compulsive disorder, PTSD, panic disorder, or bulimia nervosa.

The Medicaid Analytic Extract database consisted of 316,178 patients insured through Medicaid or the Children’s Health Insurance Program. The IBM MarketScan database consisted of 211,460 privately insured patients. Patients were followed up for a mean of 2.3 and 2.2 years, respectively.

Patients who initiated SSRI treatment were compared with those with a similar indication but who were not taking an SSRI. Secondary analyses compared new SSRI users with patients who recently initiated treatment with bupropion, which has no metabolic side effects, or with patients who recently initiated psychotherapy.

“In observational data, it is difficult to mimic a placebo group, often used in RCTs [randomized, controlled trials], therefore several comparator groups were explored to broaden our understanding,” said Dr. Sun.

In addition, the researchers compared the individual SSRI medications, using fluoxetine as a comparator.

A wide range of more than 100 potential confounders or “proxies of confounders,” were taken into account, including demographic characteristics, psychiatric diagnoses, metabolic conditions, concomitant medications, and use of health care services.

The researchers conducted two analyses. They included an intention-to-treat (ITT) analysis that was restricted to patients with one or more additional SSRI prescriptions during the 6 months following the index exposure assessment period.

 

 

Close monitoring required

An as-treated analysis estimated the association of continuous SSRI treatment (vs. untreated, bupropion treatment, and psychotherapy), with adherence assessed at 3-month intervals.

Initiation and continuation of SSRI treatment in publicly insured patients were both associated with a considerably higher risk of T2D, compared with untreated patients, and a steeper risk, compared with their privately insured counterparts.

For newly treated publicly insured patients initiated on SSRI treatment, the ITT adjusted hazard ratio was 1.13 (95% confidence interval, 1.04-1.22).

There was an even stronger association among continuously treated publicly insured patients, with an as-treated aHR of 1.33 (95% CI, 1.21-1.47). The authors noted that this corresponds to 6.6 additional T2D cases per 10,000 patients continuously treated for at least 2 years.

The association was weaker in privately insured patients (ITT aHR, 1.01; 95% CI, 0.84-1.23; as-treated aHR, 1.10; 95% CI, 0.88-1.36).

The secondary analyses yielded similar findings: When SSRI treatment was compared with psychotherapy, the as-treated aHR for publicly insured patients was 1.44 (95% CI, 1.25-1.65), whereas the aHR for privately insured patients was lower at 1.21 (95% CI, 0.93-1.57)

The investigators found no increased risk when SSRIs were compared with bupropion, and the within-class analysis showed that none of the SSRIs carried an increased hazard of T2D, compared with fluoxetine.

“Publicly insured patients are enrolled in Medicaid and the Children’s Health Insurance Program, whereas privately insured patients are generally covered by their parent’s employer-sponsored insurance,” said Dr. Sun.

“Publicly insured patients are of lower socioeconomic status and represent a population with greater overall medical burden, more comorbidities, and a higher prevalence of risk factors for T2D, such as obesity, at the time of treatment initiation,” she said.

She added that high-risk children and youth should be closely monitored and clinicians should also consider recommending dietary modifications and increased exercise to offset T2D risk.

Useful ‘real-world data’

William Cooper, MD, MPH, professor of pediatrics and health policy at Vanderbilt University Medical Center in Nashville, Tenn., said that the study “provides a fascinating look at risks of SSRI medications in children and adolescents.”

Dr. Cooper, who was not involved with the study, said that the authors “draw from real-world data representing two different populations and carefully consider factors which might confound the associations.”

The results, he said, “provide important benefits for patients, families, and clinicians as they weigh the risks and benefits of using SSRIs for children who need treatment for depression and anxiety disorders.

“As a pediatrician, I would find these results useful as I work with my patients, their families, and behavioral health colleagues in making important treatment decisions.”

The study was supported by a training grant from the program in pharmacoepidemiology at the Harvard School of Public Health. Dr. Sun disclosed no relevant financial relationships. Dr. Cooper disclosed no relevant financial relationships.

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

 

SSRIs are associated with a much lower risk of type 2 diabetes (T2D) in children and adolescents than previously reported, new research shows.

Investigators found publicly insured patients treated with SSRIs had a 13% increased risk for T2D, compared with those not treated with these agents. In addition, those taking SSRIs continuously (defined as receiving one or more prescriptions every 3 months) had a 33% increased risk of T2D.

On the other hand, privately insured youth had a much lower increased risk – a finding that may be attributable to a lower prevalence of risk factors for T2D in this group.

“We cannot exclude that children and adolescents treated with SSRIs may be at a small increased risk of developing T2D, particularly publicly insured patients, but the magnitude of association was weaker than previous thought and much smaller than other known risk factors for T2DM, such as obesity, race, and poverty,” lead investigator Jenny Sun, PhD, said in an interview.

“When weighing the known benefits and risks of SSRI treatment in children and adolescents, our findings provide reassurance that the risk of T2DM is not as substantial as initially reported,” said Dr. Sun, a postdoctoral research fellow in the department of population medicine at Harvard Medical School’s Harvard Pilgrim Health Care Institute, Boston.

The study was published online Sept. 2 in JAMA Psychiatry.

Limited evidence

Previous research suggested that SSRIs increase the risk of T2D by up to 90% in children and adolescents.

However, the investigators noted, the study reporting this finding was too small to draw conclusions about the SSRI class as a whole also did not examine specific SSRIs.

In addition, although “several studies have reported that antidepressant use may be a risk factor for T2D in adults, evidence was limited in children and adolescents,” said Dr. Sun.

“Rapid changes in growth during childhood and adolescents can alter drugs’ pharmacokinetics and pharmacodynamics, so high-quality, age-specific data are needed to inform prescribing decisions,” she said.

For the current study, the researchers analyzed claims data on almost 1.6 million patients aged 10-19 years (58.3% female; mean age, 15.1 years) from two large claims databases.

The analysis focused on those with a diagnosis warranting treatment with an SSRI, including depression, generalized or social anxiety disorder, obsessive compulsive disorder, PTSD, panic disorder, or bulimia nervosa.

The Medicaid Analytic Extract database consisted of 316,178 patients insured through Medicaid or the Children’s Health Insurance Program. The IBM MarketScan database consisted of 211,460 privately insured patients. Patients were followed up for a mean of 2.3 and 2.2 years, respectively.

Patients who initiated SSRI treatment were compared with those with a similar indication but who were not taking an SSRI. Secondary analyses compared new SSRI users with patients who recently initiated treatment with bupropion, which has no metabolic side effects, or with patients who recently initiated psychotherapy.

“In observational data, it is difficult to mimic a placebo group, often used in RCTs [randomized, controlled trials], therefore several comparator groups were explored to broaden our understanding,” said Dr. Sun.

In addition, the researchers compared the individual SSRI medications, using fluoxetine as a comparator.

A wide range of more than 100 potential confounders or “proxies of confounders,” were taken into account, including demographic characteristics, psychiatric diagnoses, metabolic conditions, concomitant medications, and use of health care services.

The researchers conducted two analyses. They included an intention-to-treat (ITT) analysis that was restricted to patients with one or more additional SSRI prescriptions during the 6 months following the index exposure assessment period.

 

 

Close monitoring required

An as-treated analysis estimated the association of continuous SSRI treatment (vs. untreated, bupropion treatment, and psychotherapy), with adherence assessed at 3-month intervals.

Initiation and continuation of SSRI treatment in publicly insured patients were both associated with a considerably higher risk of T2D, compared with untreated patients, and a steeper risk, compared with their privately insured counterparts.

For newly treated publicly insured patients initiated on SSRI treatment, the ITT adjusted hazard ratio was 1.13 (95% confidence interval, 1.04-1.22).

There was an even stronger association among continuously treated publicly insured patients, with an as-treated aHR of 1.33 (95% CI, 1.21-1.47). The authors noted that this corresponds to 6.6 additional T2D cases per 10,000 patients continuously treated for at least 2 years.

The association was weaker in privately insured patients (ITT aHR, 1.01; 95% CI, 0.84-1.23; as-treated aHR, 1.10; 95% CI, 0.88-1.36).

The secondary analyses yielded similar findings: When SSRI treatment was compared with psychotherapy, the as-treated aHR for publicly insured patients was 1.44 (95% CI, 1.25-1.65), whereas the aHR for privately insured patients was lower at 1.21 (95% CI, 0.93-1.57)

The investigators found no increased risk when SSRIs were compared with bupropion, and the within-class analysis showed that none of the SSRIs carried an increased hazard of T2D, compared with fluoxetine.

“Publicly insured patients are enrolled in Medicaid and the Children’s Health Insurance Program, whereas privately insured patients are generally covered by their parent’s employer-sponsored insurance,” said Dr. Sun.

“Publicly insured patients are of lower socioeconomic status and represent a population with greater overall medical burden, more comorbidities, and a higher prevalence of risk factors for T2D, such as obesity, at the time of treatment initiation,” she said.

She added that high-risk children and youth should be closely monitored and clinicians should also consider recommending dietary modifications and increased exercise to offset T2D risk.

Useful ‘real-world data’

William Cooper, MD, MPH, professor of pediatrics and health policy at Vanderbilt University Medical Center in Nashville, Tenn., said that the study “provides a fascinating look at risks of SSRI medications in children and adolescents.”

Dr. Cooper, who was not involved with the study, said that the authors “draw from real-world data representing two different populations and carefully consider factors which might confound the associations.”

The results, he said, “provide important benefits for patients, families, and clinicians as they weigh the risks and benefits of using SSRIs for children who need treatment for depression and anxiety disorders.

“As a pediatrician, I would find these results useful as I work with my patients, their families, and behavioral health colleagues in making important treatment decisions.”

The study was supported by a training grant from the program in pharmacoepidemiology at the Harvard School of Public Health. Dr. Sun disclosed no relevant financial relationships. Dr. Cooper disclosed no relevant financial relationships.

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

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Anorexia nervosa and COVID-19

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Anorexia nervosa and COVID-19

Recent concerns surrounding coronavirus disease 2019 (COVID-19) make it timely to reexamine the complex findings related to eating disorders and the immune system, and the risks for and detection of infection in patients with anorexia nervosa (AN) and similar disorders. To date, there are no published studies evaluating patients with eating disorders and COVID-19. However, it may be helpful to review the data on the infectious process in this patient population to improve patient communication, enhance surveillance and detection, and possibly reduce morbidity and mortality.

The Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) issued warnings that individuals who are older, have underlying medical conditions, and/or are immunocompromised face the greatest risk of serious complications and death as a result of COVID-19, the disease process caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Due to malnutrition, patients with eating disorders, especially AN, may be perceived to have an increased risk of medical conditions and infection. Despite many studies on specific changes and differences in the immune system of patients with eating disorders, the consequences of these changes remain controversial and inconclusive.

This article reviews research on eating disorders, focusing on published data regarding the effects of AN on the immune system, susceptibility to infections, infectious detection, and morbidity. We also discuss clinical considerations related to COVID-19 and patients with AN.

 

Infection risks: Conflicting data

In a 1981 study that included 9 participants, Golla et al1 concluded that patients with AN may have “resistance” to infections based on a suggested protective factor within the immune system of these patients. Because this study has been cited repeatedly in multiple articles about AN and cell-mediated immunity,2-7 some clinicians have accepted this evidence of resistance to infection in patients with AN, which may lower their suspicion for and detection of infections in patients with AN.

However, studies published both before and after Golla et al1 have shown statistically significant results that contradict those researchers’ conclusion. A study that compared the medical records of 68 patients with AN with those who did not have AN found no significant difference, and concluded that the rate of infection among patients with AN is the same as among controls.8 These researchers noted that infection rates may be higher among patients with later-stage, more severe AN. In a 1986 study of 12 patients with AN, Cason et al9 concluded that while cellular immunity function is abnormal in patients with AN, their results were not compatible with prior studies that suggested AN patients were more resistant to infection.1,2,8

More recently, researchers compared 1,592 patients with eating disorders with 6,368 matched controls; they reviewed prescriptions of antibacterial, antifungal, and antiviral medications as a measure of infection rates.10 Compared with controls, patients with binge eating disorder (BED), patients with bulimia nervosa (BN), and males with AN more often received prescriptions for antimicrobial medications. There was no statistically significant difference between controls and females with AN, which is consistent with other reports of no increased or decreased risk of infection among females with AN. In terms of antiviral use, this study showed an increased prescription of antivirals only in the BN group.

Several other studies examining the rate of infection in patients with AN concluded that there is neither an increased nor decreased rate of infection in patients with AN, and that the rate of infection in this population is similar to that of the general population.8,10-12 Because studies that have included patients with AN have evaluated only symptomatic viral infections, some researchers have proposed that patients with AN may show lower rates of symptomatic viral infection but higher rates of asymptomatic infection, as evidenced by higher viral titers.6 Further research is required. Despite controversy regarding infection rates, studies have found that patients with AN have increased rates of morbidity and mortality from infections.6,12-16

Continue to: Obstacles to detecting infections

 

 

Obstacles to detecting infections

Several factors can complicate the surveillance and detection of infections in patients with eating disorders, especially those with AN. These include:

  • an accepted predisposition to infection secondary to malnutrition
  • a lack of visual or reported infectious symptoms
  • misrepresentation and assumptions from published research.

Clinicians who report fewer observed cases of infections among patients with AN may be overlooking comorbid disease processes due to a bias from the literature and/or a lack of awareness of symptom parameters in patients with AN.

Features of AN include a loss of adipose tissue responsible for pro-inflammatory cytokines, and excessive exercise, which stimulates anti-inflammatory myokines. This can modulate the experience of illness that impacts the core features of disease,17 possibly reducing symptomatic presentation of infections.

Fever. The presence and intensity of fever may be altered in patients with eating disorders, especially those with AN. In a study of 311 inpatients with AN, researchers found that patients with AN had a significant delay in fever response in AN.12 Of 23 patients with an active bacterial infection, all but 5 had a fever <37°C, with some as low as 35.5°C. A detectable fever response and unexplained fevers were found in 2 of the 6 patients with a viral infection. A series of case studies found that patients with AN with bacterial infections also had a delayed fever response.18

For patients with infections that commonly present with fever, such as COVID-19, a delayed fever response can delay or evade the detection of infection, thus increasing potential complications as well viral exposure to others. Thus, clinicians should use caution when ruling out COVID-19 or other infections because of a lack of significant fever.

Continue to: Overlapping symptoms

 

 

Overlapping symptoms. The symptoms of viral infection can mimic the symptoms of AN, which further complicates screening and diagnosis of infection in these patients. Although up to 80% of individuals infected with COVID-19 may be asymptomatic or have a mild presentation, the most common reported symptoms are fever (92.6%), shortness of breath (50.8%), expectoration (41.4%), fatigue (46.4%), dry cough (33.3%), and myalgia (21.4%).19-21 Gastrointestinal (GI) symptoms have been reported in patients with COVID-19, as well as a loss of taste and smell.

Commonly reported physical symptoms of AN include an intolerance to cold, general fatigue, muscle aches and pains, restlessness, emesis, and a multitude of GI complaints. Patients with AN also have been reported to experience shortness of breath due to conditions such as respiratory muscle weakness,22 nutritional emphysema,23 and anxiety and panic attack.24 These conditions could lead to an increased susceptibility to COVID-19 and increased complications during treatment. Cardiac abnormalities, which are common in patients with AN and BN, may increase the risk of adverse events. While these symptoms may be an important part of screening for diseases such as COVID-19, suspicion of infection also may be lower because of the overlap of AN symptomology, underlying conditions, and a delayed fever response.

Laboratory findings. Laboratory testing results for patients with COVID-19 include lower lymphocyte counts, higher leukocyte counts, elevated levels of infection-related biomarkers and inflammatory cytokines, and significantly decreased T-cell counts.19 Similar values are also found in patients with AN.

The similar clinical presentations and laboratory values of AN and COVID-19 could lead to delayed diagnosis, increased disease transmission, cross-contamination of facilities, and higher incidences of medical complications and mortality.

The immunology of AN and correlations with COVID-19

Many studies examining the immune system of patients with eating disorders, especially those with AN, have discovered changes and differences in both cell-mediated and humoral response to infections.1,3,5,7,9,11,16,21,25-27 Whether these differences represent a dysfunctional immune system, an immunocompromised state, or even a protective factor remains unclear.

Continue to: While some studies have reported...

 

 

While some studies have reported that AN represents an immunocompromised state, others describe the immune system of patients with AN as dysfunctional or simply altered.9,11,22,28 Some studies have found that patients with AN had delayed reactions to pathogen skin exposures compared with healthy controls, which provides evidence of an impaired cell-mediated immune system.9,27,29

Some studies have considered the consequences of infection and immunologic findings as markers of or contributing to the onset of AN.2,30,31 Numerous studies have noted abnormalities in AN with regards to cell-mediated immunity, the humoral system, the lymphoreticular system, and the innate immune system, and potential contributions from increased oxidative stress, a chronically activated sympathetic nervous system and hypothalamic-pituitary-adrenal axis, altered intestinal microbiota, and an abnormal bone marrow microenvironment.2

Box 1

The immunology of COVID-19

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new beta-coronavirus that is still being studied for its effects on the immune system. It may take years to fully understand the nature of the pathogen and the response of the human immune system. To better understand COVID19, researchers have been turning to what they learned from the past outbreaks of severe acute respiratory syndrome (SARS) in 2003- 2004 and Middle East respiratory syndrome (MERS) in 2011, both caused by betacoronaviruses with a zoonotic origin.25,32

The proposed pathogenesis for infection of SARS-CoV-2 is similar to SARS and occurs when aerosolized droplets containing the virus enter the host.32 While currently there is only initial data on the host innate immune status of patients infected with SARS-CoV-2, initial findings of a report on 99 cases in Wuhan, China included increased total neutrophils (38%), reduced total lymphocytes (35%), increased serum interleukin-6 (52%), and increased C-reactive protein (84%).33 Additional findings were decreased percentages of monocytes, eosinophils, and basophils, as well as significantly decreased levels of cytokines and T-cells in more severe cases.19 Past research with SARS reported similar T-cell findings, with a more frequent CD8+ response and a greater magnitude of CD4+.34

Box 119,25,32-34 describes some of the initial immunologic findings reported in patients with COVID-19. In Box 2,5,8,11,13,14,19,26,28,35-40 we discuss reports that describe the immunologic overlay of COVID-19 and AN.

Box 2

The immunologic overlay of COVID-19 and anorexia nervosa

Leukopenia (low leukocyte levels) is a common finding in patients with anorexia nervosa (AN),8 and often leads clinicians to lower their suspicion for infection. A 2008 Hungarian study that evaluated lymphocyte activation parameters and clinical status in 11 adolescents (10 girls and 1 boy) with AN, 12 obese adolescents, and 10 healthy controls did not find any association between the variables.35 While many studies have focused on adults, it is important to note that leukopenia is a common finding in adolescents (age 12 to 17) with AN.36

Leukocyte counts are elevated in coronavirus disease 2019 (COVID-19), possibly offsetting AN’s leukopenia. In addition, neutrophil counts are elevated and monocyte, eosinophil, basophil, and especially lymphocyte counts are significantly decreased. A meta-analysis that included 22 studies and 924 participants (512 with AN and 412 controls) examined common inflammatory cytokine findings in patients with AN.11 Compared with healthy controls, patients with AN had significantly elevated levels of tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1, IL-6, and TNF-receptor II, and significantly decreased levels of C-reactive protein and IL-6 receptor. Elevated levels of TNF-alpha and IL-6 also have been reported in patients with COVID-19.19 These findings may mask suspicion for infection in patients with AN.19

In patients with AN and those with bulimia nervosa, CD4+-to-CD8+ ratios also have been found to be low as a result of normal-tohigher levels of CD4+ cells and lower levels of CD8+ cells.36-39 Researchers have also proposed that the lymphocytosis observed in AN is a result of increased naïve CD4+.36 In AN, total lymphocyte counts have been found to correlate positively with a patient’s body mass index (BMI), while the CD4+ T-lymphocyte correlated negatively with BMI and were critically low in patients with severe malnutrition.26,40 In patients with COVID-19, CD4+ levels have reported to be within normal range, naïve CD4+ cells were elevated, and CD8+ cells were slightly decreased,19 which is similar to the findings in AN.

Fewer studies have evaluated humoral immune response in AN, and results have varied. One study (N = 46) found elevated B-cell counts in adolescents with AN-restricting type,36 while another (N = 40) reported normal levels of B-cells.5 Specific decreases in immunoglobulin (Ig) G and IgM have also been reported in AN, while IgA, IgG, and IgM usually are normal in COVID-19.19

Despite differences in immune system function, cellular immunity appears to remain relatively intact in patients with AN, but can become compromised with severe malnutrition or with advanced weight loss.28,40 This compromised immunity related to severe AN with a very low BMI likely leads to the increased morbidity and mortality.8,13,14

Malnutrition and the immune system

Differences in the type of malnutrition observed in low-weight patients with AN may help explain why patients with AN can maintain a relatively intact cell-mediated immune system.1 Protein-energy malnutrition (PEM), which is found in typical states of starvation, consists of deficiencies in multiple vitamins, protein, and energy (caloric content), whereas the dietary habits of patients with AN usually result in a deficiency of carbohydrates and fats.41 Studies that examined the impact of PEM on immunity to influenza infection have suggested that balanced protein energy replenishment may be a strategy for boosting immunity against influenza viral infections.42 However, carbohydrates are the primary nutrients for human bone marrow fat cells, which play a crucial role in the maturation of white blood cells. This may account for the leukopenia that is common in patients with AN.6,43 The protein-sparing aspect of the typical AN diet may account for the immune system changes observed in patients with AN.44

Although some studies have proposed that immune deficiencies observed in patients with AN are secondary to malnutrition and return to normal with refeeding,5,40,45 others have concluded that immune function is not compromised by factors such as nutritional status or body weight in AN.26,43,46

Continue to: Clinical considerations

 

 

Clinical considerations

Neither the CDC nor the WHO have issued a specific protocol for monitoring for and treating COVID-19 in patients with eating disorders; however, the guidelines offered by these organizations for the general population should be followed for patients with eating disorders.

When screening a patient with an eating disorder, keep in mind that the symptoms of eating disorders, such as AN, may mimic an infectious process. Mood symptoms, such as depression or anxiety, could represent physiological responses to infection. Patients with GI symptoms that typically are considered part of the pathology of an eating disorder should be more carefully considered for COVID-19. Monitor a patient’s basal body temperature, and be mindful that a patient with AN may exhibit a delayed fever response. Be vigilant for a recent loss of taste or smell, which should raise suspicion for COVID-19. When monitoring vital signs, pay careful attention for any decompensation in a patient’s pulse oximetry. Whenever possible, order COVID-19 testing for any patient you suspect may be infected.

Outpatient clinicians should work closely in a collaborative manner with a patient’s eating disorder treatment team. Psychiatrists, primary care physicians, psychotherapists, nutritionists, and other clinicians should all follow CDC/WHO guidelines regarding COVID-19, provide surveillance, and communicate any suspicions to the medical team. Eating disorder treatment programs, including residential centers, partial hospital programs (PHP), and intensive outpatient programs (IOP), must enhance monitoring for COVID-19, and exercise caution by practicing social distancing and providing adequate personal protective equipment for patients and staff. To reduce the spread of COVID-19, many IOPs and PHPs have transitioned to virtual treatment. Residential centers must carefully screen patients before admission to weigh the risks and benefits of inpatient vs outpatient care.

 

Bottom Line

Differences in the immune system of patients with an eating disorder do not necessarily confer a higher or lower risk of infection. Symptoms of some infections can mimic the symptoms of anorexia nervosa. Recognizing infections in patients with eating disorders is critical because compared with the general population, they have higher rates of infection-related morbidity and mortality.

Related Resources

References

1. Golla JA, Larson LA, Anderson CF, et al. An immunological assessment of patients with anorexia nervosa. Am J Clin Nutr. 1981;34(12):2756-2762.
2. Gibson D, Mehler PS. Anorexia nervosa and the immune system—a narrative review. J Clin Med. 2019;8(11):1915. doi: 10.3390/jcm8111915.
3. Słotwin´ska SM, Słotwin´ska R. Immune disorders in anorexia. Cent Eur J Immunol. 2017;42(3):294-300.
4. Nova E, Samartín S, Gómez S, et al. The adaptive response of the immune system to the particular malnutrition of eating disorders. Eur J Clin Nutr. 2002;56(suppl 3):S34-S37.
5. Allende LM, Corell A, Manzanares J, et al. Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding. Immunology. 1998;94(4):543-551.
6. Brown RF, Bartrop R, Birmingham CL. Immunological disturbance and infectious disease in anorexia nervosa: a review. Acta Neuropsychiatr. 2008;20(3):117-128.
7. Polack E, Nahmod VE, Emeric-Sauval E, et al. Low lymphocyte interferon-gamma production and variable proliferative response in anorexia nervosa patients. J Clin Immunol. 1993;13(6):445-451.
8. Bowers TK, Eckert E. Leukopenia in anorexia nervosa. Lack of increased risk of infection. Arch Intern Med. 1978;138(10):1520-1523.
9. Cason J, Ainley CC, Wolstencroft RA, et al. Cell-mediated immunity in anorexia nervosa. Clin Exp Immunol. 1986;64(2):370-375.
10. Raevuori A, Lukkariniemi L, Suokas JT, et al. Increased use of antimicrobial medication in bulimia nervosa and binge-eating disorder prior to the eating disorder treatment. Int J Eat Disord. 2016;49(6):542-552.
11. Solmi M, Veronese N, Favaro A, et al. Inflammatory cytokines and anorexia nervosa: a meta-analysis of cross-sectional and longitudinal studies. Psychoneuroendocrinology. 2015;51:237-252.
12. Brown RF, Bartrop R, Beumont P, et al. Bacterial infections in anorexia nervosa: delayed recognition increases complications. Int J Eat Disord. 2005;37(3):261-265.
13. Theander S. Anorexia nervosa. A psychiatric investigation of 94 female patients. Acta Psychiatr Scand Suppl. 1970;214:1-194.
14. Warren MP, Vande Wiele RL. Clinical and metabolic features of anorexia nervosa. Am J Obstet Gynecol. 1973;117(3):435-449.
15. Copeland PM, Herzog DB. Hypoglycemia and death in anorexia nervosa. Psychother Psychosom. 1987;48(1-4):146-150.
16. Devuyst O, Lambert M, Rodhain J, et al. Haematological changes and infectious complications in anorexia nervosa: a case-control study. Q J Med. 1993;86(12):791-799.
17. Pisetsky DS, Trace SE, Brownley KA, et al. The expression of cytokines and chemokines in the blood of patients with severe weight loss from anorexia nervosa: an exploratory study. Cytokine. 2014;69(1):110-115.
18. Birmingham CL, Hodgson DM, Fung J, et al. Reduced febrile response to bacterial infection in anorexia nervosa patients. Int J Eat Disord. 2003;34(2):269-272.
19. Qin C, Zhou L, Hu Z, et al. Dysregulation of immune response in patients with COVID-19 in Wuhan, China [published online March 12, 2020]. Clin Infect Dis. doi: 10.1093/cid/ciaa248.
20. Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497-506.
21. Chan JF, Yuan S, Kok KH, et al. A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-to-person transmission: a study of a family cluster. Lancet. 2020;395(10223):514-523.
22. Birmingham CL, Tan AO. Respiratory muscle weakness and anorexia nervosa. Int J Eat Disord. 2003;33(2):230-233.
23. Cook VJ, Coxson HO, Mason AG, et al. Bullae, bronchiectasis and nutritional emphysema in severe anorexia nervosa. Can Respir J. 2001;8(5):361-365.
24. Khalsa SS, Hassanpour MS, Strober M, et al. Interoceptive anxiety and body representation in anorexia nervosa [published online September 21, 2018]. Front Psychiatry. 2018;9:444. doi: 10.3389/fpsyt.2018.00444.
25. van West D, Maes M. Cytokines in de obsessief compulsieve stoornis en in anorexia nervosa: een overzicht. Acta Neuropsychiatr. 1999;11(4):125-129.
26. Komorowska-Pietrzykowska R, Rajewski A, Wiktorowicz K, et al. Czynnos´c´ układu immunologicznego w jadłowstrecie psychicznym [Immunological system activity in anorexia nervosa]. Psychiatr Pol. 1996;30(5):801‐810.
27. Marcos A, Varela P, Toro O, et al. Interactions between nutrition and immunity in anorexia nervosa: a 1-y follow-up study. Am J Clin Nutr. 1997;66(2):485S-490S.
28. Pertschuk MJ, Crosby LO, Barot L, et al. Immunocompetency in anorexia nervosa. Am J Clin Nutr. 1982;35(5):968-972.
29. Varela P, Marcos A, Navarro MP. Zinc status in anorexia nervosa. Ann Nutr Metab. 1992;36(4):197-202.
30. Breithaupt L, Köhler-Forsberg O, Larsen JT, et al. Association of exposure to infections in childhood with risk of eating disorders in adolescent girls. JAMA Psychiatry. 2019;76(8):800-809.
31. Brambilla F, Monti D, Franceschi C. Plasma concentrations of interleukin-1-beta, interleukin-6 and tumor necrosis factor-alpha, and of their soluble receptors and receptor antagonist in anorexia nervosa. Psychiatry Res. 2001;103(2-3):107-114.
32. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: lessons learned from SARS and MERS epidemic [published online February 27, 2020]. Asian Pac J Allergy Immunol. doi: 10.12932/AP-200220-0772.
33. Zhou P, Yang XL, Wang XG, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature. 2020;579(7798):270-273.
34. Li CK, Wu H, Yan H, et al. T cell responses to whole SARS coronavirus in humans. J Immunol. 2008;181(8):5490-5500.
35. Páli AA, Pászthy B. Az immunrendszer muködésének megváltozása a táplálkozási magatartás zavarai esetén [Changes of the immune functions in patients with eating disorders]. Ideggyogy Sz. 2008;61(11-12):381‐384.
36. Elegido A, Graell M, Andrés P, et al. Increased naive CD4+ and B lymphocyte subsets are associated with body mass loss and drive relative lymphocytosis in anorexia nervosa patients. Nutr Res. 2017;39:43-50.
37. Marcos A, Varela P, Santacruz I, et al. Nutritional status and immunocompetence in eating disorders. A comparative study. Eur J Clin Nutr. 1993;47(11):787-793.
38. Mustafa A, Ward A, Treasure J, et al. T lymphocyte subpopulations in anorexia nervosa and refeeding. Clin Immunol Immunopathol. 1997;82(3):282-289.
39. Nagata T, Kiriike N, Tobitani W, et al. Lymphocyte subset, lymphocyte proliferative response, and soluble interleukin-2 receptor in anorexic patients. Biol Psychiatry. 1999;45(4):471-474.
40. Saito H, Nomura K, Hotta M, et al. Malnutrition induces dissociated changes in lymphocyte count and subset proportion in patients with anorexia nervosa. Int J Eat Disord. 2007;40(6):575-579.
41. Nova E, Varela P, López-Vidriero I, et al. A one-year follow-up study in anorexia nervosa. Dietary pattern and anthropometrical evolution. Eur J Clin Nutr. 2001;55(7):547-554.
42. Taylor AK, Cao W, Vora KP, et al. Protein energy malnutrition decreases immunity and increases susceptibility to influenza infection in mice. J Infect Dis. 2013;207(3):501-510.
43. Mant MJ, Faragher BS. The hematology of anorexia nervosa. Br J Haematol. 1972;23(6):737-749.
44. Marcos A. The immune system in eating disorders: an overview. Nutrition. 1997;13(10):853-862.
45. Schattner A, Tepper R, Steinbock M, et al. TNF, interferon-gamma and cell-mediated cytotoxicity in anorexia nervosa; effect of refeeding. J Clin Lab Immunol. 1990;32(4):183-184.
46. Nagata T, Tobitani W, Kiriike N, et al. Capacity to produce cytokines during weight restoration in patients with anorexia nervosa. Psychosom Med. 1999;61(3):371-377.

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Medical Director
ED-180 Treatment Programs
Garden City, New York

Lukas DeSarbo, LMSW
Staff Psychotherapist
ED-180 Treatment Programs
Garden City, New York

Disclosures
The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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Jeffrey R. DeSarbo, DO
Medical Director
ED-180 Treatment Programs
Garden City, New York

Lukas DeSarbo, LMSW
Staff Psychotherapist
ED-180 Treatment Programs
Garden City, New York

Disclosures
The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Author and Disclosure Information

Jeffrey R. DeSarbo, DO
Medical Director
ED-180 Treatment Programs
Garden City, New York

Lukas DeSarbo, LMSW
Staff Psychotherapist
ED-180 Treatment Programs
Garden City, New York

Disclosures
The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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Recent concerns surrounding coronavirus disease 2019 (COVID-19) make it timely to reexamine the complex findings related to eating disorders and the immune system, and the risks for and detection of infection in patients with anorexia nervosa (AN) and similar disorders. To date, there are no published studies evaluating patients with eating disorders and COVID-19. However, it may be helpful to review the data on the infectious process in this patient population to improve patient communication, enhance surveillance and detection, and possibly reduce morbidity and mortality.

The Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) issued warnings that individuals who are older, have underlying medical conditions, and/or are immunocompromised face the greatest risk of serious complications and death as a result of COVID-19, the disease process caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Due to malnutrition, patients with eating disorders, especially AN, may be perceived to have an increased risk of medical conditions and infection. Despite many studies on specific changes and differences in the immune system of patients with eating disorders, the consequences of these changes remain controversial and inconclusive.

This article reviews research on eating disorders, focusing on published data regarding the effects of AN on the immune system, susceptibility to infections, infectious detection, and morbidity. We also discuss clinical considerations related to COVID-19 and patients with AN.

 

Infection risks: Conflicting data

In a 1981 study that included 9 participants, Golla et al1 concluded that patients with AN may have “resistance” to infections based on a suggested protective factor within the immune system of these patients. Because this study has been cited repeatedly in multiple articles about AN and cell-mediated immunity,2-7 some clinicians have accepted this evidence of resistance to infection in patients with AN, which may lower their suspicion for and detection of infections in patients with AN.

However, studies published both before and after Golla et al1 have shown statistically significant results that contradict those researchers’ conclusion. A study that compared the medical records of 68 patients with AN with those who did not have AN found no significant difference, and concluded that the rate of infection among patients with AN is the same as among controls.8 These researchers noted that infection rates may be higher among patients with later-stage, more severe AN. In a 1986 study of 12 patients with AN, Cason et al9 concluded that while cellular immunity function is abnormal in patients with AN, their results were not compatible with prior studies that suggested AN patients were more resistant to infection.1,2,8

More recently, researchers compared 1,592 patients with eating disorders with 6,368 matched controls; they reviewed prescriptions of antibacterial, antifungal, and antiviral medications as a measure of infection rates.10 Compared with controls, patients with binge eating disorder (BED), patients with bulimia nervosa (BN), and males with AN more often received prescriptions for antimicrobial medications. There was no statistically significant difference between controls and females with AN, which is consistent with other reports of no increased or decreased risk of infection among females with AN. In terms of antiviral use, this study showed an increased prescription of antivirals only in the BN group.

Several other studies examining the rate of infection in patients with AN concluded that there is neither an increased nor decreased rate of infection in patients with AN, and that the rate of infection in this population is similar to that of the general population.8,10-12 Because studies that have included patients with AN have evaluated only symptomatic viral infections, some researchers have proposed that patients with AN may show lower rates of symptomatic viral infection but higher rates of asymptomatic infection, as evidenced by higher viral titers.6 Further research is required. Despite controversy regarding infection rates, studies have found that patients with AN have increased rates of morbidity and mortality from infections.6,12-16

Continue to: Obstacles to detecting infections

 

 

Obstacles to detecting infections

Several factors can complicate the surveillance and detection of infections in patients with eating disorders, especially those with AN. These include:

  • an accepted predisposition to infection secondary to malnutrition
  • a lack of visual or reported infectious symptoms
  • misrepresentation and assumptions from published research.

Clinicians who report fewer observed cases of infections among patients with AN may be overlooking comorbid disease processes due to a bias from the literature and/or a lack of awareness of symptom parameters in patients with AN.

Features of AN include a loss of adipose tissue responsible for pro-inflammatory cytokines, and excessive exercise, which stimulates anti-inflammatory myokines. This can modulate the experience of illness that impacts the core features of disease,17 possibly reducing symptomatic presentation of infections.

Fever. The presence and intensity of fever may be altered in patients with eating disorders, especially those with AN. In a study of 311 inpatients with AN, researchers found that patients with AN had a significant delay in fever response in AN.12 Of 23 patients with an active bacterial infection, all but 5 had a fever <37°C, with some as low as 35.5°C. A detectable fever response and unexplained fevers were found in 2 of the 6 patients with a viral infection. A series of case studies found that patients with AN with bacterial infections also had a delayed fever response.18

For patients with infections that commonly present with fever, such as COVID-19, a delayed fever response can delay or evade the detection of infection, thus increasing potential complications as well viral exposure to others. Thus, clinicians should use caution when ruling out COVID-19 or other infections because of a lack of significant fever.

Continue to: Overlapping symptoms

 

 

Overlapping symptoms. The symptoms of viral infection can mimic the symptoms of AN, which further complicates screening and diagnosis of infection in these patients. Although up to 80% of individuals infected with COVID-19 may be asymptomatic or have a mild presentation, the most common reported symptoms are fever (92.6%), shortness of breath (50.8%), expectoration (41.4%), fatigue (46.4%), dry cough (33.3%), and myalgia (21.4%).19-21 Gastrointestinal (GI) symptoms have been reported in patients with COVID-19, as well as a loss of taste and smell.

Commonly reported physical symptoms of AN include an intolerance to cold, general fatigue, muscle aches and pains, restlessness, emesis, and a multitude of GI complaints. Patients with AN also have been reported to experience shortness of breath due to conditions such as respiratory muscle weakness,22 nutritional emphysema,23 and anxiety and panic attack.24 These conditions could lead to an increased susceptibility to COVID-19 and increased complications during treatment. Cardiac abnormalities, which are common in patients with AN and BN, may increase the risk of adverse events. While these symptoms may be an important part of screening for diseases such as COVID-19, suspicion of infection also may be lower because of the overlap of AN symptomology, underlying conditions, and a delayed fever response.

Laboratory findings. Laboratory testing results for patients with COVID-19 include lower lymphocyte counts, higher leukocyte counts, elevated levels of infection-related biomarkers and inflammatory cytokines, and significantly decreased T-cell counts.19 Similar values are also found in patients with AN.

The similar clinical presentations and laboratory values of AN and COVID-19 could lead to delayed diagnosis, increased disease transmission, cross-contamination of facilities, and higher incidences of medical complications and mortality.

The immunology of AN and correlations with COVID-19

Many studies examining the immune system of patients with eating disorders, especially those with AN, have discovered changes and differences in both cell-mediated and humoral response to infections.1,3,5,7,9,11,16,21,25-27 Whether these differences represent a dysfunctional immune system, an immunocompromised state, or even a protective factor remains unclear.

Continue to: While some studies have reported...

 

 

While some studies have reported that AN represents an immunocompromised state, others describe the immune system of patients with AN as dysfunctional or simply altered.9,11,22,28 Some studies have found that patients with AN had delayed reactions to pathogen skin exposures compared with healthy controls, which provides evidence of an impaired cell-mediated immune system.9,27,29

Some studies have considered the consequences of infection and immunologic findings as markers of or contributing to the onset of AN.2,30,31 Numerous studies have noted abnormalities in AN with regards to cell-mediated immunity, the humoral system, the lymphoreticular system, and the innate immune system, and potential contributions from increased oxidative stress, a chronically activated sympathetic nervous system and hypothalamic-pituitary-adrenal axis, altered intestinal microbiota, and an abnormal bone marrow microenvironment.2

Box 1

The immunology of COVID-19

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new beta-coronavirus that is still being studied for its effects on the immune system. It may take years to fully understand the nature of the pathogen and the response of the human immune system. To better understand COVID19, researchers have been turning to what they learned from the past outbreaks of severe acute respiratory syndrome (SARS) in 2003- 2004 and Middle East respiratory syndrome (MERS) in 2011, both caused by betacoronaviruses with a zoonotic origin.25,32

The proposed pathogenesis for infection of SARS-CoV-2 is similar to SARS and occurs when aerosolized droplets containing the virus enter the host.32 While currently there is only initial data on the host innate immune status of patients infected with SARS-CoV-2, initial findings of a report on 99 cases in Wuhan, China included increased total neutrophils (38%), reduced total lymphocytes (35%), increased serum interleukin-6 (52%), and increased C-reactive protein (84%).33 Additional findings were decreased percentages of monocytes, eosinophils, and basophils, as well as significantly decreased levels of cytokines and T-cells in more severe cases.19 Past research with SARS reported similar T-cell findings, with a more frequent CD8+ response and a greater magnitude of CD4+.34

Box 119,25,32-34 describes some of the initial immunologic findings reported in patients with COVID-19. In Box 2,5,8,11,13,14,19,26,28,35-40 we discuss reports that describe the immunologic overlay of COVID-19 and AN.

Box 2

The immunologic overlay of COVID-19 and anorexia nervosa

Leukopenia (low leukocyte levels) is a common finding in patients with anorexia nervosa (AN),8 and often leads clinicians to lower their suspicion for infection. A 2008 Hungarian study that evaluated lymphocyte activation parameters and clinical status in 11 adolescents (10 girls and 1 boy) with AN, 12 obese adolescents, and 10 healthy controls did not find any association between the variables.35 While many studies have focused on adults, it is important to note that leukopenia is a common finding in adolescents (age 12 to 17) with AN.36

Leukocyte counts are elevated in coronavirus disease 2019 (COVID-19), possibly offsetting AN’s leukopenia. In addition, neutrophil counts are elevated and monocyte, eosinophil, basophil, and especially lymphocyte counts are significantly decreased. A meta-analysis that included 22 studies and 924 participants (512 with AN and 412 controls) examined common inflammatory cytokine findings in patients with AN.11 Compared with healthy controls, patients with AN had significantly elevated levels of tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1, IL-6, and TNF-receptor II, and significantly decreased levels of C-reactive protein and IL-6 receptor. Elevated levels of TNF-alpha and IL-6 also have been reported in patients with COVID-19.19 These findings may mask suspicion for infection in patients with AN.19

In patients with AN and those with bulimia nervosa, CD4+-to-CD8+ ratios also have been found to be low as a result of normal-tohigher levels of CD4+ cells and lower levels of CD8+ cells.36-39 Researchers have also proposed that the lymphocytosis observed in AN is a result of increased naïve CD4+.36 In AN, total lymphocyte counts have been found to correlate positively with a patient’s body mass index (BMI), while the CD4+ T-lymphocyte correlated negatively with BMI and were critically low in patients with severe malnutrition.26,40 In patients with COVID-19, CD4+ levels have reported to be within normal range, naïve CD4+ cells were elevated, and CD8+ cells were slightly decreased,19 which is similar to the findings in AN.

Fewer studies have evaluated humoral immune response in AN, and results have varied. One study (N = 46) found elevated B-cell counts in adolescents with AN-restricting type,36 while another (N = 40) reported normal levels of B-cells.5 Specific decreases in immunoglobulin (Ig) G and IgM have also been reported in AN, while IgA, IgG, and IgM usually are normal in COVID-19.19

Despite differences in immune system function, cellular immunity appears to remain relatively intact in patients with AN, but can become compromised with severe malnutrition or with advanced weight loss.28,40 This compromised immunity related to severe AN with a very low BMI likely leads to the increased morbidity and mortality.8,13,14

Malnutrition and the immune system

Differences in the type of malnutrition observed in low-weight patients with AN may help explain why patients with AN can maintain a relatively intact cell-mediated immune system.1 Protein-energy malnutrition (PEM), which is found in typical states of starvation, consists of deficiencies in multiple vitamins, protein, and energy (caloric content), whereas the dietary habits of patients with AN usually result in a deficiency of carbohydrates and fats.41 Studies that examined the impact of PEM on immunity to influenza infection have suggested that balanced protein energy replenishment may be a strategy for boosting immunity against influenza viral infections.42 However, carbohydrates are the primary nutrients for human bone marrow fat cells, which play a crucial role in the maturation of white blood cells. This may account for the leukopenia that is common in patients with AN.6,43 The protein-sparing aspect of the typical AN diet may account for the immune system changes observed in patients with AN.44

Although some studies have proposed that immune deficiencies observed in patients with AN are secondary to malnutrition and return to normal with refeeding,5,40,45 others have concluded that immune function is not compromised by factors such as nutritional status or body weight in AN.26,43,46

Continue to: Clinical considerations

 

 

Clinical considerations

Neither the CDC nor the WHO have issued a specific protocol for monitoring for and treating COVID-19 in patients with eating disorders; however, the guidelines offered by these organizations for the general population should be followed for patients with eating disorders.

When screening a patient with an eating disorder, keep in mind that the symptoms of eating disorders, such as AN, may mimic an infectious process. Mood symptoms, such as depression or anxiety, could represent physiological responses to infection. Patients with GI symptoms that typically are considered part of the pathology of an eating disorder should be more carefully considered for COVID-19. Monitor a patient’s basal body temperature, and be mindful that a patient with AN may exhibit a delayed fever response. Be vigilant for a recent loss of taste or smell, which should raise suspicion for COVID-19. When monitoring vital signs, pay careful attention for any decompensation in a patient’s pulse oximetry. Whenever possible, order COVID-19 testing for any patient you suspect may be infected.

Outpatient clinicians should work closely in a collaborative manner with a patient’s eating disorder treatment team. Psychiatrists, primary care physicians, psychotherapists, nutritionists, and other clinicians should all follow CDC/WHO guidelines regarding COVID-19, provide surveillance, and communicate any suspicions to the medical team. Eating disorder treatment programs, including residential centers, partial hospital programs (PHP), and intensive outpatient programs (IOP), must enhance monitoring for COVID-19, and exercise caution by practicing social distancing and providing adequate personal protective equipment for patients and staff. To reduce the spread of COVID-19, many IOPs and PHPs have transitioned to virtual treatment. Residential centers must carefully screen patients before admission to weigh the risks and benefits of inpatient vs outpatient care.

 

Bottom Line

Differences in the immune system of patients with an eating disorder do not necessarily confer a higher or lower risk of infection. Symptoms of some infections can mimic the symptoms of anorexia nervosa. Recognizing infections in patients with eating disorders is critical because compared with the general population, they have higher rates of infection-related morbidity and mortality.

Related Resources

Recent concerns surrounding coronavirus disease 2019 (COVID-19) make it timely to reexamine the complex findings related to eating disorders and the immune system, and the risks for and detection of infection in patients with anorexia nervosa (AN) and similar disorders. To date, there are no published studies evaluating patients with eating disorders and COVID-19. However, it may be helpful to review the data on the infectious process in this patient population to improve patient communication, enhance surveillance and detection, and possibly reduce morbidity and mortality.

The Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) issued warnings that individuals who are older, have underlying medical conditions, and/or are immunocompromised face the greatest risk of serious complications and death as a result of COVID-19, the disease process caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Due to malnutrition, patients with eating disorders, especially AN, may be perceived to have an increased risk of medical conditions and infection. Despite many studies on specific changes and differences in the immune system of patients with eating disorders, the consequences of these changes remain controversial and inconclusive.

This article reviews research on eating disorders, focusing on published data regarding the effects of AN on the immune system, susceptibility to infections, infectious detection, and morbidity. We also discuss clinical considerations related to COVID-19 and patients with AN.

 

Infection risks: Conflicting data

In a 1981 study that included 9 participants, Golla et al1 concluded that patients with AN may have “resistance” to infections based on a suggested protective factor within the immune system of these patients. Because this study has been cited repeatedly in multiple articles about AN and cell-mediated immunity,2-7 some clinicians have accepted this evidence of resistance to infection in patients with AN, which may lower their suspicion for and detection of infections in patients with AN.

However, studies published both before and after Golla et al1 have shown statistically significant results that contradict those researchers’ conclusion. A study that compared the medical records of 68 patients with AN with those who did not have AN found no significant difference, and concluded that the rate of infection among patients with AN is the same as among controls.8 These researchers noted that infection rates may be higher among patients with later-stage, more severe AN. In a 1986 study of 12 patients with AN, Cason et al9 concluded that while cellular immunity function is abnormal in patients with AN, their results were not compatible with prior studies that suggested AN patients were more resistant to infection.1,2,8

More recently, researchers compared 1,592 patients with eating disorders with 6,368 matched controls; they reviewed prescriptions of antibacterial, antifungal, and antiviral medications as a measure of infection rates.10 Compared with controls, patients with binge eating disorder (BED), patients with bulimia nervosa (BN), and males with AN more often received prescriptions for antimicrobial medications. There was no statistically significant difference between controls and females with AN, which is consistent with other reports of no increased or decreased risk of infection among females with AN. In terms of antiviral use, this study showed an increased prescription of antivirals only in the BN group.

Several other studies examining the rate of infection in patients with AN concluded that there is neither an increased nor decreased rate of infection in patients with AN, and that the rate of infection in this population is similar to that of the general population.8,10-12 Because studies that have included patients with AN have evaluated only symptomatic viral infections, some researchers have proposed that patients with AN may show lower rates of symptomatic viral infection but higher rates of asymptomatic infection, as evidenced by higher viral titers.6 Further research is required. Despite controversy regarding infection rates, studies have found that patients with AN have increased rates of morbidity and mortality from infections.6,12-16

Continue to: Obstacles to detecting infections

 

 

Obstacles to detecting infections

Several factors can complicate the surveillance and detection of infections in patients with eating disorders, especially those with AN. These include:

  • an accepted predisposition to infection secondary to malnutrition
  • a lack of visual or reported infectious symptoms
  • misrepresentation and assumptions from published research.

Clinicians who report fewer observed cases of infections among patients with AN may be overlooking comorbid disease processes due to a bias from the literature and/or a lack of awareness of symptom parameters in patients with AN.

Features of AN include a loss of adipose tissue responsible for pro-inflammatory cytokines, and excessive exercise, which stimulates anti-inflammatory myokines. This can modulate the experience of illness that impacts the core features of disease,17 possibly reducing symptomatic presentation of infections.

Fever. The presence and intensity of fever may be altered in patients with eating disorders, especially those with AN. In a study of 311 inpatients with AN, researchers found that patients with AN had a significant delay in fever response in AN.12 Of 23 patients with an active bacterial infection, all but 5 had a fever <37°C, with some as low as 35.5°C. A detectable fever response and unexplained fevers were found in 2 of the 6 patients with a viral infection. A series of case studies found that patients with AN with bacterial infections also had a delayed fever response.18

For patients with infections that commonly present with fever, such as COVID-19, a delayed fever response can delay or evade the detection of infection, thus increasing potential complications as well viral exposure to others. Thus, clinicians should use caution when ruling out COVID-19 or other infections because of a lack of significant fever.

Continue to: Overlapping symptoms

 

 

Overlapping symptoms. The symptoms of viral infection can mimic the symptoms of AN, which further complicates screening and diagnosis of infection in these patients. Although up to 80% of individuals infected with COVID-19 may be asymptomatic or have a mild presentation, the most common reported symptoms are fever (92.6%), shortness of breath (50.8%), expectoration (41.4%), fatigue (46.4%), dry cough (33.3%), and myalgia (21.4%).19-21 Gastrointestinal (GI) symptoms have been reported in patients with COVID-19, as well as a loss of taste and smell.

Commonly reported physical symptoms of AN include an intolerance to cold, general fatigue, muscle aches and pains, restlessness, emesis, and a multitude of GI complaints. Patients with AN also have been reported to experience shortness of breath due to conditions such as respiratory muscle weakness,22 nutritional emphysema,23 and anxiety and panic attack.24 These conditions could lead to an increased susceptibility to COVID-19 and increased complications during treatment. Cardiac abnormalities, which are common in patients with AN and BN, may increase the risk of adverse events. While these symptoms may be an important part of screening for diseases such as COVID-19, suspicion of infection also may be lower because of the overlap of AN symptomology, underlying conditions, and a delayed fever response.

Laboratory findings. Laboratory testing results for patients with COVID-19 include lower lymphocyte counts, higher leukocyte counts, elevated levels of infection-related biomarkers and inflammatory cytokines, and significantly decreased T-cell counts.19 Similar values are also found in patients with AN.

The similar clinical presentations and laboratory values of AN and COVID-19 could lead to delayed diagnosis, increased disease transmission, cross-contamination of facilities, and higher incidences of medical complications and mortality.

The immunology of AN and correlations with COVID-19

Many studies examining the immune system of patients with eating disorders, especially those with AN, have discovered changes and differences in both cell-mediated and humoral response to infections.1,3,5,7,9,11,16,21,25-27 Whether these differences represent a dysfunctional immune system, an immunocompromised state, or even a protective factor remains unclear.

Continue to: While some studies have reported...

 

 

While some studies have reported that AN represents an immunocompromised state, others describe the immune system of patients with AN as dysfunctional or simply altered.9,11,22,28 Some studies have found that patients with AN had delayed reactions to pathogen skin exposures compared with healthy controls, which provides evidence of an impaired cell-mediated immune system.9,27,29

Some studies have considered the consequences of infection and immunologic findings as markers of or contributing to the onset of AN.2,30,31 Numerous studies have noted abnormalities in AN with regards to cell-mediated immunity, the humoral system, the lymphoreticular system, and the innate immune system, and potential contributions from increased oxidative stress, a chronically activated sympathetic nervous system and hypothalamic-pituitary-adrenal axis, altered intestinal microbiota, and an abnormal bone marrow microenvironment.2

Box 1

The immunology of COVID-19

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new beta-coronavirus that is still being studied for its effects on the immune system. It may take years to fully understand the nature of the pathogen and the response of the human immune system. To better understand COVID19, researchers have been turning to what they learned from the past outbreaks of severe acute respiratory syndrome (SARS) in 2003- 2004 and Middle East respiratory syndrome (MERS) in 2011, both caused by betacoronaviruses with a zoonotic origin.25,32

The proposed pathogenesis for infection of SARS-CoV-2 is similar to SARS and occurs when aerosolized droplets containing the virus enter the host.32 While currently there is only initial data on the host innate immune status of patients infected with SARS-CoV-2, initial findings of a report on 99 cases in Wuhan, China included increased total neutrophils (38%), reduced total lymphocytes (35%), increased serum interleukin-6 (52%), and increased C-reactive protein (84%).33 Additional findings were decreased percentages of monocytes, eosinophils, and basophils, as well as significantly decreased levels of cytokines and T-cells in more severe cases.19 Past research with SARS reported similar T-cell findings, with a more frequent CD8+ response and a greater magnitude of CD4+.34

Box 119,25,32-34 describes some of the initial immunologic findings reported in patients with COVID-19. In Box 2,5,8,11,13,14,19,26,28,35-40 we discuss reports that describe the immunologic overlay of COVID-19 and AN.

Box 2

The immunologic overlay of COVID-19 and anorexia nervosa

Leukopenia (low leukocyte levels) is a common finding in patients with anorexia nervosa (AN),8 and often leads clinicians to lower their suspicion for infection. A 2008 Hungarian study that evaluated lymphocyte activation parameters and clinical status in 11 adolescents (10 girls and 1 boy) with AN, 12 obese adolescents, and 10 healthy controls did not find any association between the variables.35 While many studies have focused on adults, it is important to note that leukopenia is a common finding in adolescents (age 12 to 17) with AN.36

Leukocyte counts are elevated in coronavirus disease 2019 (COVID-19), possibly offsetting AN’s leukopenia. In addition, neutrophil counts are elevated and monocyte, eosinophil, basophil, and especially lymphocyte counts are significantly decreased. A meta-analysis that included 22 studies and 924 participants (512 with AN and 412 controls) examined common inflammatory cytokine findings in patients with AN.11 Compared with healthy controls, patients with AN had significantly elevated levels of tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1, IL-6, and TNF-receptor II, and significantly decreased levels of C-reactive protein and IL-6 receptor. Elevated levels of TNF-alpha and IL-6 also have been reported in patients with COVID-19.19 These findings may mask suspicion for infection in patients with AN.19

In patients with AN and those with bulimia nervosa, CD4+-to-CD8+ ratios also have been found to be low as a result of normal-tohigher levels of CD4+ cells and lower levels of CD8+ cells.36-39 Researchers have also proposed that the lymphocytosis observed in AN is a result of increased naïve CD4+.36 In AN, total lymphocyte counts have been found to correlate positively with a patient’s body mass index (BMI), while the CD4+ T-lymphocyte correlated negatively with BMI and were critically low in patients with severe malnutrition.26,40 In patients with COVID-19, CD4+ levels have reported to be within normal range, naïve CD4+ cells were elevated, and CD8+ cells were slightly decreased,19 which is similar to the findings in AN.

Fewer studies have evaluated humoral immune response in AN, and results have varied. One study (N = 46) found elevated B-cell counts in adolescents with AN-restricting type,36 while another (N = 40) reported normal levels of B-cells.5 Specific decreases in immunoglobulin (Ig) G and IgM have also been reported in AN, while IgA, IgG, and IgM usually are normal in COVID-19.19

Despite differences in immune system function, cellular immunity appears to remain relatively intact in patients with AN, but can become compromised with severe malnutrition or with advanced weight loss.28,40 This compromised immunity related to severe AN with a very low BMI likely leads to the increased morbidity and mortality.8,13,14

Malnutrition and the immune system

Differences in the type of malnutrition observed in low-weight patients with AN may help explain why patients with AN can maintain a relatively intact cell-mediated immune system.1 Protein-energy malnutrition (PEM), which is found in typical states of starvation, consists of deficiencies in multiple vitamins, protein, and energy (caloric content), whereas the dietary habits of patients with AN usually result in a deficiency of carbohydrates and fats.41 Studies that examined the impact of PEM on immunity to influenza infection have suggested that balanced protein energy replenishment may be a strategy for boosting immunity against influenza viral infections.42 However, carbohydrates are the primary nutrients for human bone marrow fat cells, which play a crucial role in the maturation of white blood cells. This may account for the leukopenia that is common in patients with AN.6,43 The protein-sparing aspect of the typical AN diet may account for the immune system changes observed in patients with AN.44

Although some studies have proposed that immune deficiencies observed in patients with AN are secondary to malnutrition and return to normal with refeeding,5,40,45 others have concluded that immune function is not compromised by factors such as nutritional status or body weight in AN.26,43,46

Continue to: Clinical considerations

 

 

Clinical considerations

Neither the CDC nor the WHO have issued a specific protocol for monitoring for and treating COVID-19 in patients with eating disorders; however, the guidelines offered by these organizations for the general population should be followed for patients with eating disorders.

When screening a patient with an eating disorder, keep in mind that the symptoms of eating disorders, such as AN, may mimic an infectious process. Mood symptoms, such as depression or anxiety, could represent physiological responses to infection. Patients with GI symptoms that typically are considered part of the pathology of an eating disorder should be more carefully considered for COVID-19. Monitor a patient’s basal body temperature, and be mindful that a patient with AN may exhibit a delayed fever response. Be vigilant for a recent loss of taste or smell, which should raise suspicion for COVID-19. When monitoring vital signs, pay careful attention for any decompensation in a patient’s pulse oximetry. Whenever possible, order COVID-19 testing for any patient you suspect may be infected.

Outpatient clinicians should work closely in a collaborative manner with a patient’s eating disorder treatment team. Psychiatrists, primary care physicians, psychotherapists, nutritionists, and other clinicians should all follow CDC/WHO guidelines regarding COVID-19, provide surveillance, and communicate any suspicions to the medical team. Eating disorder treatment programs, including residential centers, partial hospital programs (PHP), and intensive outpatient programs (IOP), must enhance monitoring for COVID-19, and exercise caution by practicing social distancing and providing adequate personal protective equipment for patients and staff. To reduce the spread of COVID-19, many IOPs and PHPs have transitioned to virtual treatment. Residential centers must carefully screen patients before admission to weigh the risks and benefits of inpatient vs outpatient care.

 

Bottom Line

Differences in the immune system of patients with an eating disorder do not necessarily confer a higher or lower risk of infection. Symptoms of some infections can mimic the symptoms of anorexia nervosa. Recognizing infections in patients with eating disorders is critical because compared with the general population, they have higher rates of infection-related morbidity and mortality.

Related Resources

References

1. Golla JA, Larson LA, Anderson CF, et al. An immunological assessment of patients with anorexia nervosa. Am J Clin Nutr. 1981;34(12):2756-2762.
2. Gibson D, Mehler PS. Anorexia nervosa and the immune system—a narrative review. J Clin Med. 2019;8(11):1915. doi: 10.3390/jcm8111915.
3. Słotwin´ska SM, Słotwin´ska R. Immune disorders in anorexia. Cent Eur J Immunol. 2017;42(3):294-300.
4. Nova E, Samartín S, Gómez S, et al. The adaptive response of the immune system to the particular malnutrition of eating disorders. Eur J Clin Nutr. 2002;56(suppl 3):S34-S37.
5. Allende LM, Corell A, Manzanares J, et al. Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding. Immunology. 1998;94(4):543-551.
6. Brown RF, Bartrop R, Birmingham CL. Immunological disturbance and infectious disease in anorexia nervosa: a review. Acta Neuropsychiatr. 2008;20(3):117-128.
7. Polack E, Nahmod VE, Emeric-Sauval E, et al. Low lymphocyte interferon-gamma production and variable proliferative response in anorexia nervosa patients. J Clin Immunol. 1993;13(6):445-451.
8. Bowers TK, Eckert E. Leukopenia in anorexia nervosa. Lack of increased risk of infection. Arch Intern Med. 1978;138(10):1520-1523.
9. Cason J, Ainley CC, Wolstencroft RA, et al. Cell-mediated immunity in anorexia nervosa. Clin Exp Immunol. 1986;64(2):370-375.
10. Raevuori A, Lukkariniemi L, Suokas JT, et al. Increased use of antimicrobial medication in bulimia nervosa and binge-eating disorder prior to the eating disorder treatment. Int J Eat Disord. 2016;49(6):542-552.
11. Solmi M, Veronese N, Favaro A, et al. Inflammatory cytokines and anorexia nervosa: a meta-analysis of cross-sectional and longitudinal studies. Psychoneuroendocrinology. 2015;51:237-252.
12. Brown RF, Bartrop R, Beumont P, et al. Bacterial infections in anorexia nervosa: delayed recognition increases complications. Int J Eat Disord. 2005;37(3):261-265.
13. Theander S. Anorexia nervosa. A psychiatric investigation of 94 female patients. Acta Psychiatr Scand Suppl. 1970;214:1-194.
14. Warren MP, Vande Wiele RL. Clinical and metabolic features of anorexia nervosa. Am J Obstet Gynecol. 1973;117(3):435-449.
15. Copeland PM, Herzog DB. Hypoglycemia and death in anorexia nervosa. Psychother Psychosom. 1987;48(1-4):146-150.
16. Devuyst O, Lambert M, Rodhain J, et al. Haematological changes and infectious complications in anorexia nervosa: a case-control study. Q J Med. 1993;86(12):791-799.
17. Pisetsky DS, Trace SE, Brownley KA, et al. The expression of cytokines and chemokines in the blood of patients with severe weight loss from anorexia nervosa: an exploratory study. Cytokine. 2014;69(1):110-115.
18. Birmingham CL, Hodgson DM, Fung J, et al. Reduced febrile response to bacterial infection in anorexia nervosa patients. Int J Eat Disord. 2003;34(2):269-272.
19. Qin C, Zhou L, Hu Z, et al. Dysregulation of immune response in patients with COVID-19 in Wuhan, China [published online March 12, 2020]. Clin Infect Dis. doi: 10.1093/cid/ciaa248.
20. Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497-506.
21. Chan JF, Yuan S, Kok KH, et al. A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-to-person transmission: a study of a family cluster. Lancet. 2020;395(10223):514-523.
22. Birmingham CL, Tan AO. Respiratory muscle weakness and anorexia nervosa. Int J Eat Disord. 2003;33(2):230-233.
23. Cook VJ, Coxson HO, Mason AG, et al. Bullae, bronchiectasis and nutritional emphysema in severe anorexia nervosa. Can Respir J. 2001;8(5):361-365.
24. Khalsa SS, Hassanpour MS, Strober M, et al. Interoceptive anxiety and body representation in anorexia nervosa [published online September 21, 2018]. Front Psychiatry. 2018;9:444. doi: 10.3389/fpsyt.2018.00444.
25. van West D, Maes M. Cytokines in de obsessief compulsieve stoornis en in anorexia nervosa: een overzicht. Acta Neuropsychiatr. 1999;11(4):125-129.
26. Komorowska-Pietrzykowska R, Rajewski A, Wiktorowicz K, et al. Czynnos´c´ układu immunologicznego w jadłowstrecie psychicznym [Immunological system activity in anorexia nervosa]. Psychiatr Pol. 1996;30(5):801‐810.
27. Marcos A, Varela P, Toro O, et al. Interactions between nutrition and immunity in anorexia nervosa: a 1-y follow-up study. Am J Clin Nutr. 1997;66(2):485S-490S.
28. Pertschuk MJ, Crosby LO, Barot L, et al. Immunocompetency in anorexia nervosa. Am J Clin Nutr. 1982;35(5):968-972.
29. Varela P, Marcos A, Navarro MP. Zinc status in anorexia nervosa. Ann Nutr Metab. 1992;36(4):197-202.
30. Breithaupt L, Köhler-Forsberg O, Larsen JT, et al. Association of exposure to infections in childhood with risk of eating disorders in adolescent girls. JAMA Psychiatry. 2019;76(8):800-809.
31. Brambilla F, Monti D, Franceschi C. Plasma concentrations of interleukin-1-beta, interleukin-6 and tumor necrosis factor-alpha, and of their soluble receptors and receptor antagonist in anorexia nervosa. Psychiatry Res. 2001;103(2-3):107-114.
32. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: lessons learned from SARS and MERS epidemic [published online February 27, 2020]. Asian Pac J Allergy Immunol. doi: 10.12932/AP-200220-0772.
33. Zhou P, Yang XL, Wang XG, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature. 2020;579(7798):270-273.
34. Li CK, Wu H, Yan H, et al. T cell responses to whole SARS coronavirus in humans. J Immunol. 2008;181(8):5490-5500.
35. Páli AA, Pászthy B. Az immunrendszer muködésének megváltozása a táplálkozási magatartás zavarai esetén [Changes of the immune functions in patients with eating disorders]. Ideggyogy Sz. 2008;61(11-12):381‐384.
36. Elegido A, Graell M, Andrés P, et al. Increased naive CD4+ and B lymphocyte subsets are associated with body mass loss and drive relative lymphocytosis in anorexia nervosa patients. Nutr Res. 2017;39:43-50.
37. Marcos A, Varela P, Santacruz I, et al. Nutritional status and immunocompetence in eating disorders. A comparative study. Eur J Clin Nutr. 1993;47(11):787-793.
38. Mustafa A, Ward A, Treasure J, et al. T lymphocyte subpopulations in anorexia nervosa and refeeding. Clin Immunol Immunopathol. 1997;82(3):282-289.
39. Nagata T, Kiriike N, Tobitani W, et al. Lymphocyte subset, lymphocyte proliferative response, and soluble interleukin-2 receptor in anorexic patients. Biol Psychiatry. 1999;45(4):471-474.
40. Saito H, Nomura K, Hotta M, et al. Malnutrition induces dissociated changes in lymphocyte count and subset proportion in patients with anorexia nervosa. Int J Eat Disord. 2007;40(6):575-579.
41. Nova E, Varela P, López-Vidriero I, et al. A one-year follow-up study in anorexia nervosa. Dietary pattern and anthropometrical evolution. Eur J Clin Nutr. 2001;55(7):547-554.
42. Taylor AK, Cao W, Vora KP, et al. Protein energy malnutrition decreases immunity and increases susceptibility to influenza infection in mice. J Infect Dis. 2013;207(3):501-510.
43. Mant MJ, Faragher BS. The hematology of anorexia nervosa. Br J Haematol. 1972;23(6):737-749.
44. Marcos A. The immune system in eating disorders: an overview. Nutrition. 1997;13(10):853-862.
45. Schattner A, Tepper R, Steinbock M, et al. TNF, interferon-gamma and cell-mediated cytotoxicity in anorexia nervosa; effect of refeeding. J Clin Lab Immunol. 1990;32(4):183-184.
46. Nagata T, Tobitani W, Kiriike N, et al. Capacity to produce cytokines during weight restoration in patients with anorexia nervosa. Psychosom Med. 1999;61(3):371-377.

References

1. Golla JA, Larson LA, Anderson CF, et al. An immunological assessment of patients with anorexia nervosa. Am J Clin Nutr. 1981;34(12):2756-2762.
2. Gibson D, Mehler PS. Anorexia nervosa and the immune system—a narrative review. J Clin Med. 2019;8(11):1915. doi: 10.3390/jcm8111915.
3. Słotwin´ska SM, Słotwin´ska R. Immune disorders in anorexia. Cent Eur J Immunol. 2017;42(3):294-300.
4. Nova E, Samartín S, Gómez S, et al. The adaptive response of the immune system to the particular malnutrition of eating disorders. Eur J Clin Nutr. 2002;56(suppl 3):S34-S37.
5. Allende LM, Corell A, Manzanares J, et al. Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding. Immunology. 1998;94(4):543-551.
6. Brown RF, Bartrop R, Birmingham CL. Immunological disturbance and infectious disease in anorexia nervosa: a review. Acta Neuropsychiatr. 2008;20(3):117-128.
7. Polack E, Nahmod VE, Emeric-Sauval E, et al. Low lymphocyte interferon-gamma production and variable proliferative response in anorexia nervosa patients. J Clin Immunol. 1993;13(6):445-451.
8. Bowers TK, Eckert E. Leukopenia in anorexia nervosa. Lack of increased risk of infection. Arch Intern Med. 1978;138(10):1520-1523.
9. Cason J, Ainley CC, Wolstencroft RA, et al. Cell-mediated immunity in anorexia nervosa. Clin Exp Immunol. 1986;64(2):370-375.
10. Raevuori A, Lukkariniemi L, Suokas JT, et al. Increased use of antimicrobial medication in bulimia nervosa and binge-eating disorder prior to the eating disorder treatment. Int J Eat Disord. 2016;49(6):542-552.
11. Solmi M, Veronese N, Favaro A, et al. Inflammatory cytokines and anorexia nervosa: a meta-analysis of cross-sectional and longitudinal studies. Psychoneuroendocrinology. 2015;51:237-252.
12. Brown RF, Bartrop R, Beumont P, et al. Bacterial infections in anorexia nervosa: delayed recognition increases complications. Int J Eat Disord. 2005;37(3):261-265.
13. Theander S. Anorexia nervosa. A psychiatric investigation of 94 female patients. Acta Psychiatr Scand Suppl. 1970;214:1-194.
14. Warren MP, Vande Wiele RL. Clinical and metabolic features of anorexia nervosa. Am J Obstet Gynecol. 1973;117(3):435-449.
15. Copeland PM, Herzog DB. Hypoglycemia and death in anorexia nervosa. Psychother Psychosom. 1987;48(1-4):146-150.
16. Devuyst O, Lambert M, Rodhain J, et al. Haematological changes and infectious complications in anorexia nervosa: a case-control study. Q J Med. 1993;86(12):791-799.
17. Pisetsky DS, Trace SE, Brownley KA, et al. The expression of cytokines and chemokines in the blood of patients with severe weight loss from anorexia nervosa: an exploratory study. Cytokine. 2014;69(1):110-115.
18. Birmingham CL, Hodgson DM, Fung J, et al. Reduced febrile response to bacterial infection in anorexia nervosa patients. Int J Eat Disord. 2003;34(2):269-272.
19. Qin C, Zhou L, Hu Z, et al. Dysregulation of immune response in patients with COVID-19 in Wuhan, China [published online March 12, 2020]. Clin Infect Dis. doi: 10.1093/cid/ciaa248.
20. Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497-506.
21. Chan JF, Yuan S, Kok KH, et al. A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-to-person transmission: a study of a family cluster. Lancet. 2020;395(10223):514-523.
22. Birmingham CL, Tan AO. Respiratory muscle weakness and anorexia nervosa. Int J Eat Disord. 2003;33(2):230-233.
23. Cook VJ, Coxson HO, Mason AG, et al. Bullae, bronchiectasis and nutritional emphysema in severe anorexia nervosa. Can Respir J. 2001;8(5):361-365.
24. Khalsa SS, Hassanpour MS, Strober M, et al. Interoceptive anxiety and body representation in anorexia nervosa [published online September 21, 2018]. Front Psychiatry. 2018;9:444. doi: 10.3389/fpsyt.2018.00444.
25. van West D, Maes M. Cytokines in de obsessief compulsieve stoornis en in anorexia nervosa: een overzicht. Acta Neuropsychiatr. 1999;11(4):125-129.
26. Komorowska-Pietrzykowska R, Rajewski A, Wiktorowicz K, et al. Czynnos´c´ układu immunologicznego w jadłowstrecie psychicznym [Immunological system activity in anorexia nervosa]. Psychiatr Pol. 1996;30(5):801‐810.
27. Marcos A, Varela P, Toro O, et al. Interactions between nutrition and immunity in anorexia nervosa: a 1-y follow-up study. Am J Clin Nutr. 1997;66(2):485S-490S.
28. Pertschuk MJ, Crosby LO, Barot L, et al. Immunocompetency in anorexia nervosa. Am J Clin Nutr. 1982;35(5):968-972.
29. Varela P, Marcos A, Navarro MP. Zinc status in anorexia nervosa. Ann Nutr Metab. 1992;36(4):197-202.
30. Breithaupt L, Köhler-Forsberg O, Larsen JT, et al. Association of exposure to infections in childhood with risk of eating disorders in adolescent girls. JAMA Psychiatry. 2019;76(8):800-809.
31. Brambilla F, Monti D, Franceschi C. Plasma concentrations of interleukin-1-beta, interleukin-6 and tumor necrosis factor-alpha, and of their soluble receptors and receptor antagonist in anorexia nervosa. Psychiatry Res. 2001;103(2-3):107-114.
32. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: lessons learned from SARS and MERS epidemic [published online February 27, 2020]. Asian Pac J Allergy Immunol. doi: 10.12932/AP-200220-0772.
33. Zhou P, Yang XL, Wang XG, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature. 2020;579(7798):270-273.
34. Li CK, Wu H, Yan H, et al. T cell responses to whole SARS coronavirus in humans. J Immunol. 2008;181(8):5490-5500.
35. Páli AA, Pászthy B. Az immunrendszer muködésének megváltozása a táplálkozási magatartás zavarai esetén [Changes of the immune functions in patients with eating disorders]. Ideggyogy Sz. 2008;61(11-12):381‐384.
36. Elegido A, Graell M, Andrés P, et al. Increased naive CD4+ and B lymphocyte subsets are associated with body mass loss and drive relative lymphocytosis in anorexia nervosa patients. Nutr Res. 2017;39:43-50.
37. Marcos A, Varela P, Santacruz I, et al. Nutritional status and immunocompetence in eating disorders. A comparative study. Eur J Clin Nutr. 1993;47(11):787-793.
38. Mustafa A, Ward A, Treasure J, et al. T lymphocyte subpopulations in anorexia nervosa and refeeding. Clin Immunol Immunopathol. 1997;82(3):282-289.
39. Nagata T, Kiriike N, Tobitani W, et al. Lymphocyte subset, lymphocyte proliferative response, and soluble interleukin-2 receptor in anorexic patients. Biol Psychiatry. 1999;45(4):471-474.
40. Saito H, Nomura K, Hotta M, et al. Malnutrition induces dissociated changes in lymphocyte count and subset proportion in patients with anorexia nervosa. Int J Eat Disord. 2007;40(6):575-579.
41. Nova E, Varela P, López-Vidriero I, et al. A one-year follow-up study in anorexia nervosa. Dietary pattern and anthropometrical evolution. Eur J Clin Nutr. 2001;55(7):547-554.
42. Taylor AK, Cao W, Vora KP, et al. Protein energy malnutrition decreases immunity and increases susceptibility to influenza infection in mice. J Infect Dis. 2013;207(3):501-510.
43. Mant MJ, Faragher BS. The hematology of anorexia nervosa. Br J Haematol. 1972;23(6):737-749.
44. Marcos A. The immune system in eating disorders: an overview. Nutrition. 1997;13(10):853-862.
45. Schattner A, Tepper R, Steinbock M, et al. TNF, interferon-gamma and cell-mediated cytotoxicity in anorexia nervosa; effect of refeeding. J Clin Lab Immunol. 1990;32(4):183-184.
46. Nagata T, Tobitani W, Kiriike N, et al. Capacity to produce cytokines during weight restoration in patients with anorexia nervosa. Psychosom Med. 1999;61(3):371-377.

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Consider adjunctive olanzapine for feeding disturbance

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Best treatment for avoidant/restrictive food intake disorder is multidisciplinary

– No evidence-based medications are approved for the treatment of avoidant/restrictive food intake disorder, but olanzapine is a sensible option to consider, according to Timothy D. Brewerton, MD.

Doug Brunk/MDedge News
Dr. Timothy D. Brewerton

A newly classified disorder in the DSM-5, avoidant/restrictive food intake disorder (ARFID) is an eating/feeding disturbance manifested by the persistent failure to meet appropriate nutritional energy needs associated with one or more of the following factors: significant weight loss or failure to achieve expected growth, significant nutritional deficiency, dependence on enteral feeding or oral nutritional supplements to survive, and marked interference with psychosocial functioning. ARFID “is not better explained by lack of available food or by culturally sanctioned practices,” Dr. Brewerton, an affiliate professor of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “It does not occur during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which one’s body weight or shape is experienced. That’s what distinguishes it from anorexia nervosa.”

He added that, although many cases of ARFID have autism spectrum disorder traits, ARFID “is not attributable to a concurrent medical condition or to mental disorder.” When it does occur, the severity of the feeding disorder far outweighs that of the medical condition.”

Several ARFID case reports have been published in the medical literature, yet no randomized controlled trials exist to date. “Treatment is multidisciplinary and involves cognitive-behavioral therapy, sometimes occupational therapy,” said Dr. Brewerton, who is a founding fellow and former board member of the Academy for Eating Disorders.

He and his colleagues published a report on nine ARFID cases treated in an eating disorders program (J Child Adolesc Psychopharmacol. 2017;27[10]:920-2). The patients were treated with adjunctive olanzapine at a starting dose of 0.9 mg/day and discharge dose 2.8 mg/day. For the starting dose, “you have to break the [olanzapine pills] in pieces,” he said. “You have to have a pill cutter. What you don’t want to do is overwhelm the patient or their family members with oversedation. Too often, people start them with 2.5 mg or 5 mg [of olanzapine] right off the bat.”



The researchers found a significant increase in weight gain pre- versus post-olanzapine treatment (a mean of 3.3 pounds vs. 13.1 pounds, respectively; P less than .04) and BMI-for-weight percentiles (P less than .009). “Patients also had improvements in their Clinical Global Impressions Scale scores and a reduction in their associated anxious, depressive, and cognitive symptoms,” Dr. Brewerton said.

Similar findings were observed in a subsequent Canadian study of six ARFID cases (J Eat Disord. 2018;6:20). Five females and one male were treated with a combination of medical monitoring, family therapy, medication (including olanzapine, fluoxetine and in two cases, cyproheptadine), and CBT. At treatment termination, all six patients had achieved their goal weight.

At the University of California, San Diego, researchers led by Emily Gray, MD, conducted a retrospective chart review of six females and eight males with ARFID who ranged in age from 7 to 23 years. All but one of the 14 patients had a co-occurring diagnosis, including general anxiety disorder, social anxiety, unspecified anxiety, ADHD, major depressive disorder, and autism spectrum disorder (J Am Acad Child Adoles Psychiatry. 2018;57[4]:288-9). They were treated with mirtazapine at a dosing range of 7.5-45 mg per day. The average change in BMI per week rose from 0.10 BMI points per week pretreatment to 0.23 BMI points per week post-treatment (P less than .05).

“These cases illustrate that the judicious use of low-dose olanzapine, when used as an adjunct to other treatment modalities, may facilitate eating, weight gain, and the reduction of anxious, depressive, and cognitive symptoms,” said Dr. Brewerton, who also has a private practice in Charleston.

Dr. Brewerton disclosed that he is a consultant to Monte Nido & Affiliates and Sunovion. He receives royalties from Taylor & Francis and Springer-Verlag, and holds ownership interest in Monte Nido & Affiliates.

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Best treatment for avoidant/restrictive food intake disorder is multidisciplinary

Best treatment for avoidant/restrictive food intake disorder is multidisciplinary

– No evidence-based medications are approved for the treatment of avoidant/restrictive food intake disorder, but olanzapine is a sensible option to consider, according to Timothy D. Brewerton, MD.

Doug Brunk/MDedge News
Dr. Timothy D. Brewerton

A newly classified disorder in the DSM-5, avoidant/restrictive food intake disorder (ARFID) is an eating/feeding disturbance manifested by the persistent failure to meet appropriate nutritional energy needs associated with one or more of the following factors: significant weight loss or failure to achieve expected growth, significant nutritional deficiency, dependence on enteral feeding or oral nutritional supplements to survive, and marked interference with psychosocial functioning. ARFID “is not better explained by lack of available food or by culturally sanctioned practices,” Dr. Brewerton, an affiliate professor of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “It does not occur during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which one’s body weight or shape is experienced. That’s what distinguishes it from anorexia nervosa.”

He added that, although many cases of ARFID have autism spectrum disorder traits, ARFID “is not attributable to a concurrent medical condition or to mental disorder.” When it does occur, the severity of the feeding disorder far outweighs that of the medical condition.”

Several ARFID case reports have been published in the medical literature, yet no randomized controlled trials exist to date. “Treatment is multidisciplinary and involves cognitive-behavioral therapy, sometimes occupational therapy,” said Dr. Brewerton, who is a founding fellow and former board member of the Academy for Eating Disorders.

He and his colleagues published a report on nine ARFID cases treated in an eating disorders program (J Child Adolesc Psychopharmacol. 2017;27[10]:920-2). The patients were treated with adjunctive olanzapine at a starting dose of 0.9 mg/day and discharge dose 2.8 mg/day. For the starting dose, “you have to break the [olanzapine pills] in pieces,” he said. “You have to have a pill cutter. What you don’t want to do is overwhelm the patient or their family members with oversedation. Too often, people start them with 2.5 mg or 5 mg [of olanzapine] right off the bat.”



The researchers found a significant increase in weight gain pre- versus post-olanzapine treatment (a mean of 3.3 pounds vs. 13.1 pounds, respectively; P less than .04) and BMI-for-weight percentiles (P less than .009). “Patients also had improvements in their Clinical Global Impressions Scale scores and a reduction in their associated anxious, depressive, and cognitive symptoms,” Dr. Brewerton said.

Similar findings were observed in a subsequent Canadian study of six ARFID cases (J Eat Disord. 2018;6:20). Five females and one male were treated with a combination of medical monitoring, family therapy, medication (including olanzapine, fluoxetine and in two cases, cyproheptadine), and CBT. At treatment termination, all six patients had achieved their goal weight.

At the University of California, San Diego, researchers led by Emily Gray, MD, conducted a retrospective chart review of six females and eight males with ARFID who ranged in age from 7 to 23 years. All but one of the 14 patients had a co-occurring diagnosis, including general anxiety disorder, social anxiety, unspecified anxiety, ADHD, major depressive disorder, and autism spectrum disorder (J Am Acad Child Adoles Psychiatry. 2018;57[4]:288-9). They were treated with mirtazapine at a dosing range of 7.5-45 mg per day. The average change in BMI per week rose from 0.10 BMI points per week pretreatment to 0.23 BMI points per week post-treatment (P less than .05).

“These cases illustrate that the judicious use of low-dose olanzapine, when used as an adjunct to other treatment modalities, may facilitate eating, weight gain, and the reduction of anxious, depressive, and cognitive symptoms,” said Dr. Brewerton, who also has a private practice in Charleston.

Dr. Brewerton disclosed that he is a consultant to Monte Nido & Affiliates and Sunovion. He receives royalties from Taylor & Francis and Springer-Verlag, and holds ownership interest in Monte Nido & Affiliates.

– No evidence-based medications are approved for the treatment of avoidant/restrictive food intake disorder, but olanzapine is a sensible option to consider, according to Timothy D. Brewerton, MD.

Doug Brunk/MDedge News
Dr. Timothy D. Brewerton

A newly classified disorder in the DSM-5, avoidant/restrictive food intake disorder (ARFID) is an eating/feeding disturbance manifested by the persistent failure to meet appropriate nutritional energy needs associated with one or more of the following factors: significant weight loss or failure to achieve expected growth, significant nutritional deficiency, dependence on enteral feeding or oral nutritional supplements to survive, and marked interference with psychosocial functioning. ARFID “is not better explained by lack of available food or by culturally sanctioned practices,” Dr. Brewerton, an affiliate professor of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “It does not occur during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which one’s body weight or shape is experienced. That’s what distinguishes it from anorexia nervosa.”

He added that, although many cases of ARFID have autism spectrum disorder traits, ARFID “is not attributable to a concurrent medical condition or to mental disorder.” When it does occur, the severity of the feeding disorder far outweighs that of the medical condition.”

Several ARFID case reports have been published in the medical literature, yet no randomized controlled trials exist to date. “Treatment is multidisciplinary and involves cognitive-behavioral therapy, sometimes occupational therapy,” said Dr. Brewerton, who is a founding fellow and former board member of the Academy for Eating Disorders.

He and his colleagues published a report on nine ARFID cases treated in an eating disorders program (J Child Adolesc Psychopharmacol. 2017;27[10]:920-2). The patients were treated with adjunctive olanzapine at a starting dose of 0.9 mg/day and discharge dose 2.8 mg/day. For the starting dose, “you have to break the [olanzapine pills] in pieces,” he said. “You have to have a pill cutter. What you don’t want to do is overwhelm the patient or their family members with oversedation. Too often, people start them with 2.5 mg or 5 mg [of olanzapine] right off the bat.”



The researchers found a significant increase in weight gain pre- versus post-olanzapine treatment (a mean of 3.3 pounds vs. 13.1 pounds, respectively; P less than .04) and BMI-for-weight percentiles (P less than .009). “Patients also had improvements in their Clinical Global Impressions Scale scores and a reduction in their associated anxious, depressive, and cognitive symptoms,” Dr. Brewerton said.

Similar findings were observed in a subsequent Canadian study of six ARFID cases (J Eat Disord. 2018;6:20). Five females and one male were treated with a combination of medical monitoring, family therapy, medication (including olanzapine, fluoxetine and in two cases, cyproheptadine), and CBT. At treatment termination, all six patients had achieved their goal weight.

At the University of California, San Diego, researchers led by Emily Gray, MD, conducted a retrospective chart review of six females and eight males with ARFID who ranged in age from 7 to 23 years. All but one of the 14 patients had a co-occurring diagnosis, including general anxiety disorder, social anxiety, unspecified anxiety, ADHD, major depressive disorder, and autism spectrum disorder (J Am Acad Child Adoles Psychiatry. 2018;57[4]:288-9). They were treated with mirtazapine at a dosing range of 7.5-45 mg per day. The average change in BMI per week rose from 0.10 BMI points per week pretreatment to 0.23 BMI points per week post-treatment (P less than .05).

“These cases illustrate that the judicious use of low-dose olanzapine, when used as an adjunct to other treatment modalities, may facilitate eating, weight gain, and the reduction of anxious, depressive, and cognitive symptoms,” said Dr. Brewerton, who also has a private practice in Charleston.

Dr. Brewerton disclosed that he is a consultant to Monte Nido & Affiliates and Sunovion. He receives royalties from Taylor & Francis and Springer-Verlag, and holds ownership interest in Monte Nido & Affiliates.

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The woman who couldn’t stop eating

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The woman who couldn’t stop eating

CASE Uncontrollable eating and weight gain

Ms. C, age 33, presents to an outpatient clinic with complaints of weight gain and “uncontrollable eating.” Ms. C says she’s gained >50 lb over the last year. She describes progressively frequent episodes of overeating during which she feels that she has no control over the amount of food she consumes. She reports eating as often as 10 times a day, and overeating to the point of physical discomfort during most meals. She gives an example of having recently consumed a large pizza, several portions of Chinese food, approximately 20 chicken wings, and half a chocolate cake for dinner. Ms. C admits that on several occasions she has vomited after meals due to feeling extremely full; however, she denies having done so intentionally. She also denies restricting her food intake, misusing laxatives or diuretics, or exercising excessively.

Ms. C expresses frustration and embarrassment with her eating and resulting weight gain. She says she has poor self-esteem, low energy and motivation, and poor concentration. She feels that her condition has significantly impacted her social life, romantic relationships, and family life. She admits she’s been avoiding dating and seeing friends due to her weight gain, and has been irritable with her teenage daughter.

During her initial evaluation, Ms. C is alert and oriented, with a linear and goal-directed thought process. She is somewhat irritable and guarded, wearing large sunglasses that cover most of her face, but is not overtly paranoid. Although she appears frustrated when discussing her condition, she denies feeling hopeless or helpless.

 

HISTORY Thyroid cancer and mood swings

Ms. C, who is single and unemployed, lives in an apartment with her teenage daughter, with whom she describes having a good relationship. She has been receiving disability benefits for the past 2 years after a motor vehicle accident resulted in multiple fractures of her arm and elbow, and subsequent chronic pain. Ms. C reports a distant history of “problems with alcohol,” but denies drinking any alcohol since being charged with driving under the influence several years ago. She has a 10 pack-year history of smoking and denies any history of illicit drug use.

Two years ago, Ms. C was diagnosed with thyroid carcinoma, and treated with surgical resection and a course of radiation. She has regular visits with her endocrinologist and has been prescribed oral levothyroxine, 150 mcg/d.

Ms. C reports a history of “mood swings” characterized by “snapping at people” and becoming irritable in response to stressful situations, but denies any past symptoms consistent with a manic or hypomanic episode. Ms. C has not been admitted to a psychiatric hospital, nor has she received any prior psychiatric treatment. She reluctantly discloses that approximately 3 years ago she had a less severe episode of uncontrollable eating and weight gain (20 to 30 lb). At that time, she was able to regain her desired physical appearance by going on the “Subway diet” and undergoing liposuction and plastic surgery.

At her current outpatient clinic visit, Ms. C expresses an interest in exploring bariatric surgery as a potential solution to her weight gain.

[polldaddy:10446186]

Continue to: EVALUATION Obese; stable thyroid function

 

 

EVALUATION Obese; stable thyroid function

We refer Ms. C for a physical examination and routine blood analysis to rule out any medical contributors to her condition. Her physical examination is reported as normal, with no signs of skin changes, goiter, or exophthalmos. Ms. C is noted to be obese, with a body mass index of 37.2 kg/m2, and an abdominal circumference of 38.5 in.

A blood analysis shows that Ms. C has elevated triglyceride levels (202 mg/dL) and elevated cholesterol levels (210 mg/dL). Her thyroid function tests are within normal limits based on the dose of levothyroxine she’s been receiving. A pregnancy test is negative.

Ms. C gives the team at the clinic permission to contact her endocrinologist, who reports that he does not suspect that Ms. C’s drastic weight gain and abnormal eating patterns are attributable to her history of thyroid carcinoma because her thyroid function tests have been stable on her current regimen.

The authors’ observations

Based on Ms. C’s initial presentation, we strongly suspected a diagnosis of binge eating disorder (BED). Several differential diagnoses were considered and carefully ruled out; Ms. C’s medical workup did not suggest that her weight gain was due to an active medical condition, and she did not meet DSM-5 criteria for a mood or psychotic disorder or anorexia nervosa or bulimia nervosa.

With an estimated lifetime prevalence in the United States of 2.6%, BED is the most prevalent eating disorder (compared with 0.6% for anorexia nervosa and 1% for bulimia nervosa).1 BED is more prevalent in women than in men, and the mean age of onset is mid-20s.

Continue to: BED may be difficult...

 

 

BED may be difficult to detect because patients may feel ashamed or guilty and are often hesitant to disclose and discuss their symptoms. Furthermore, they are frequently frustrated by the subjective loss of control over their behaviors. Patients with BED often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics.

Screening for eating disorders

Several screening instruments have been developed to help clinicians identify patients who may need further evaluation for possible diagnosis of an eating disorder, including anorexia nervosa, bulimia nervosa, and BED.2 The SCOFF questionnaire is composed of 5 brief clinician-administered questions to screen for eating disorders.2 The 7-item Binge Eating Disorder Screener (BED-7) is a screening instrument specific for BED that examines a patient’s eating patterns and behaviors during the past 3 months.3

In general, suspect BED in patients who have significant weight dissatisfaction, fluctuation in weight, and depressive symptoms. The DSM-5 criteria for binge eating disorder are shown in Table 14.

DSM-5 criteria for binge eating disorder

BED and comorbid psychiatric disorders

Patients with BED are more likely than the general population to have comorbid psychiatric disorders, including mood and anxiety disorders, attention-deficit/hyperactivity disorder, posttraumatic stress disorder, and substance use disorders. Swanson et al5 found that 83.5% of adolescents who met criteria for BED also met criteria for at least 1 other psychiatric disorder, and 37% endorsed >3 concurrent psychiatric conditions. Once BED is confirmed, it is important to screen for other psychiatric and medical comorbidities that are often present in individuals with BED (Table 21,6).

Psychiatric and medical comorbidities associated with BED

The rates of diagnosis and treatment of BED remain low. This is likely due to patient factors such as shame and fear of stigma and clinician factors such as lack of awareness, ineffective communication, hesitation to discuss the sensitive topic, or insufficient knowledge about treatment options once BED is diagnosed.

[polldaddy:10446187]

Continue to: TREATMENT Combination therapy

 

 

TREATMENT Combination therapy

Ms. C is ambivalent about her BED diagnosis, and becomes angry about it when the proposed treatments do not involve bariatric surgery or cosmetic procedures. Ms. C is enrolled in weekly individual psychotherapy, where she receives a combination of CBT and psychodynamic therapy; however, her attendance is inconsistent. Ms. C is offered a trial of fluoxetine, but adamantly refuses, citing a relative who experienced adverse effects while receiving this type of antidepressant. Ms. C also refuses a trial of topiramate due to concerns of feeling sedated. Finally, she is offered a trial of lisdexamfetamine, 30 mg/d, which was FDA-approved in 2015 to treat moderate to severe BED. We discuss the risks, benefits, and adverse effects of lisdexamfetamine with Ms. C; however, she is hesitant to start this medication and expresses increasing interest in obtaining a consultation for bariatric surgery. Ms. C is provided with extensive education about the risks and dangers of surgery before addressing her eating patterns, and the clinician provides validation, verbal support, and counseling. Ms. C eventually agrees to a trial of lisdexamfetamine, but her insurance denies coverage of this medication.

The authors’ observations

When developing an individualized treatment plan for a patient with BED, the patient’s psychiatric and medical comorbidities should be considered. Treatment goals for patients with BED include:

  • abstinence from binge eating
  • sustainable weight loss and metabolic health
  • reduction in symptoms associated with comorbid conditions
  • improvement in self-esteem and overall quality of life.

A 2015 comparative effectiveness review of management and outcomes for patients with BED evaluated pharmacologic, psychologic, behavioral, and combined approaches for treating patients with BED.7 The results suggested that second-generation antidepressants, topiramate, and lisdexamfetamine were superior to placebo in reducing binge-eating episodes and achieving abstinence from binge-eating. Weight reduction was also achieved with topiramate and lisdexamfetamine, and antidepressants helped relieve symptoms of comorbid depression.

Various formats of CBT, including therapist-led and guided self-help, were also superior to placebo in reducing the frequency of binge-eating and promoting abstinence; however, they were generally not effective in treating depression or reducing patients’ weight.7

OUTCOME Fixated on surgery

We appeal the decision of Ms. C’s insurance company; however, during the appeals process, Ms. C becomes increasingly irritable and informs us that she has changed her mind and, with the reported support of her medical doctors, wishes to undergo bariatric surgery. Although we made multiple attempts to engage Ms. C in further treatment, she is lost to follow-up.

Continue to: Bottom Line

 

 

Bottom Line

Diagnosing and managing patients with binge eating disorder (BED) can be challenging because patients may hesitate to seek help, and/or have psychiatric and medical comorbidities. They often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics. Once BED is confirmed, screen for other psychiatric and medical comorbidities. A combination of pharmacologic and psychotherapeutic interventions can benefit some patients with BED, but treatment should be individualized.

Related Resources

  • National Eating Disorders Association. NEDA. www.nationaleatingdisorders.org/.
  • Safer D, Telch C, Chen EY. Dialectical behavior therapy for binge eating and bulimia. New York, NY: Guilford Press; 2017.

Drug Brand Names

Fluoxetine • Prozac
Levothyroxine • Synthroid
Lisdexamfetamine • Vyvanse
Topiramate • Topamax

References

1. Hudson JI, Hiripi E, Pope HG Jr, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;61(3):348-358.
2. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: assessment of a new screening tool for eating disorders. BMJ. 1999;319(7223):1467-1468.
3. Herman BK, Deal LS, DiBenedetti DB, et al. Development of the 7-Item Binge-Eating Disorder screener (BEDS-7). Prim Care Companion CNS Disord. 2016;18(2):10.4088/PCC.15m01896. doi:10.4088/PCC.15m01896.
4. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
5. Swanson SA, Crow SJ, Le Grange D, et al. Prevalence and correlates of eating disorders in adolescents. Results from the national comorbidity survey replication adolescent supplement. Arch Gen Psychiatry. 2011;68(7):714.
6. Guerdjikova AI, Mori N, Casuto LS, et al. Binge eating disorder. Psychiatric Clinics of North America. 2017;40(2):255-266.
7. Berkman ND, Brownley KA, Peat CM, et al. Management and outcomes of binge-eating disorder. Comparative Effectiveness Reviews, No. 160. Agency for Healthcare Research and Quality (US). https://www.ncbi.nlm.nih.gov/books/NBK338312/. Published December 2015. Accessed July 29, 2019.

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The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Author and Disclosure Information

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CASE Uncontrollable eating and weight gain

Ms. C, age 33, presents to an outpatient clinic with complaints of weight gain and “uncontrollable eating.” Ms. C says she’s gained >50 lb over the last year. She describes progressively frequent episodes of overeating during which she feels that she has no control over the amount of food she consumes. She reports eating as often as 10 times a day, and overeating to the point of physical discomfort during most meals. She gives an example of having recently consumed a large pizza, several portions of Chinese food, approximately 20 chicken wings, and half a chocolate cake for dinner. Ms. C admits that on several occasions she has vomited after meals due to feeling extremely full; however, she denies having done so intentionally. She also denies restricting her food intake, misusing laxatives or diuretics, or exercising excessively.

Ms. C expresses frustration and embarrassment with her eating and resulting weight gain. She says she has poor self-esteem, low energy and motivation, and poor concentration. She feels that her condition has significantly impacted her social life, romantic relationships, and family life. She admits she’s been avoiding dating and seeing friends due to her weight gain, and has been irritable with her teenage daughter.

During her initial evaluation, Ms. C is alert and oriented, with a linear and goal-directed thought process. She is somewhat irritable and guarded, wearing large sunglasses that cover most of her face, but is not overtly paranoid. Although she appears frustrated when discussing her condition, she denies feeling hopeless or helpless.

 

HISTORY Thyroid cancer and mood swings

Ms. C, who is single and unemployed, lives in an apartment with her teenage daughter, with whom she describes having a good relationship. She has been receiving disability benefits for the past 2 years after a motor vehicle accident resulted in multiple fractures of her arm and elbow, and subsequent chronic pain. Ms. C reports a distant history of “problems with alcohol,” but denies drinking any alcohol since being charged with driving under the influence several years ago. She has a 10 pack-year history of smoking and denies any history of illicit drug use.

Two years ago, Ms. C was diagnosed with thyroid carcinoma, and treated with surgical resection and a course of radiation. She has regular visits with her endocrinologist and has been prescribed oral levothyroxine, 150 mcg/d.

Ms. C reports a history of “mood swings” characterized by “snapping at people” and becoming irritable in response to stressful situations, but denies any past symptoms consistent with a manic or hypomanic episode. Ms. C has not been admitted to a psychiatric hospital, nor has she received any prior psychiatric treatment. She reluctantly discloses that approximately 3 years ago she had a less severe episode of uncontrollable eating and weight gain (20 to 30 lb). At that time, she was able to regain her desired physical appearance by going on the “Subway diet” and undergoing liposuction and plastic surgery.

At her current outpatient clinic visit, Ms. C expresses an interest in exploring bariatric surgery as a potential solution to her weight gain.

[polldaddy:10446186]

Continue to: EVALUATION Obese; stable thyroid function

 

 

EVALUATION Obese; stable thyroid function

We refer Ms. C for a physical examination and routine blood analysis to rule out any medical contributors to her condition. Her physical examination is reported as normal, with no signs of skin changes, goiter, or exophthalmos. Ms. C is noted to be obese, with a body mass index of 37.2 kg/m2, and an abdominal circumference of 38.5 in.

A blood analysis shows that Ms. C has elevated triglyceride levels (202 mg/dL) and elevated cholesterol levels (210 mg/dL). Her thyroid function tests are within normal limits based on the dose of levothyroxine she’s been receiving. A pregnancy test is negative.

Ms. C gives the team at the clinic permission to contact her endocrinologist, who reports that he does not suspect that Ms. C’s drastic weight gain and abnormal eating patterns are attributable to her history of thyroid carcinoma because her thyroid function tests have been stable on her current regimen.

The authors’ observations

Based on Ms. C’s initial presentation, we strongly suspected a diagnosis of binge eating disorder (BED). Several differential diagnoses were considered and carefully ruled out; Ms. C’s medical workup did not suggest that her weight gain was due to an active medical condition, and she did not meet DSM-5 criteria for a mood or psychotic disorder or anorexia nervosa or bulimia nervosa.

With an estimated lifetime prevalence in the United States of 2.6%, BED is the most prevalent eating disorder (compared with 0.6% for anorexia nervosa and 1% for bulimia nervosa).1 BED is more prevalent in women than in men, and the mean age of onset is mid-20s.

Continue to: BED may be difficult...

 

 

BED may be difficult to detect because patients may feel ashamed or guilty and are often hesitant to disclose and discuss their symptoms. Furthermore, they are frequently frustrated by the subjective loss of control over their behaviors. Patients with BED often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics.

Screening for eating disorders

Several screening instruments have been developed to help clinicians identify patients who may need further evaluation for possible diagnosis of an eating disorder, including anorexia nervosa, bulimia nervosa, and BED.2 The SCOFF questionnaire is composed of 5 brief clinician-administered questions to screen for eating disorders.2 The 7-item Binge Eating Disorder Screener (BED-7) is a screening instrument specific for BED that examines a patient’s eating patterns and behaviors during the past 3 months.3

In general, suspect BED in patients who have significant weight dissatisfaction, fluctuation in weight, and depressive symptoms. The DSM-5 criteria for binge eating disorder are shown in Table 14.

DSM-5 criteria for binge eating disorder

BED and comorbid psychiatric disorders

Patients with BED are more likely than the general population to have comorbid psychiatric disorders, including mood and anxiety disorders, attention-deficit/hyperactivity disorder, posttraumatic stress disorder, and substance use disorders. Swanson et al5 found that 83.5% of adolescents who met criteria for BED also met criteria for at least 1 other psychiatric disorder, and 37% endorsed >3 concurrent psychiatric conditions. Once BED is confirmed, it is important to screen for other psychiatric and medical comorbidities that are often present in individuals with BED (Table 21,6).

Psychiatric and medical comorbidities associated with BED

The rates of diagnosis and treatment of BED remain low. This is likely due to patient factors such as shame and fear of stigma and clinician factors such as lack of awareness, ineffective communication, hesitation to discuss the sensitive topic, or insufficient knowledge about treatment options once BED is diagnosed.

[polldaddy:10446187]

Continue to: TREATMENT Combination therapy

 

 

TREATMENT Combination therapy

Ms. C is ambivalent about her BED diagnosis, and becomes angry about it when the proposed treatments do not involve bariatric surgery or cosmetic procedures. Ms. C is enrolled in weekly individual psychotherapy, where she receives a combination of CBT and psychodynamic therapy; however, her attendance is inconsistent. Ms. C is offered a trial of fluoxetine, but adamantly refuses, citing a relative who experienced adverse effects while receiving this type of antidepressant. Ms. C also refuses a trial of topiramate due to concerns of feeling sedated. Finally, she is offered a trial of lisdexamfetamine, 30 mg/d, which was FDA-approved in 2015 to treat moderate to severe BED. We discuss the risks, benefits, and adverse effects of lisdexamfetamine with Ms. C; however, she is hesitant to start this medication and expresses increasing interest in obtaining a consultation for bariatric surgery. Ms. C is provided with extensive education about the risks and dangers of surgery before addressing her eating patterns, and the clinician provides validation, verbal support, and counseling. Ms. C eventually agrees to a trial of lisdexamfetamine, but her insurance denies coverage of this medication.

The authors’ observations

When developing an individualized treatment plan for a patient with BED, the patient’s psychiatric and medical comorbidities should be considered. Treatment goals for patients with BED include:

  • abstinence from binge eating
  • sustainable weight loss and metabolic health
  • reduction in symptoms associated with comorbid conditions
  • improvement in self-esteem and overall quality of life.

A 2015 comparative effectiveness review of management and outcomes for patients with BED evaluated pharmacologic, psychologic, behavioral, and combined approaches for treating patients with BED.7 The results suggested that second-generation antidepressants, topiramate, and lisdexamfetamine were superior to placebo in reducing binge-eating episodes and achieving abstinence from binge-eating. Weight reduction was also achieved with topiramate and lisdexamfetamine, and antidepressants helped relieve symptoms of comorbid depression.

Various formats of CBT, including therapist-led and guided self-help, were also superior to placebo in reducing the frequency of binge-eating and promoting abstinence; however, they were generally not effective in treating depression or reducing patients’ weight.7

OUTCOME Fixated on surgery

We appeal the decision of Ms. C’s insurance company; however, during the appeals process, Ms. C becomes increasingly irritable and informs us that she has changed her mind and, with the reported support of her medical doctors, wishes to undergo bariatric surgery. Although we made multiple attempts to engage Ms. C in further treatment, she is lost to follow-up.

Continue to: Bottom Line

 

 

Bottom Line

Diagnosing and managing patients with binge eating disorder (BED) can be challenging because patients may hesitate to seek help, and/or have psychiatric and medical comorbidities. They often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics. Once BED is confirmed, screen for other psychiatric and medical comorbidities. A combination of pharmacologic and psychotherapeutic interventions can benefit some patients with BED, but treatment should be individualized.

Related Resources

  • National Eating Disorders Association. NEDA. www.nationaleatingdisorders.org/.
  • Safer D, Telch C, Chen EY. Dialectical behavior therapy for binge eating and bulimia. New York, NY: Guilford Press; 2017.

Drug Brand Names

Fluoxetine • Prozac
Levothyroxine • Synthroid
Lisdexamfetamine • Vyvanse
Topiramate • Topamax

CASE Uncontrollable eating and weight gain

Ms. C, age 33, presents to an outpatient clinic with complaints of weight gain and “uncontrollable eating.” Ms. C says she’s gained >50 lb over the last year. She describes progressively frequent episodes of overeating during which she feels that she has no control over the amount of food she consumes. She reports eating as often as 10 times a day, and overeating to the point of physical discomfort during most meals. She gives an example of having recently consumed a large pizza, several portions of Chinese food, approximately 20 chicken wings, and half a chocolate cake for dinner. Ms. C admits that on several occasions she has vomited after meals due to feeling extremely full; however, she denies having done so intentionally. She also denies restricting her food intake, misusing laxatives or diuretics, or exercising excessively.

Ms. C expresses frustration and embarrassment with her eating and resulting weight gain. She says she has poor self-esteem, low energy and motivation, and poor concentration. She feels that her condition has significantly impacted her social life, romantic relationships, and family life. She admits she’s been avoiding dating and seeing friends due to her weight gain, and has been irritable with her teenage daughter.

During her initial evaluation, Ms. C is alert and oriented, with a linear and goal-directed thought process. She is somewhat irritable and guarded, wearing large sunglasses that cover most of her face, but is not overtly paranoid. Although she appears frustrated when discussing her condition, she denies feeling hopeless or helpless.

 

HISTORY Thyroid cancer and mood swings

Ms. C, who is single and unemployed, lives in an apartment with her teenage daughter, with whom she describes having a good relationship. She has been receiving disability benefits for the past 2 years after a motor vehicle accident resulted in multiple fractures of her arm and elbow, and subsequent chronic pain. Ms. C reports a distant history of “problems with alcohol,” but denies drinking any alcohol since being charged with driving under the influence several years ago. She has a 10 pack-year history of smoking and denies any history of illicit drug use.

Two years ago, Ms. C was diagnosed with thyroid carcinoma, and treated with surgical resection and a course of radiation. She has regular visits with her endocrinologist and has been prescribed oral levothyroxine, 150 mcg/d.

Ms. C reports a history of “mood swings” characterized by “snapping at people” and becoming irritable in response to stressful situations, but denies any past symptoms consistent with a manic or hypomanic episode. Ms. C has not been admitted to a psychiatric hospital, nor has she received any prior psychiatric treatment. She reluctantly discloses that approximately 3 years ago she had a less severe episode of uncontrollable eating and weight gain (20 to 30 lb). At that time, she was able to regain her desired physical appearance by going on the “Subway diet” and undergoing liposuction and plastic surgery.

At her current outpatient clinic visit, Ms. C expresses an interest in exploring bariatric surgery as a potential solution to her weight gain.

[polldaddy:10446186]

Continue to: EVALUATION Obese; stable thyroid function

 

 

EVALUATION Obese; stable thyroid function

We refer Ms. C for a physical examination and routine blood analysis to rule out any medical contributors to her condition. Her physical examination is reported as normal, with no signs of skin changes, goiter, or exophthalmos. Ms. C is noted to be obese, with a body mass index of 37.2 kg/m2, and an abdominal circumference of 38.5 in.

A blood analysis shows that Ms. C has elevated triglyceride levels (202 mg/dL) and elevated cholesterol levels (210 mg/dL). Her thyroid function tests are within normal limits based on the dose of levothyroxine she’s been receiving. A pregnancy test is negative.

Ms. C gives the team at the clinic permission to contact her endocrinologist, who reports that he does not suspect that Ms. C’s drastic weight gain and abnormal eating patterns are attributable to her history of thyroid carcinoma because her thyroid function tests have been stable on her current regimen.

The authors’ observations

Based on Ms. C’s initial presentation, we strongly suspected a diagnosis of binge eating disorder (BED). Several differential diagnoses were considered and carefully ruled out; Ms. C’s medical workup did not suggest that her weight gain was due to an active medical condition, and she did not meet DSM-5 criteria for a mood or psychotic disorder or anorexia nervosa or bulimia nervosa.

With an estimated lifetime prevalence in the United States of 2.6%, BED is the most prevalent eating disorder (compared with 0.6% for anorexia nervosa and 1% for bulimia nervosa).1 BED is more prevalent in women than in men, and the mean age of onset is mid-20s.

Continue to: BED may be difficult...

 

 

BED may be difficult to detect because patients may feel ashamed or guilty and are often hesitant to disclose and discuss their symptoms. Furthermore, they are frequently frustrated by the subjective loss of control over their behaviors. Patients with BED often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics.

Screening for eating disorders

Several screening instruments have been developed to help clinicians identify patients who may need further evaluation for possible diagnosis of an eating disorder, including anorexia nervosa, bulimia nervosa, and BED.2 The SCOFF questionnaire is composed of 5 brief clinician-administered questions to screen for eating disorders.2 The 7-item Binge Eating Disorder Screener (BED-7) is a screening instrument specific for BED that examines a patient’s eating patterns and behaviors during the past 3 months.3

In general, suspect BED in patients who have significant weight dissatisfaction, fluctuation in weight, and depressive symptoms. The DSM-5 criteria for binge eating disorder are shown in Table 14.

DSM-5 criteria for binge eating disorder

BED and comorbid psychiatric disorders

Patients with BED are more likely than the general population to have comorbid psychiatric disorders, including mood and anxiety disorders, attention-deficit/hyperactivity disorder, posttraumatic stress disorder, and substance use disorders. Swanson et al5 found that 83.5% of adolescents who met criteria for BED also met criteria for at least 1 other psychiatric disorder, and 37% endorsed >3 concurrent psychiatric conditions. Once BED is confirmed, it is important to screen for other psychiatric and medical comorbidities that are often present in individuals with BED (Table 21,6).

Psychiatric and medical comorbidities associated with BED

The rates of diagnosis and treatment of BED remain low. This is likely due to patient factors such as shame and fear of stigma and clinician factors such as lack of awareness, ineffective communication, hesitation to discuss the sensitive topic, or insufficient knowledge about treatment options once BED is diagnosed.

[polldaddy:10446187]

Continue to: TREATMENT Combination therapy

 

 

TREATMENT Combination therapy

Ms. C is ambivalent about her BED diagnosis, and becomes angry about it when the proposed treatments do not involve bariatric surgery or cosmetic procedures. Ms. C is enrolled in weekly individual psychotherapy, where she receives a combination of CBT and psychodynamic therapy; however, her attendance is inconsistent. Ms. C is offered a trial of fluoxetine, but adamantly refuses, citing a relative who experienced adverse effects while receiving this type of antidepressant. Ms. C also refuses a trial of topiramate due to concerns of feeling sedated. Finally, she is offered a trial of lisdexamfetamine, 30 mg/d, which was FDA-approved in 2015 to treat moderate to severe BED. We discuss the risks, benefits, and adverse effects of lisdexamfetamine with Ms. C; however, she is hesitant to start this medication and expresses increasing interest in obtaining a consultation for bariatric surgery. Ms. C is provided with extensive education about the risks and dangers of surgery before addressing her eating patterns, and the clinician provides validation, verbal support, and counseling. Ms. C eventually agrees to a trial of lisdexamfetamine, but her insurance denies coverage of this medication.

The authors’ observations

When developing an individualized treatment plan for a patient with BED, the patient’s psychiatric and medical comorbidities should be considered. Treatment goals for patients with BED include:

  • abstinence from binge eating
  • sustainable weight loss and metabolic health
  • reduction in symptoms associated with comorbid conditions
  • improvement in self-esteem and overall quality of life.

A 2015 comparative effectiveness review of management and outcomes for patients with BED evaluated pharmacologic, psychologic, behavioral, and combined approaches for treating patients with BED.7 The results suggested that second-generation antidepressants, topiramate, and lisdexamfetamine were superior to placebo in reducing binge-eating episodes and achieving abstinence from binge-eating. Weight reduction was also achieved with topiramate and lisdexamfetamine, and antidepressants helped relieve symptoms of comorbid depression.

Various formats of CBT, including therapist-led and guided self-help, were also superior to placebo in reducing the frequency of binge-eating and promoting abstinence; however, they were generally not effective in treating depression or reducing patients’ weight.7

OUTCOME Fixated on surgery

We appeal the decision of Ms. C’s insurance company; however, during the appeals process, Ms. C becomes increasingly irritable and informs us that she has changed her mind and, with the reported support of her medical doctors, wishes to undergo bariatric surgery. Although we made multiple attempts to engage Ms. C in further treatment, she is lost to follow-up.

Continue to: Bottom Line

 

 

Bottom Line

Diagnosing and managing patients with binge eating disorder (BED) can be challenging because patients may hesitate to seek help, and/or have psychiatric and medical comorbidities. They often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics. Once BED is confirmed, screen for other psychiatric and medical comorbidities. A combination of pharmacologic and psychotherapeutic interventions can benefit some patients with BED, but treatment should be individualized.

Related Resources

  • National Eating Disorders Association. NEDA. www.nationaleatingdisorders.org/.
  • Safer D, Telch C, Chen EY. Dialectical behavior therapy for binge eating and bulimia. New York, NY: Guilford Press; 2017.

Drug Brand Names

Fluoxetine • Prozac
Levothyroxine • Synthroid
Lisdexamfetamine • Vyvanse
Topiramate • Topamax

References

1. Hudson JI, Hiripi E, Pope HG Jr, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;61(3):348-358.
2. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: assessment of a new screening tool for eating disorders. BMJ. 1999;319(7223):1467-1468.
3. Herman BK, Deal LS, DiBenedetti DB, et al. Development of the 7-Item Binge-Eating Disorder screener (BEDS-7). Prim Care Companion CNS Disord. 2016;18(2):10.4088/PCC.15m01896. doi:10.4088/PCC.15m01896.
4. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
5. Swanson SA, Crow SJ, Le Grange D, et al. Prevalence and correlates of eating disorders in adolescents. Results from the national comorbidity survey replication adolescent supplement. Arch Gen Psychiatry. 2011;68(7):714.
6. Guerdjikova AI, Mori N, Casuto LS, et al. Binge eating disorder. Psychiatric Clinics of North America. 2017;40(2):255-266.
7. Berkman ND, Brownley KA, Peat CM, et al. Management and outcomes of binge-eating disorder. Comparative Effectiveness Reviews, No. 160. Agency for Healthcare Research and Quality (US). https://www.ncbi.nlm.nih.gov/books/NBK338312/. Published December 2015. Accessed July 29, 2019.

References

1. Hudson JI, Hiripi E, Pope HG Jr, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;61(3):348-358.
2. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: assessment of a new screening tool for eating disorders. BMJ. 1999;319(7223):1467-1468.
3. Herman BK, Deal LS, DiBenedetti DB, et al. Development of the 7-Item Binge-Eating Disorder screener (BEDS-7). Prim Care Companion CNS Disord. 2016;18(2):10.4088/PCC.15m01896. doi:10.4088/PCC.15m01896.
4. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
5. Swanson SA, Crow SJ, Le Grange D, et al. Prevalence and correlates of eating disorders in adolescents. Results from the national comorbidity survey replication adolescent supplement. Arch Gen Psychiatry. 2011;68(7):714.
6. Guerdjikova AI, Mori N, Casuto LS, et al. Binge eating disorder. Psychiatric Clinics of North America. 2017;40(2):255-266.
7. Berkman ND, Brownley KA, Peat CM, et al. Management and outcomes of binge-eating disorder. Comparative Effectiveness Reviews, No. 160. Agency for Healthcare Research and Quality (US). https://www.ncbi.nlm.nih.gov/books/NBK338312/. Published December 2015. Accessed July 29, 2019.

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Eating disorders may add to poor type 2 control, but BMI confounds the issue

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Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.

“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.

In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.

Although FBG and HbA1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.

The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.

However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.

The researchers had no financial conflicts to disclose.
 

SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.

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Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.

“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.

In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.

Although FBG and HbA1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.

The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.

However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.

The researchers had no financial conflicts to disclose.
 

SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.

Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.

“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.

In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.

Although FBG and HbA1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.

The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.

However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.

The researchers had no financial conflicts to disclose.
 

SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.

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Duloxetine ‘sprinkle’ launches for patients with difficulty swallowing

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Drizalma Sprinkle (duloxetine delayed-release capsule) has launched for the treatment of various neuropsychiatric and pain disorders in patients with difficulty swallowing, according to a release from Sun Pharma. It can be swallowed whole, sprinkled on applesauce, or administered via nasogastric tube.

Difficulty swallowing affects approximately 30%-35% of long-term care residents, but the main alternative – crushing tablets – introduces risks of its own to the administration process.

This sprinkle is indicated for the treatment of major depressive disorder in adults, generalized anxiety disorder in patients aged 7 years and older, diabetic peripheral neuropathic pain in adults, and chronic musculoskeletal pain in adults. It was approved by the Food and Drug Administration for these indications July 19, 2019.

It carries a boxed warning for suicidal thoughts and behaviors. The most common adverse reactions (5% or more of treated participants and twice the incidence with placebo) were nausea, dry mouth, somnolence, constipation, decreased appetite, and hyperhidrosis. The full prescribing information can be found on the FDA website.

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Drizalma Sprinkle (duloxetine delayed-release capsule) has launched for the treatment of various neuropsychiatric and pain disorders in patients with difficulty swallowing, according to a release from Sun Pharma. It can be swallowed whole, sprinkled on applesauce, or administered via nasogastric tube.

Difficulty swallowing affects approximately 30%-35% of long-term care residents, but the main alternative – crushing tablets – introduces risks of its own to the administration process.

This sprinkle is indicated for the treatment of major depressive disorder in adults, generalized anxiety disorder in patients aged 7 years and older, diabetic peripheral neuropathic pain in adults, and chronic musculoskeletal pain in adults. It was approved by the Food and Drug Administration for these indications July 19, 2019.

It carries a boxed warning for suicidal thoughts and behaviors. The most common adverse reactions (5% or more of treated participants and twice the incidence with placebo) were nausea, dry mouth, somnolence, constipation, decreased appetite, and hyperhidrosis. The full prescribing information can be found on the FDA website.

[email protected]

Drizalma Sprinkle (duloxetine delayed-release capsule) has launched for the treatment of various neuropsychiatric and pain disorders in patients with difficulty swallowing, according to a release from Sun Pharma. It can be swallowed whole, sprinkled on applesauce, or administered via nasogastric tube.

Difficulty swallowing affects approximately 30%-35% of long-term care residents, but the main alternative – crushing tablets – introduces risks of its own to the administration process.

This sprinkle is indicated for the treatment of major depressive disorder in adults, generalized anxiety disorder in patients aged 7 years and older, diabetic peripheral neuropathic pain in adults, and chronic musculoskeletal pain in adults. It was approved by the Food and Drug Administration for these indications July 19, 2019.

It carries a boxed warning for suicidal thoughts and behaviors. The most common adverse reactions (5% or more of treated participants and twice the incidence with placebo) were nausea, dry mouth, somnolence, constipation, decreased appetite, and hyperhidrosis. The full prescribing information can be found on the FDA website.

[email protected]

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Yale-Brown Obsessive Scale shows value for assessing binge eating patients

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Mon, 10/21/2019 - 09:49

Symptoms of binge eating disorder can be assessed with a modified version of the Yale-Brown Obsessive Compulsive Scale, based on data from an analysis of three phase III studies.

The Yale-Brown Obsessive Compulsive Scale Modified for Binge Eating (Y-BOCS-BE) is designed to assess symptoms of binge eating disorder (BED), including binge eating thoughts and compulsiveness. “Psychometric testing and analysis of the Y-BOCS-BE is being conducted as a multistage process to optimize the characterization of BED,” wrote Karen Yee, PhD, of Shire (now part of Takeda), Boston, and colleagues.

In a study published in Quality of Life Research, investigators examined the validity of the Y-BOCS-BE in terms of dimensionality, internal consistency, convergent validity, test-retest reliability, and determination of clinically meaningful improvement. The Y-BOCS-BE is a 10-item clinician-rated scale with total scores from 0 to 4 on which 0 equals no symptoms and 4 equals extreme symptoms.

Overall, the Y-BOCS-BE’s internal consistency and convergent validity were maximized at 12 weeks, and test-retest reliability was maximized in an 8-week retest interval, minimal clinically important improvement could not be assessed in the two short-term efficacy studies, but “estimates in score reductions of 12-17 points were taken to represent the best estimates of clinically meaningful improvement,” the researchers said.

The findings were limited by several factors including the use of a study population of BED patients without psychiatric comorbidities, and the inclusion only of those who did not relapse the researchers noted. However, the results “set the stage for normalizing the Y-BOCS-BE and increasing the understanding of the clinical significance of Y-BOCS-BE scores and score changes to be useful both for clinical practice and clinical research,” they said.

Dr. Yee disclosed being employed by Shire and owning stock in Takeda. The studies were funded by Shire.

SOURCE: Yee K et al. Qual Life Res. 2019 Aug 31. doi: 10.1007/s11136-019-02277-8 .

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Symptoms of binge eating disorder can be assessed with a modified version of the Yale-Brown Obsessive Compulsive Scale, based on data from an analysis of three phase III studies.

The Yale-Brown Obsessive Compulsive Scale Modified for Binge Eating (Y-BOCS-BE) is designed to assess symptoms of binge eating disorder (BED), including binge eating thoughts and compulsiveness. “Psychometric testing and analysis of the Y-BOCS-BE is being conducted as a multistage process to optimize the characterization of BED,” wrote Karen Yee, PhD, of Shire (now part of Takeda), Boston, and colleagues.

In a study published in Quality of Life Research, investigators examined the validity of the Y-BOCS-BE in terms of dimensionality, internal consistency, convergent validity, test-retest reliability, and determination of clinically meaningful improvement. The Y-BOCS-BE is a 10-item clinician-rated scale with total scores from 0 to 4 on which 0 equals no symptoms and 4 equals extreme symptoms.

Overall, the Y-BOCS-BE’s internal consistency and convergent validity were maximized at 12 weeks, and test-retest reliability was maximized in an 8-week retest interval, minimal clinically important improvement could not be assessed in the two short-term efficacy studies, but “estimates in score reductions of 12-17 points were taken to represent the best estimates of clinically meaningful improvement,” the researchers said.

The findings were limited by several factors including the use of a study population of BED patients without psychiatric comorbidities, and the inclusion only of those who did not relapse the researchers noted. However, the results “set the stage for normalizing the Y-BOCS-BE and increasing the understanding of the clinical significance of Y-BOCS-BE scores and score changes to be useful both for clinical practice and clinical research,” they said.

Dr. Yee disclosed being employed by Shire and owning stock in Takeda. The studies were funded by Shire.

SOURCE: Yee K et al. Qual Life Res. 2019 Aug 31. doi: 10.1007/s11136-019-02277-8 .

Symptoms of binge eating disorder can be assessed with a modified version of the Yale-Brown Obsessive Compulsive Scale, based on data from an analysis of three phase III studies.

The Yale-Brown Obsessive Compulsive Scale Modified for Binge Eating (Y-BOCS-BE) is designed to assess symptoms of binge eating disorder (BED), including binge eating thoughts and compulsiveness. “Psychometric testing and analysis of the Y-BOCS-BE is being conducted as a multistage process to optimize the characterization of BED,” wrote Karen Yee, PhD, of Shire (now part of Takeda), Boston, and colleagues.

In a study published in Quality of Life Research, investigators examined the validity of the Y-BOCS-BE in terms of dimensionality, internal consistency, convergent validity, test-retest reliability, and determination of clinically meaningful improvement. The Y-BOCS-BE is a 10-item clinician-rated scale with total scores from 0 to 4 on which 0 equals no symptoms and 4 equals extreme symptoms.

Overall, the Y-BOCS-BE’s internal consistency and convergent validity were maximized at 12 weeks, and test-retest reliability was maximized in an 8-week retest interval, minimal clinically important improvement could not be assessed in the two short-term efficacy studies, but “estimates in score reductions of 12-17 points were taken to represent the best estimates of clinically meaningful improvement,” the researchers said.

The findings were limited by several factors including the use of a study population of BED patients without psychiatric comorbidities, and the inclusion only of those who did not relapse the researchers noted. However, the results “set the stage for normalizing the Y-BOCS-BE and increasing the understanding of the clinical significance of Y-BOCS-BE scores and score changes to be useful both for clinical practice and clinical research,” they said.

Dr. Yee disclosed being employed by Shire and owning stock in Takeda. The studies were funded by Shire.

SOURCE: Yee K et al. Qual Life Res. 2019 Aug 31. doi: 10.1007/s11136-019-02277-8 .

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Study: Half of college women exhibited binge eating symptoms

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Mon, 10/21/2019 - 09:50

Approximately half of college-aged women exhibit binge eating symptoms, and these women scored significantly higher on measures of depression, stress, and anxiety than do non–binge eaters, based on data from 154 women at a Palestine Polytechnic University in Hebron.

Previous studies show that binge eating disorder is multifactorial and associated with depression and anxiety, however, “To our knowledge, no study has yet assessed the prevalence of binge eating symptoms among female university students,” wrote Manal M. Badrasawi, PhD, of An-Najah National University, Tulkarm, Palestine, and colleagues.

In a cross-sectional study published in the Journal of Eating Disorders, the researchers interviewed 154 female college students in Palestine using the using BEDS-7 (Binge Eating Disorder Screener-7). The average age of the participants was 20 years.

Overall, 50% of the students showed positive binge eating symptoms, and these individuals had significantly higher scores on measures of depression, stress, and anxiety compared to individuals without binge eating symptoms.

Binge eating also was significantly associated with greater frequency of eating between meals and increased snacking, but no significant association was noted between binge eating and sociodemographic variables, including place of residence, marital status, and years of study. Binge eating was not significantly associated with weight status.

The researchers had no financial conflicts to disclose.

SOURCE: Badrasawi MM et al. J Eat Disord. 2019 Oct 2;7:33. doi: 10.1186/s40337-019-0263-1.2019.

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Approximately half of college-aged women exhibit binge eating symptoms, and these women scored significantly higher on measures of depression, stress, and anxiety than do non–binge eaters, based on data from 154 women at a Palestine Polytechnic University in Hebron.

Previous studies show that binge eating disorder is multifactorial and associated with depression and anxiety, however, “To our knowledge, no study has yet assessed the prevalence of binge eating symptoms among female university students,” wrote Manal M. Badrasawi, PhD, of An-Najah National University, Tulkarm, Palestine, and colleagues.

In a cross-sectional study published in the Journal of Eating Disorders, the researchers interviewed 154 female college students in Palestine using the using BEDS-7 (Binge Eating Disorder Screener-7). The average age of the participants was 20 years.

Overall, 50% of the students showed positive binge eating symptoms, and these individuals had significantly higher scores on measures of depression, stress, and anxiety compared to individuals without binge eating symptoms.

Binge eating also was significantly associated with greater frequency of eating between meals and increased snacking, but no significant association was noted between binge eating and sociodemographic variables, including place of residence, marital status, and years of study. Binge eating was not significantly associated with weight status.

The researchers had no financial conflicts to disclose.

SOURCE: Badrasawi MM et al. J Eat Disord. 2019 Oct 2;7:33. doi: 10.1186/s40337-019-0263-1.2019.

Approximately half of college-aged women exhibit binge eating symptoms, and these women scored significantly higher on measures of depression, stress, and anxiety than do non–binge eaters, based on data from 154 women at a Palestine Polytechnic University in Hebron.

Previous studies show that binge eating disorder is multifactorial and associated with depression and anxiety, however, “To our knowledge, no study has yet assessed the prevalence of binge eating symptoms among female university students,” wrote Manal M. Badrasawi, PhD, of An-Najah National University, Tulkarm, Palestine, and colleagues.

In a cross-sectional study published in the Journal of Eating Disorders, the researchers interviewed 154 female college students in Palestine using the using BEDS-7 (Binge Eating Disorder Screener-7). The average age of the participants was 20 years.

Overall, 50% of the students showed positive binge eating symptoms, and these individuals had significantly higher scores on measures of depression, stress, and anxiety compared to individuals without binge eating symptoms.

Binge eating also was significantly associated with greater frequency of eating between meals and increased snacking, but no significant association was noted between binge eating and sociodemographic variables, including place of residence, marital status, and years of study. Binge eating was not significantly associated with weight status.

The researchers had no financial conflicts to disclose.

SOURCE: Badrasawi MM et al. J Eat Disord. 2019 Oct 2;7:33. doi: 10.1186/s40337-019-0263-1.2019.

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FDA accepts dasotraline NDA for binge-eating disorder

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Wed, 07/31/2019 - 15:03

 

The Food and Drug Administration has accepted the new drug application for dasotraline for the treatment of moderate to severe binge-eating disorder, the drug’s developer, Sunovion, announced July 30.

Dasotraline, a dopamine and norepinephrine reuptake inhibitor, demonstrated significant efficacy in a pair of 12-week, randomized, placebo-controlled studies (SEP360-221 and SEP360-321). The drug also was found to be well tolerated by patients with binge-eating disorder (BED), both in those studies and in a long-term safety study that followed patients for up to a year (SEP360-322).

The medication – characterized by an extended half-life – is to be taken once a day. The most common adverse events reported by patients who took dasotraline include insomnia, dry mouth, decreased appetite, anxiety, nausea, and decreased weight.

BED is more common than any other eating disorder, with an estimated lifetime prevalence among U.S. adults of 1.25% for women and 0.42% for men (CNS Spectr. 2019 Jun 14. doi: 10.1017/S109285291900103). The condition also might run in families. BED often is comorbid with other psychiatric and behavioral disorders, such as depression, substance use, and PTSD, noted Antony Loebel, MD, president and CEO of Sunovion, in a press release. He also said BED often is underrecognized and undertreated.

Meta-analytic reviews show that cognitive-behavioral therapy is considered first-line treatment for BED. However, limited access to such psychological treatments makes the development of medication options such as dasotraline important.

Last year, the agency rejected a new drug application for dasotraline for the treatment of ADHD, citing a need for additional data. The action date by the FDA on dasotraline for BED is May 14, 2020, Sunovion reported.

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The Food and Drug Administration has accepted the new drug application for dasotraline for the treatment of moderate to severe binge-eating disorder, the drug’s developer, Sunovion, announced July 30.

Dasotraline, a dopamine and norepinephrine reuptake inhibitor, demonstrated significant efficacy in a pair of 12-week, randomized, placebo-controlled studies (SEP360-221 and SEP360-321). The drug also was found to be well tolerated by patients with binge-eating disorder (BED), both in those studies and in a long-term safety study that followed patients for up to a year (SEP360-322).

The medication – characterized by an extended half-life – is to be taken once a day. The most common adverse events reported by patients who took dasotraline include insomnia, dry mouth, decreased appetite, anxiety, nausea, and decreased weight.

BED is more common than any other eating disorder, with an estimated lifetime prevalence among U.S. adults of 1.25% for women and 0.42% for men (CNS Spectr. 2019 Jun 14. doi: 10.1017/S109285291900103). The condition also might run in families. BED often is comorbid with other psychiatric and behavioral disorders, such as depression, substance use, and PTSD, noted Antony Loebel, MD, president and CEO of Sunovion, in a press release. He also said BED often is underrecognized and undertreated.

Meta-analytic reviews show that cognitive-behavioral therapy is considered first-line treatment for BED. However, limited access to such psychological treatments makes the development of medication options such as dasotraline important.

Last year, the agency rejected a new drug application for dasotraline for the treatment of ADHD, citing a need for additional data. The action date by the FDA on dasotraline for BED is May 14, 2020, Sunovion reported.

 

The Food and Drug Administration has accepted the new drug application for dasotraline for the treatment of moderate to severe binge-eating disorder, the drug’s developer, Sunovion, announced July 30.

Dasotraline, a dopamine and norepinephrine reuptake inhibitor, demonstrated significant efficacy in a pair of 12-week, randomized, placebo-controlled studies (SEP360-221 and SEP360-321). The drug also was found to be well tolerated by patients with binge-eating disorder (BED), both in those studies and in a long-term safety study that followed patients for up to a year (SEP360-322).

The medication – characterized by an extended half-life – is to be taken once a day. The most common adverse events reported by patients who took dasotraline include insomnia, dry mouth, decreased appetite, anxiety, nausea, and decreased weight.

BED is more common than any other eating disorder, with an estimated lifetime prevalence among U.S. adults of 1.25% for women and 0.42% for men (CNS Spectr. 2019 Jun 14. doi: 10.1017/S109285291900103). The condition also might run in families. BED often is comorbid with other psychiatric and behavioral disorders, such as depression, substance use, and PTSD, noted Antony Loebel, MD, president and CEO of Sunovion, in a press release. He also said BED often is underrecognized and undertreated.

Meta-analytic reviews show that cognitive-behavioral therapy is considered first-line treatment for BED. However, limited access to such psychological treatments makes the development of medication options such as dasotraline important.

Last year, the agency rejected a new drug application for dasotraline for the treatment of ADHD, citing a need for additional data. The action date by the FDA on dasotraline for BED is May 14, 2020, Sunovion reported.

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