Child Psychiatry Consult

While it is well established that medications can be an important aspect of treatment for youth who meet the criteria for attention-deficit/hyperactivity disorder (ADHD), too often clinicians neglect to address important nonpharmacologic interventions that have increasingly been shown to be effective. This column is devoted to reviewing some of the many components of a treatment plan other than medications that could be utilized to provide a more comprehensive and wellness-informed approach to children who struggle with ADHD symptoms.

Case summary

Ethan is a 7-year-old boy who presents with his parents for an ADHD evaluation. The pediatrician conducts the evaluation according to American Academy of Pediatrics guidelines, which include the use of rating scales from multiple sources. The outcome of the assessment is that Ethan does indeed meet criteria for ADHD and his symptoms are causing impairment in his school work, home environment, and interactions with his peers. Treatment is recommended.

Discussion

It is easy to rely exclusively on medications when the focus of the evaluation is solely about symptoms. When clinicians expand their view to assess various domains of wellness and health promotion, however, several other potential avenues for intervention often become apparent. Asking about sleep routines, nutrition, participation in the arts and music, physical activity, reading, and screen time – among other things – can reveal the following specific areas that require guidance and support:

•  Exercise. Children today are increasingly sedentary, and there is increasing evidence that physical activity is inversely related to several ADHD behaviors (J Am Acad Child Adolesc Psychiatry. 2015 Jul;54:565-70). Counsel families about the importance of exercise and try to help the family develop a plan that includes the provision for regular physical activity. Joining sports teams may be particularly useful as it ensures that regular exercise takes place and offers some additional benefits inherent in playing with a team.

•  Screen time. Although there has been active discussion lately about what constitutes “too much” screen time, it is clear that many children well exceed even the most liberal thresholds. Furthermore, there is increasing evidence that excessive screen time can lead to worsening attention problems over time (Pediatrics. 2004;113:708-13). One technique that can be effective, especially for younger children, is to have them “earn” their screen time by engaging in other activities such as reading or exercise.

•  Nutrition. Apart from any specific deficiency states, research shows that a healthier diet in general is associated with lower levels of behavioral problems. With regard to ADHD, one aspect that is often worth investigating specifically is whether the child gets a nutritious breakfast each morning that can help keep attentional skills optimal.

•  Musical training. Some intriguing new research is showing links between brain maturation and musical training, and in some of the very regions of the brain that have been implicated in ADHD (J Am Acad Child Adolesc Psychiatry. 2014;53:1153-61).

•  Omega-3s. A meta-analysis demonstrated that omega-3 supplementation can improve ADHD symptoms (J Am Acad Child Adolesc Psychiatry. 2011 Oct;50:991-1000). While the optimal dose remains under investigation, there is some evidence that improved response was related to higher eicosapentaenoic acid doses.

•  Skills training. To some degree, many skills associated with ADHD (disorganization, forgetfulness, distractibility) can be specifically taught with techniques such as mindfulness (J Atten Disord. 2015 Feb;19[2]:147-57). Having families work with counselors who have specific training in ADHD can be a very useful part of treatment and can help teach important lifelong skills. Parent behavioral therapy also can be effective around many behaviors such as defiance and aggression that accompany ADHD.

Case follow-up

The pediatrician decides to enhance her assessment by inquiring about many domains of wellness, and she discovers that Ethan has chronic problems getting to sleep, and he spends many hours each day playing video games to the exclusion of physical activity. She offers some strategies to improve these areas while the family investigates working with a counselor who has specific expertise in enhancing cognitive skills. Initial improvements are encouraging, and the family decides to pursue these avenues further while delaying medication treatment, at least for now.

By keeping in mind these important other treatment domains, pediatricians can avoid the trap of overrelying on medications as the sole method of treatment while encouraging techniques that will provide long-term benefits in overall health and wellness.

Dr. Rettew is an associate professor of psychiatry and pediatrics at the University of Vermont, Burlington. Dr. Rettew said he has no relevant financial disclosures. Follow him on Twitter @pedipsych. E-mail him at [email protected].

While it is well established that medications can be an important aspect of treatment for youth who meet the criteria for attention-deficit/hyperactivity disorder (ADHD), too often clinicians neglect to address important nonpharmacologic interventions that have increasingly been shown to be effective. This column is devoted to reviewing some of the many components of a treatment plan other than medications that could be utilized to provide a more comprehensive and wellness-informed approach to children who struggle with ADHD symptoms.

Case summary

Ethan is a 7-year-old boy who presents with his parents for an ADHD evaluation. The pediatrician conducts the evaluation according to American Academy of Pediatrics guidelines, which include the use of rating scales from multiple sources. The outcome of the assessment is that Ethan does indeed meet criteria for ADHD and his symptoms are causing impairment in his school work, home environment, and interactions with his peers. Treatment is recommended.

Discussion

It is easy to rely exclusively on medications when the focus of the evaluation is solely about symptoms. When clinicians expand their view to assess various domains of wellness and health promotion, however, several other potential avenues for intervention often become apparent. Asking about sleep routines, nutrition, participation in the arts and music, physical activity, reading, and screen time – among other things – can reveal the following specific areas that require guidance and support:

•  Exercise. Children today are increasingly sedentary, and there is increasing evidence that physical activity is inversely related to several ADHD behaviors (J Am Acad Child Adolesc Psychiatry. 2015 Jul;54:565-70). Counsel families about the importance of exercise and try to help the family develop a plan that includes the provision for regular physical activity. Joining sports teams may be particularly useful as it ensures that regular exercise takes place and offers some additional benefits inherent in playing with a team.

•  Screen time. Although there has been active discussion lately about what constitutes “too much” screen time, it is clear that many children well exceed even the most liberal thresholds. Furthermore, there is increasing evidence that excessive screen time can lead to worsening attention problems over time (Pediatrics. 2004;113:708-13). One technique that can be effective, especially for younger children, is to have them “earn” their screen time by engaging in other activities such as reading or exercise.

•  Nutrition. Apart from any specific deficiency states, research shows that a healthier diet in general is associated with lower levels of behavioral problems. With regard to ADHD, one aspect that is often worth investigating specifically is whether the child gets a nutritious breakfast each morning that can help keep attentional skills optimal.

•  Musical training. Some intriguing new research is showing links between brain maturation and musical training, and in some of the very regions of the brain that have been implicated in ADHD (J Am Acad Child Adolesc Psychiatry. 2014;53:1153-61).

•  Omega-3s. A meta-analysis demonstrated that omega-3 supplementation can improve ADHD symptoms (J Am Acad Child Adolesc Psychiatry. 2011 Oct;50:991-1000). While the optimal dose remains under investigation, there is some evidence that improved response was related to higher eicosapentaenoic acid doses.

•  Skills training. To some degree, many skills associated with ADHD (disorganization, forgetfulness, distractibility) can be specifically taught with techniques such as mindfulness (J Atten Disord. 2015 Feb;19[2]:147-57). Having families work with counselors who have specific training in ADHD can be a very useful part of treatment and can help teach important lifelong skills. Parent behavioral therapy also can be effective around many behaviors such as defiance and aggression that accompany ADHD.

Case follow-up

The pediatrician decides to enhance her assessment by inquiring about many domains of wellness, and she discovers that Ethan has chronic problems getting to sleep, and he spends many hours each day playing video games to the exclusion of physical activity. She offers some strategies to improve these areas while the family investigates working with a counselor who has specific expertise in enhancing cognitive skills. Initial improvements are encouraging, and the family decides to pursue these avenues further while delaying medication treatment, at least for now.

By keeping in mind these important other treatment domains, pediatricians can avoid the trap of overrelying on medications as the sole method of treatment while encouraging techniques that will provide long-term benefits in overall health and wellness.

Dr. Rettew is an associate professor of psychiatry and pediatrics at the University of Vermont, Burlington. Dr. Rettew said he has no relevant financial disclosures. Follow him on Twitter @pedipsych. E-mail him at [email protected].

While it is well established that medications can be an important aspect of treatment for youth who meet the criteria for attention-deficit/hyperactivity disorder (ADHD), too often clinicians neglect to address important nonpharmacologic interventions that have increasingly been shown to be effective. This column is devoted to reviewing some of the many components of a treatment plan other than medications that could be utilized to provide a more comprehensive and wellness-informed approach to children who struggle with ADHD symptoms.

Case summary

Ethan is a 7-year-old boy who presents with his parents for an ADHD evaluation. The pediatrician conducts the evaluation according to American Academy of Pediatrics guidelines, which include the use of rating scales from multiple sources. The outcome of the assessment is that Ethan does indeed meet criteria for ADHD and his symptoms are causing impairment in his school work, home environment, and interactions with his peers. Treatment is recommended.

Discussion

It is easy to rely exclusively on medications when the focus of the evaluation is solely about symptoms. When clinicians expand their view to assess various domains of wellness and health promotion, however, several other potential avenues for intervention often become apparent. Asking about sleep routines, nutrition, participation in the arts and music, physical activity, reading, and screen time – among other things – can reveal the following specific areas that require guidance and support:

•  Exercise. Children today are increasingly sedentary, and there is increasing evidence that physical activity is inversely related to several ADHD behaviors (J Am Acad Child Adolesc Psychiatry. 2015 Jul;54:565-70). Counsel families about the importance of exercise and try to help the family develop a plan that includes the provision for regular physical activity. Joining sports teams may be particularly useful as it ensures that regular exercise takes place and offers some additional benefits inherent in playing with a team.

•  Screen time. Although there has been active discussion lately about what constitutes “too much” screen time, it is clear that many children well exceed even the most liberal thresholds. Furthermore, there is increasing evidence that excessive screen time can lead to worsening attention problems over time (Pediatrics. 2004;113:708-13). One technique that can be effective, especially for younger children, is to have them “earn” their screen time by engaging in other activities such as reading or exercise.

•  Nutrition. Apart from any specific deficiency states, research shows that a healthier diet in general is associated with lower levels of behavioral problems. With regard to ADHD, one aspect that is often worth investigating specifically is whether the child gets a nutritious breakfast each morning that can help keep attentional skills optimal.

•  Musical training. Some intriguing new research is showing links between brain maturation and musical training, and in some of the very regions of the brain that have been implicated in ADHD (J Am Acad Child Adolesc Psychiatry. 2014;53:1153-61).

•  Omega-3s. A meta-analysis demonstrated that omega-3 supplementation can improve ADHD symptoms (J Am Acad Child Adolesc Psychiatry. 2011 Oct;50:991-1000). While the optimal dose remains under investigation, there is some evidence that improved response was related to higher eicosapentaenoic acid doses.

•  Skills training. To some degree, many skills associated with ADHD (disorganization, forgetfulness, distractibility) can be specifically taught with techniques such as mindfulness (J Atten Disord. 2015 Feb;19[2]:147-57). Having families work with counselors who have specific training in ADHD can be a very useful part of treatment and can help teach important lifelong skills. Parent behavioral therapy also can be effective around many behaviors such as defiance and aggression that accompany ADHD.

Case follow-up

The pediatrician decides to enhance her assessment by inquiring about many domains of wellness, and she discovers that Ethan has chronic problems getting to sleep, and he spends many hours each day playing video games to the exclusion of physical activity. She offers some strategies to improve these areas while the family investigates working with a counselor who has specific expertise in enhancing cognitive skills. Initial improvements are encouraging, and the family decides to pursue these avenues further while delaying medication treatment, at least for now.

By keeping in mind these important other treatment domains, pediatricians can avoid the trap of overrelying on medications as the sole method of treatment while encouraging techniques that will provide long-term benefits in overall health and wellness.

Dr. Rettew is an associate professor of psychiatry and pediatrics at the University of Vermont, Burlington. Dr. Rettew said he has no relevant financial disclosures. Follow him on Twitter @pedipsych. E-mail him at [email protected].

Chronic cough is defined by the American College of Chest Physicians as a cough lasting longer than 8 weeks. Chronic cough is a troubling disorder, mostly for the patients, who frequently make several outpatient visits to seek help for their symptoms, and whose quality of life can be severely impaired.

An algorithmic approach should be used in the diagnosis of chronic cough. Once we have ruled out the “bad actors” and have run through our nasal sprays, proton pump inhibitors, and antihistamines, it is time to get creative. Don’t neglect to provide lung cancer screening for your smokers – which, in the case of chronic cough, is actually case finding.

Dr. Peter G. Gibson of the University of Newcastle, Australia, and his colleagues published an article presenting some new concepts for chronic cough, an assessment tool, and a literature review on the use of gabapentin for this troubling disorder (Pulm Pharmacol Ther. 2015 Jul 2. pii:S1094-5539[15]00072-3).

The new concepts include laryngeal hypersensitivity, central reflex hypersensitivity, and cough hypersensitivity syndrome. The authors posit that these concepts reformulate into chronic cough as a neuropathic disorder, which may be amenable to treatment with neuromodulatory agents such as gabapentin.

I have several patients in my panel who might benefit from this therapy. But there are a couple of things to remember. First, gabapentin can be taken with food, but antacids decrease the bioavailability by 20% when taken together or up to 2 hours after gabapentin ingestion. Also, gabapentin has a wide therapeutic window, which will make it easier to find an individualized dose for our patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

Chronic cough is defined by the American College of Chest Physicians as a cough lasting longer than 8 weeks. Chronic cough is a troubling disorder, mostly for the patients, who frequently make several outpatient visits to seek help for their symptoms, and whose quality of life can be severely impaired.

An algorithmic approach should be used in the diagnosis of chronic cough. Once we have ruled out the “bad actors” and have run through our nasal sprays, proton pump inhibitors, and antihistamines, it is time to get creative. Don’t neglect to provide lung cancer screening for your smokers – which, in the case of chronic cough, is actually case finding.

Dr. Peter G. Gibson of the University of Newcastle, Australia, and his colleagues published an article presenting some new concepts for chronic cough, an assessment tool, and a literature review on the use of gabapentin for this troubling disorder (Pulm Pharmacol Ther. 2015 Jul 2. pii:S1094-5539[15]00072-3).

The new concepts include laryngeal hypersensitivity, central reflex hypersensitivity, and cough hypersensitivity syndrome. The authors posit that these concepts reformulate into chronic cough as a neuropathic disorder, which may be amenable to treatment with neuromodulatory agents such as gabapentin.

I have several patients in my panel who might benefit from this therapy. But there are a couple of things to remember. First, gabapentin can be taken with food, but antacids decrease the bioavailability by 20% when taken together or up to 2 hours after gabapentin ingestion. Also, gabapentin has a wide therapeutic window, which will make it easier to find an individualized dose for our patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

Chronic cough is defined by the American College of Chest Physicians as a cough lasting longer than 8 weeks. Chronic cough is a troubling disorder, mostly for the patients, who frequently make several outpatient visits to seek help for their symptoms, and whose quality of life can be severely impaired.

An algorithmic approach should be used in the diagnosis of chronic cough. Once we have ruled out the “bad actors” and have run through our nasal sprays, proton pump inhibitors, and antihistamines, it is time to get creative. Don’t neglect to provide lung cancer screening for your smokers – which, in the case of chronic cough, is actually case finding.

Dr. Peter G. Gibson of the University of Newcastle, Australia, and his colleagues published an article presenting some new concepts for chronic cough, an assessment tool, and a literature review on the use of gabapentin for this troubling disorder (Pulm Pharmacol Ther. 2015 Jul 2. pii:S1094-5539[15]00072-3).

The new concepts include laryngeal hypersensitivity, central reflex hypersensitivity, and cough hypersensitivity syndrome. The authors posit that these concepts reformulate into chronic cough as a neuropathic disorder, which may be amenable to treatment with neuromodulatory agents such as gabapentin.

I have several patients in my panel who might benefit from this therapy. But there are a couple of things to remember. First, gabapentin can be taken with food, but antacids decrease the bioavailability by 20% when taken together or up to 2 hours after gabapentin ingestion. Also, gabapentin has a wide therapeutic window, which will make it easier to find an individualized dose for our patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

What Matters prides itself on reviewing the literature and presenting thoughtful commentary on articles that are relevant and applicable to the practicing clinician. We separate the wheat from the chaff. We are not, however, above taking on attention-grabbing articles.

Over the years, this column has reported on various methods to facilitate the expulsion of kidney stones, including tamsulosin, phosphodiesterase type 5 (PDE5) inhibitors, and steroids. But this one called out for our assessment: sex to expel kidney stones. Erroneously perceived prurient interests must be forgiven.

Dr. Omer Gokhan Doluoglu of the Clinic of Ankara (Turkey) Training and Research Hospital and colleagues conducted a randomized trial evaluating the effectiveness of sexual intercourse, tamsulosin, or standard medical therapy for kidney stone expulsion (Urology. 2015;86[1]:19-24). Potential subjects were eligible for inclusion if they had radiopaque distal ureteral stones. Subjects were excluded if the stones were larger than 6 mm.

Subjects were randomized to encouragement to have sexual intercourse at least three times per week, tamsulosin 0.4 mg/day, or symptomatic therapy alone. All patients received an antispasmodic and an anti-inflammatory, and were told to drink 2 L of water per day. Sexual intercourse and masturbation were prohibited in groups 2 and 3 during the treatment period, which lasted 4 weeks.

Ninety patients were randomized to the three groups. The mean stone size was 4.7-5.0 mm and not significantly different between the groups.

At 2 weeks, 83.9% (26 of 31) of the patients in the intercourse group, 47.6% (10 of 21) in the tamsulosin group, and 34.8% (8 of 23) passed the stones (P = .001). There was no difference between the groups at 4 weeks. Mean expulsion times were 10 days, 16.6 days, and 18 days, respectively (P = .0001).

The study’s authors propose that nitrous oxide is operant here by causing ureteric relaxation when released to create penile tumescence and during sexual activity. Because masturbation could achieve the same effect, patients in the other groups were told they could not. How effective this instruction was in the current study is unknown, because only “sexual intercourses” were collected on follow-up.

The random-envelope method used is less than ideal, and no data were reported on differences in the number of sexual experiences between groups. If we assume for a moment that a real effect exists, one is left wondering if more would be better. Does the requirement of a partner decrease the likelihood of more frequent stone-expelling sexual experiences? If our patients do not have sexual partners, do we not share these data with them?

And if we use PDE5 inhibitors and encourage sexual activity, do we … kill two birds with one stone?

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

What Matters prides itself on reviewing the literature and presenting thoughtful commentary on articles that are relevant and applicable to the practicing clinician. We separate the wheat from the chaff. We are not, however, above taking on attention-grabbing articles.

Over the years, this column has reported on various methods to facilitate the expulsion of kidney stones, including tamsulosin, phosphodiesterase type 5 (PDE5) inhibitors, and steroids. But this one called out for our assessment: sex to expel kidney stones. Erroneously perceived prurient interests must be forgiven.

Dr. Omer Gokhan Doluoglu of the Clinic of Ankara (Turkey) Training and Research Hospital and colleagues conducted a randomized trial evaluating the effectiveness of sexual intercourse, tamsulosin, or standard medical therapy for kidney stone expulsion (Urology. 2015;86[1]:19-24). Potential subjects were eligible for inclusion if they had radiopaque distal ureteral stones. Subjects were excluded if the stones were larger than 6 mm.

Subjects were randomized to encouragement to have sexual intercourse at least three times per week, tamsulosin 0.4 mg/day, or symptomatic therapy alone. All patients received an antispasmodic and an anti-inflammatory, and were told to drink 2 L of water per day. Sexual intercourse and masturbation were prohibited in groups 2 and 3 during the treatment period, which lasted 4 weeks.

Ninety patients were randomized to the three groups. The mean stone size was 4.7-5.0 mm and not significantly different between the groups.

At 2 weeks, 83.9% (26 of 31) of the patients in the intercourse group, 47.6% (10 of 21) in the tamsulosin group, and 34.8% (8 of 23) passed the stones (P = .001). There was no difference between the groups at 4 weeks. Mean expulsion times were 10 days, 16.6 days, and 18 days, respectively (P = .0001).

The study’s authors propose that nitrous oxide is operant here by causing ureteric relaxation when released to create penile tumescence and during sexual activity. Because masturbation could achieve the same effect, patients in the other groups were told they could not. How effective this instruction was in the current study is unknown, because only “sexual intercourses” were collected on follow-up.

The random-envelope method used is less than ideal, and no data were reported on differences in the number of sexual experiences between groups. If we assume for a moment that a real effect exists, one is left wondering if more would be better. Does the requirement of a partner decrease the likelihood of more frequent stone-expelling sexual experiences? If our patients do not have sexual partners, do we not share these data with them?

And if we use PDE5 inhibitors and encourage sexual activity, do we … kill two birds with one stone?

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

What Matters prides itself on reviewing the literature and presenting thoughtful commentary on articles that are relevant and applicable to the practicing clinician. We separate the wheat from the chaff. We are not, however, above taking on attention-grabbing articles.

Over the years, this column has reported on various methods to facilitate the expulsion of kidney stones, including tamsulosin, phosphodiesterase type 5 (PDE5) inhibitors, and steroids. But this one called out for our assessment: sex to expel kidney stones. Erroneously perceived prurient interests must be forgiven.

Dr. Omer Gokhan Doluoglu of the Clinic of Ankara (Turkey) Training and Research Hospital and colleagues conducted a randomized trial evaluating the effectiveness of sexual intercourse, tamsulosin, or standard medical therapy for kidney stone expulsion (Urology. 2015;86[1]:19-24). Potential subjects were eligible for inclusion if they had radiopaque distal ureteral stones. Subjects were excluded if the stones were larger than 6 mm.

Subjects were randomized to encouragement to have sexual intercourse at least three times per week, tamsulosin 0.4 mg/day, or symptomatic therapy alone. All patients received an antispasmodic and an anti-inflammatory, and were told to drink 2 L of water per day. Sexual intercourse and masturbation were prohibited in groups 2 and 3 during the treatment period, which lasted 4 weeks.

Ninety patients were randomized to the three groups. The mean stone size was 4.7-5.0 mm and not significantly different between the groups.

At 2 weeks, 83.9% (26 of 31) of the patients in the intercourse group, 47.6% (10 of 21) in the tamsulosin group, and 34.8% (8 of 23) passed the stones (P = .001). There was no difference between the groups at 4 weeks. Mean expulsion times were 10 days, 16.6 days, and 18 days, respectively (P = .0001).

The study’s authors propose that nitrous oxide is operant here by causing ureteric relaxation when released to create penile tumescence and during sexual activity. Because masturbation could achieve the same effect, patients in the other groups were told they could not. How effective this instruction was in the current study is unknown, because only “sexual intercourses” were collected on follow-up.

The random-envelope method used is less than ideal, and no data were reported on differences in the number of sexual experiences between groups. If we assume for a moment that a real effect exists, one is left wondering if more would be better. Does the requirement of a partner decrease the likelihood of more frequent stone-expelling sexual experiences? If our patients do not have sexual partners, do we not share these data with them?

And if we use PDE5 inhibitors and encourage sexual activity, do we … kill two birds with one stone?

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

Introduction

The use of antipsychotic medications has become more common in children and adolescents over the past 2 decades (Arch Gen Psychiatry. 2012 Dec;69[12]:1247-56). Whether or not one agrees that the trend in prescribing these agents is problematic (and I do), often the prescription and monitoring of antipsychotic medication falls to the primary care clinician who may have concerns about how to manage them. Here, we present a case to illustrate just such an issue.

Case summary

James is a 17-year-old young man with a diagnosis of bipolar disorder made earlier this year after an inpatient day at a local hospital. James had a history of attention-deficit/hyperactivity disorder (ADHD) growing up, but also had a strong family history of bipolar disorder. He began having increasing difficulty during the summer after his junior year, and then had a clear manic episode with elation and grandiosity that necessitated the hospitalization. During the relatively short stay on the psychiatric unit, he was placed on lithium carbonate and risperidone to treat the mania, which did respond. Although it was recommended that he follow up with a child and adolescent psychiatrist, through a series of happenstances he missed two appointments for an intake. He is now only able to get a new intake that is 4 months off.

You have continued to prescribe for him, waiting for what always seemed to be an imminent appointment. But now he comes to the office for a follow-up visit that can no longer wait. His mood symptoms are actually doing quite well. However, you have always known James to have a relatively thin build in the 25th percentile for weight and the 75th percentile for height. Now (is it possible?) 6 months after starting the risperidone and lithium, he returns to the office in the 50th percentile for weight and remains in the 75th percentile for height. There is nothing else noted to be concerning on physical or mental status examination, but you wonder what should be done for monitoring of his weight, should you be doing it, and whether there are other metabolic parameters that you should be measuring?

Case discussion

Regardless of your stance on pediatric bipolar disorder and the treatments for it, James has been placed on medications that need to be monitored. While it appears that James will, eventually, have a prescriber who can monitor his medication for side effects, it is incumbent on all of his providers to make sure that monitoring is occurring. Recent studies have demonstrated that guidelines for monitoring of antipsychotic use are not consistently being adhered to. For example, Rettew et al. (Pediatrics. 2015 Apr;135[4]:658-65) recently reported that metabolic monitoring that included laboratory tests was reported in only 57.2% of cases where an antipsychotic was prescribed.

Children and adolescents placed on these agents should be monitored in a number of ways. First, height and weight should be taken at baseline and at follow-up visits – at least every 6 months. The American Academy of Child and Adolescent Psychiatry practice parameters state that “consideration of weight management interventions and increased regularity of blood glucose and lipid levels should be implemented if [atypical antipsychotic agent]–induced weight gain exceeds 90th percentile body mass index (BMI) for age, or a change of five BMI units in those youths who were obese at the beginning of treatment.” Fasting blood sugar, fasting triglyceride, and cholesterol panels should be done at baseline and at approximately 6-month intervals. Screening for dystonic movements with an Abnormal Involuntary Movement Scale (AIMS) should be done at 6-month intervals. In the case of risperidone, if there are any questions about gynecomastia, galactorrhea, and/or sexual dysfunction, a prolactin level should be considered. Certain other antipsychotics require specific monitoring (for example, ECG for prolonged QT interval for ziprasidone, CBC for clozapine, and an eye exam for quetiapine).

The most important kinds of monitoring are for dose and efficacy. While the antipsychotic medications may have a role, they are not a panacea and do carry longer-term risks of metabolic problems and obesity, among others. If it is possible to provide interventions to reduce the dose or duration of use, that is preferable. If not, it’s best to work with the psychiatrist (if available) to determine who will perform the monitoring and how often it will be done to stave off metabolic problems as early as possible.

Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Dr. Althoff receives no funding from pharmaceutical companies or industry. He has grant funding from the National Institute of General Medical Sciences and the Klingenstein Third Generation Foundation and is employed, in part, by the nonprofit Research Center for Children, Youth, and Families that develops the Child Behavior Checklist and associated instruments. E-mail him at [email protected].

Introduction

The use of antipsychotic medications has become more common in children and adolescents over the past 2 decades (Arch Gen Psychiatry. 2012 Dec;69[12]:1247-56). Whether or not one agrees that the trend in prescribing these agents is problematic (and I do), often the prescription and monitoring of antipsychotic medication falls to the primary care clinician who may have concerns about how to manage them. Here, we present a case to illustrate just such an issue.

Case summary

James is a 17-year-old young man with a diagnosis of bipolar disorder made earlier this year after an inpatient day at a local hospital. James had a history of attention-deficit/hyperactivity disorder (ADHD) growing up, but also had a strong family history of bipolar disorder. He began having increasing difficulty during the summer after his junior year, and then had a clear manic episode with elation and grandiosity that necessitated the hospitalization. During the relatively short stay on the psychiatric unit, he was placed on lithium carbonate and risperidone to treat the mania, which did respond. Although it was recommended that he follow up with a child and adolescent psychiatrist, through a series of happenstances he missed two appointments for an intake. He is now only able to get a new intake that is 4 months off.

You have continued to prescribe for him, waiting for what always seemed to be an imminent appointment. But now he comes to the office for a follow-up visit that can no longer wait. His mood symptoms are actually doing quite well. However, you have always known James to have a relatively thin build in the 25th percentile for weight and the 75th percentile for height. Now (is it possible?) 6 months after starting the risperidone and lithium, he returns to the office in the 50th percentile for weight and remains in the 75th percentile for height. There is nothing else noted to be concerning on physical or mental status examination, but you wonder what should be done for monitoring of his weight, should you be doing it, and whether there are other metabolic parameters that you should be measuring?

Case discussion

Regardless of your stance on pediatric bipolar disorder and the treatments for it, James has been placed on medications that need to be monitored. While it appears that James will, eventually, have a prescriber who can monitor his medication for side effects, it is incumbent on all of his providers to make sure that monitoring is occurring. Recent studies have demonstrated that guidelines for monitoring of antipsychotic use are not consistently being adhered to. For example, Rettew et al. (Pediatrics. 2015 Apr;135[4]:658-65) recently reported that metabolic monitoring that included laboratory tests was reported in only 57.2% of cases where an antipsychotic was prescribed.

Children and adolescents placed on these agents should be monitored in a number of ways. First, height and weight should be taken at baseline and at follow-up visits – at least every 6 months. The American Academy of Child and Adolescent Psychiatry practice parameters state that “consideration of weight management interventions and increased regularity of blood glucose and lipid levels should be implemented if [atypical antipsychotic agent]–induced weight gain exceeds 90th percentile body mass index (BMI) for age, or a change of five BMI units in those youths who were obese at the beginning of treatment.” Fasting blood sugar, fasting triglyceride, and cholesterol panels should be done at baseline and at approximately 6-month intervals. Screening for dystonic movements with an Abnormal Involuntary Movement Scale (AIMS) should be done at 6-month intervals. In the case of risperidone, if there are any questions about gynecomastia, galactorrhea, and/or sexual dysfunction, a prolactin level should be considered. Certain other antipsychotics require specific monitoring (for example, ECG for prolonged QT interval for ziprasidone, CBC for clozapine, and an eye exam for quetiapine).

The most important kinds of monitoring are for dose and efficacy. While the antipsychotic medications may have a role, they are not a panacea and do carry longer-term risks of metabolic problems and obesity, among others. If it is possible to provide interventions to reduce the dose or duration of use, that is preferable. If not, it’s best to work with the psychiatrist (if available) to determine who will perform the monitoring and how often it will be done to stave off metabolic problems as early as possible.

Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Dr. Althoff receives no funding from pharmaceutical companies or industry. He has grant funding from the National Institute of General Medical Sciences and the Klingenstein Third Generation Foundation and is employed, in part, by the nonprofit Research Center for Children, Youth, and Families that develops the Child Behavior Checklist and associated instruments. E-mail him at [email protected].

Introduction

The use of antipsychotic medications has become more common in children and adolescents over the past 2 decades (Arch Gen Psychiatry. 2012 Dec;69[12]:1247-56). Whether or not one agrees that the trend in prescribing these agents is problematic (and I do), often the prescription and monitoring of antipsychotic medication falls to the primary care clinician who may have concerns about how to manage them. Here, we present a case to illustrate just such an issue.

Case summary

James is a 17-year-old young man with a diagnosis of bipolar disorder made earlier this year after an inpatient day at a local hospital. James had a history of attention-deficit/hyperactivity disorder (ADHD) growing up, but also had a strong family history of bipolar disorder. He began having increasing difficulty during the summer after his junior year, and then had a clear manic episode with elation and grandiosity that necessitated the hospitalization. During the relatively short stay on the psychiatric unit, he was placed on lithium carbonate and risperidone to treat the mania, which did respond. Although it was recommended that he follow up with a child and adolescent psychiatrist, through a series of happenstances he missed two appointments for an intake. He is now only able to get a new intake that is 4 months off.

You have continued to prescribe for him, waiting for what always seemed to be an imminent appointment. But now he comes to the office for a follow-up visit that can no longer wait. His mood symptoms are actually doing quite well. However, you have always known James to have a relatively thin build in the 25th percentile for weight and the 75th percentile for height. Now (is it possible?) 6 months after starting the risperidone and lithium, he returns to the office in the 50th percentile for weight and remains in the 75th percentile for height. There is nothing else noted to be concerning on physical or mental status examination, but you wonder what should be done for monitoring of his weight, should you be doing it, and whether there are other metabolic parameters that you should be measuring?

Case discussion

Regardless of your stance on pediatric bipolar disorder and the treatments for it, James has been placed on medications that need to be monitored. While it appears that James will, eventually, have a prescriber who can monitor his medication for side effects, it is incumbent on all of his providers to make sure that monitoring is occurring. Recent studies have demonstrated that guidelines for monitoring of antipsychotic use are not consistently being adhered to. For example, Rettew et al. (Pediatrics. 2015 Apr;135[4]:658-65) recently reported that metabolic monitoring that included laboratory tests was reported in only 57.2% of cases where an antipsychotic was prescribed.

Children and adolescents placed on these agents should be monitored in a number of ways. First, height and weight should be taken at baseline and at follow-up visits – at least every 6 months. The American Academy of Child and Adolescent Psychiatry practice parameters state that “consideration of weight management interventions and increased regularity of blood glucose and lipid levels should be implemented if [atypical antipsychotic agent]–induced weight gain exceeds 90th percentile body mass index (BMI) for age, or a change of five BMI units in those youths who were obese at the beginning of treatment.” Fasting blood sugar, fasting triglyceride, and cholesterol panels should be done at baseline and at approximately 6-month intervals. Screening for dystonic movements with an Abnormal Involuntary Movement Scale (AIMS) should be done at 6-month intervals. In the case of risperidone, if there are any questions about gynecomastia, galactorrhea, and/or sexual dysfunction, a prolactin level should be considered. Certain other antipsychotics require specific monitoring (for example, ECG for prolonged QT interval for ziprasidone, CBC for clozapine, and an eye exam for quetiapine).

The most important kinds of monitoring are for dose and efficacy. While the antipsychotic medications may have a role, they are not a panacea and do carry longer-term risks of metabolic problems and obesity, among others. If it is possible to provide interventions to reduce the dose or duration of use, that is preferable. If not, it’s best to work with the psychiatrist (if available) to determine who will perform the monitoring and how often it will be done to stave off metabolic problems as early as possible.

Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Dr. Althoff receives no funding from pharmaceutical companies or industry. He has grant funding from the National Institute of General Medical Sciences and the Klingenstein Third Generation Foundation and is employed, in part, by the nonprofit Research Center for Children, Youth, and Families that develops the Child Behavior Checklist and associated instruments. E-mail him at [email protected].

The prevalence of fibromyalgia in our clinical practices is about 2%-3%. But it may feel much higher, because some of these patients use a lot of staff and office time. Vacillations in our certainty about the diagnosis, inadequate time to differentiate new problems from the underlying one, failing to engage the patient in disease self-management, and inadequately exhausting the plethora of pharmacologic management options (however weak the data may be for each one) make care of patients with fibromyalgia challenging. Unfortunately, many of these patients are treated with chronic opioids.

So, maybe you have tried every pharmacologic option under the sun. But have you tried memantine?

Dr. Bárbara Olivan-Blázquez of the University of Zaragoza, Spain, and colleagues evaluated the efficacy of memantine for pain symptom control in fibromyalgia (Pain. 2014 Dec;155[12]:2517-25).

In this study, 63 patients with fibromyalgia were randomized to 20 mg/day of memantine or matching placebo for a total of 6 months, including an initial 1-month up-titration period. Follow-up occurred at 3 months and 6 months.

Compared with placebo, memantine decreased pain and depression at 3 months and 6 months. It also increased cognitive function and overall perceptions of function at 3 months and 6 months. More than 80% of patients completed the trial. Dizziness and headaches were the most commonly reported symptoms.

Why does it work? Memantine blocks glutamate, and glutamate may be a player in perpetuating the pain cycle for patients with fibromyalgia. Previously, memantine had been shown to be effective in other pain conditions such as complex regional pain syndrome and phantom limb pain. Memantine is well tolerated and is generically available. In my location, I was able to locate it for less than $1 per day of therapy.

So, before giving up hope or reaching for the opioid du jour, memantine may be worth a trial to decrease pain and improve function in our patients with fibromyalgia.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of fibromyalgia in our clinical practices is about 2%-3%. But it may feel much higher, because some of these patients use a lot of staff and office time. Vacillations in our certainty about the diagnosis, inadequate time to differentiate new problems from the underlying one, failing to engage the patient in disease self-management, and inadequately exhausting the plethora of pharmacologic management options (however weak the data may be for each one) make care of patients with fibromyalgia challenging. Unfortunately, many of these patients are treated with chronic opioids.

So, maybe you have tried every pharmacologic option under the sun. But have you tried memantine?

Dr. Bárbara Olivan-Blázquez of the University of Zaragoza, Spain, and colleagues evaluated the efficacy of memantine for pain symptom control in fibromyalgia (Pain. 2014 Dec;155[12]:2517-25).

In this study, 63 patients with fibromyalgia were randomized to 20 mg/day of memantine or matching placebo for a total of 6 months, including an initial 1-month up-titration period. Follow-up occurred at 3 months and 6 months.

Compared with placebo, memantine decreased pain and depression at 3 months and 6 months. It also increased cognitive function and overall perceptions of function at 3 months and 6 months. More than 80% of patients completed the trial. Dizziness and headaches were the most commonly reported symptoms.

Why does it work? Memantine blocks glutamate, and glutamate may be a player in perpetuating the pain cycle for patients with fibromyalgia. Previously, memantine had been shown to be effective in other pain conditions such as complex regional pain syndrome and phantom limb pain. Memantine is well tolerated and is generically available. In my location, I was able to locate it for less than $1 per day of therapy.

So, before giving up hope or reaching for the opioid du jour, memantine may be worth a trial to decrease pain and improve function in our patients with fibromyalgia.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of fibromyalgia in our clinical practices is about 2%-3%. But it may feel much higher, because some of these patients use a lot of staff and office time. Vacillations in our certainty about the diagnosis, inadequate time to differentiate new problems from the underlying one, failing to engage the patient in disease self-management, and inadequately exhausting the plethora of pharmacologic management options (however weak the data may be for each one) make care of patients with fibromyalgia challenging. Unfortunately, many of these patients are treated with chronic opioids.

So, maybe you have tried every pharmacologic option under the sun. But have you tried memantine?

Dr. Bárbara Olivan-Blázquez of the University of Zaragoza, Spain, and colleagues evaluated the efficacy of memantine for pain symptom control in fibromyalgia (Pain. 2014 Dec;155[12]:2517-25).

In this study, 63 patients with fibromyalgia were randomized to 20 mg/day of memantine or matching placebo for a total of 6 months, including an initial 1-month up-titration period. Follow-up occurred at 3 months and 6 months.

Compared with placebo, memantine decreased pain and depression at 3 months and 6 months. It also increased cognitive function and overall perceptions of function at 3 months and 6 months. More than 80% of patients completed the trial. Dizziness and headaches were the most commonly reported symptoms.

Why does it work? Memantine blocks glutamate, and glutamate may be a player in perpetuating the pain cycle for patients with fibromyalgia. Previously, memantine had been shown to be effective in other pain conditions such as complex regional pain syndrome and phantom limb pain. Memantine is well tolerated and is generically available. In my location, I was able to locate it for less than $1 per day of therapy.

So, before giving up hope or reaching for the opioid du jour, memantine may be worth a trial to decrease pain and improve function in our patients with fibromyalgia.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of diabetes increases as patients age and gain weight. More than one-third of nursing home residents have diabetes. The overall treatment goals for elderly patients with diabetes are similar to those for younger patients, but somehow the stakes feel higher. Polypharmacy, decreased activity, shifting dietary patterns, hyperglycemia, fears of hypoglycemia leading to falls, worsening comorbid conditions, and hospitalization pose great challenges to ideal management.

Because of these concerns, caution is raised about the use of insulin or oral agents that cause hypoglycemia in frail older adults in long-term care facilities. But these agents are used, and perhaps we understand little about their comparative risks.

Dr. Francisco J. Pasquel of Emory University, Atlanta, and his colleagues conducted a randomized clinical trial evaluating the comparative safety and effectiveness of basal insulin or an oral antidiabetic drug (OAD) for 26 weeks (BMJ Open Diab Res Care. 2015;3:e000104).

A total of 150 patients, average age 79 years, with a blood glucose level greater than 180 mg/dL or a hemoglobin A_1c greater than 7.5%, treated with diet or an oral agent, were randomized to either 0.1 U/kg per day of glargine or continuation of oral agents (metformin, insulin secretagogues, thiazolidinediones, or DPP-4 inhibitors). Glargine was adjusted based on blood sugar readings.

In the OAD group, 16% of patients were treated with metformin plus sulfonylurea, 27% with a sulfonylurea alone, and 8% with sulfonylurea and a DPP-4 inhibitor.

There were 62 hypoglycemic events in the OAD group and 43 in the basal insulin group (P = .4). Overall, daily blood glucose levels did not differ between the groups. Rates of cardiovascular events, renal failure, infection, falls, emergency department visits, hospital admissions, and mortality were similar between the two groups.

Although these data are somewhat reassuring, power may have been an issue, and a larger sample size may have resulted in detection of more hypoglycemic events in the OAD group. On the other hand, the data are balanced and resonate with previous data showing that in older adults with diabetes (about 74 years of age), intensive glycemic control is associated with an increased risk of falls in insulin users but not in those treated with OADs. The goal of the current study was not intensive glycemic control.

So, for patients in a long-term care facility, metformin and the DPP-4 inhibitors will be weight neutral without risk of hypoglycemia. Therefore, these may be the “go-to” drugs if the DPP-4 inhibitors are affordable and you do not have a long way to go for control (DPP-4 inhibitors tend to be relatively mild agents, lowering HbA_1c by 0.6%). If a sulfonylurea must be used, glipizide should be chosen, because it has a shorter half-life.

Balance all of this with appropriate HbA_1c goals for your patient adjusted for medical comorbidity, goals of care, and life expectancy.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of diabetes increases as patients age and gain weight. More than one-third of nursing home residents have diabetes. The overall treatment goals for elderly patients with diabetes are similar to those for younger patients, but somehow the stakes feel higher. Polypharmacy, decreased activity, shifting dietary patterns, hyperglycemia, fears of hypoglycemia leading to falls, worsening comorbid conditions, and hospitalization pose great challenges to ideal management.

Because of these concerns, caution is raised about the use of insulin or oral agents that cause hypoglycemia in frail older adults in long-term care facilities. But these agents are used, and perhaps we understand little about their comparative risks.

Dr. Francisco J. Pasquel of Emory University, Atlanta, and his colleagues conducted a randomized clinical trial evaluating the comparative safety and effectiveness of basal insulin or an oral antidiabetic drug (OAD) for 26 weeks (BMJ Open Diab Res Care. 2015;3:e000104).

A total of 150 patients, average age 79 years, with a blood glucose level greater than 180 mg/dL or a hemoglobin A_1c greater than 7.5%, treated with diet or an oral agent, were randomized to either 0.1 U/kg per day of glargine or continuation of oral agents (metformin, insulin secretagogues, thiazolidinediones, or DPP-4 inhibitors). Glargine was adjusted based on blood sugar readings.

In the OAD group, 16% of patients were treated with metformin plus sulfonylurea, 27% with a sulfonylurea alone, and 8% with sulfonylurea and a DPP-4 inhibitor.

There were 62 hypoglycemic events in the OAD group and 43 in the basal insulin group (P = .4). Overall, daily blood glucose levels did not differ between the groups. Rates of cardiovascular events, renal failure, infection, falls, emergency department visits, hospital admissions, and mortality were similar between the two groups.

Although these data are somewhat reassuring, power may have been an issue, and a larger sample size may have resulted in detection of more hypoglycemic events in the OAD group. On the other hand, the data are balanced and resonate with previous data showing that in older adults with diabetes (about 74 years of age), intensive glycemic control is associated with an increased risk of falls in insulin users but not in those treated with OADs. The goal of the current study was not intensive glycemic control.

So, for patients in a long-term care facility, metformin and the DPP-4 inhibitors will be weight neutral without risk of hypoglycemia. Therefore, these may be the “go-to” drugs if the DPP-4 inhibitors are affordable and you do not have a long way to go for control (DPP-4 inhibitors tend to be relatively mild agents, lowering HbA_1c by 0.6%). If a sulfonylurea must be used, glipizide should be chosen, because it has a shorter half-life.

Balance all of this with appropriate HbA_1c goals for your patient adjusted for medical comorbidity, goals of care, and life expectancy.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of diabetes increases as patients age and gain weight. More than one-third of nursing home residents have diabetes. The overall treatment goals for elderly patients with diabetes are similar to those for younger patients, but somehow the stakes feel higher. Polypharmacy, decreased activity, shifting dietary patterns, hyperglycemia, fears of hypoglycemia leading to falls, worsening comorbid conditions, and hospitalization pose great challenges to ideal management.

Because of these concerns, caution is raised about the use of insulin or oral agents that cause hypoglycemia in frail older adults in long-term care facilities. But these agents are used, and perhaps we understand little about their comparative risks.

Dr. Francisco J. Pasquel of Emory University, Atlanta, and his colleagues conducted a randomized clinical trial evaluating the comparative safety and effectiveness of basal insulin or an oral antidiabetic drug (OAD) for 26 weeks (BMJ Open Diab Res Care. 2015;3:e000104).

A total of 150 patients, average age 79 years, with a blood glucose level greater than 180 mg/dL or a hemoglobin A_1c greater than 7.5%, treated with diet or an oral agent, were randomized to either 0.1 U/kg per day of glargine or continuation of oral agents (metformin, insulin secretagogues, thiazolidinediones, or DPP-4 inhibitors). Glargine was adjusted based on blood sugar readings.

In the OAD group, 16% of patients were treated with metformin plus sulfonylurea, 27% with a sulfonylurea alone, and 8% with sulfonylurea and a DPP-4 inhibitor.

There were 62 hypoglycemic events in the OAD group and 43 in the basal insulin group (P = .4). Overall, daily blood glucose levels did not differ between the groups. Rates of cardiovascular events, renal failure, infection, falls, emergency department visits, hospital admissions, and mortality were similar between the two groups.

Although these data are somewhat reassuring, power may have been an issue, and a larger sample size may have resulted in detection of more hypoglycemic events in the OAD group. On the other hand, the data are balanced and resonate with previous data showing that in older adults with diabetes (about 74 years of age), intensive glycemic control is associated with an increased risk of falls in insulin users but not in those treated with OADs. The goal of the current study was not intensive glycemic control.

So, for patients in a long-term care facility, metformin and the DPP-4 inhibitors will be weight neutral without risk of hypoglycemia. Therefore, these may be the “go-to” drugs if the DPP-4 inhibitors are affordable and you do not have a long way to go for control (DPP-4 inhibitors tend to be relatively mild agents, lowering HbA_1c by 0.6%). If a sulfonylurea must be used, glipizide should be chosen, because it has a shorter half-life.

Balance all of this with appropriate HbA_1c goals for your patient adjusted for medical comorbidity, goals of care, and life expectancy.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

As we head into influenza season, we are likely steeling our nerves for the inevitable debate with some of our patients about receiving the influenza vaccination.

We are used to hearing patients say, “I have never had it, and I have never gotten the flu,” or (my favorite), “Last time I got the shot, I got the flu.” Arguments that – while defying chance, logic, and science in general – keep us rooted in the daily joys of clinical practice.

Some handy influenza facts:

1. In well-matched years, the number needed to treat (NNT) to prevent one flu-like illness is 33.

2. In unmatched years, the NNT is 100.

We should be adding to this discussion some information about the observed association between the influenza vaccine and acute myocardial infarction (AMI). If compelling arguments about preventing flu-like symptoms don’t carry the day, maybe preventing heart attack will.

Dr. Michelle Barnes and her colleagues at UNSW Australia, Sydney, published the results of a systematic review of case-control studies evaluating the association between the influenza vaccine and AMI (Heart, 2015 Aug. 26. doi:10.1136/heartjnl-2015-307691). In this study, the investigators identified 16 studies on AMI and influenza vaccination or influenza infection.

The odds of influenza infection, influenza-like illness, or respiratory infection were significantly greater in patients with AMI (odds ratio, 2.01; 95% confidence interval: 1.47-2.76). Influenza vaccine was associated with a lower risk of AMI (OR, 0.71; 95% CI: 0.56-0.91).

This is the first meta-analysis compiling all case-control data on the relationship between AMI and the influenza vaccine. Overall, cases had double the risk of influenza or respiratory tract infection, compared with controls.

Influenza has been hypothesized to cause coronary artery occlusion through stenosis of subcritical atherosclerotic plaque, and it has been shown to promote atherogenesis in animal models. The connection between AMI and influenza was first observed in the 1930s during the flu season.

But medicine has a short memory, and our patients sometimes do as well. So, it is time we remind them about this link and encourage them to get their flu shots.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

As we head into influenza season, we are likely steeling our nerves for the inevitable debate with some of our patients about receiving the influenza vaccination.

We are used to hearing patients say, “I have never had it, and I have never gotten the flu,” or (my favorite), “Last time I got the shot, I got the flu.” Arguments that – while defying chance, logic, and science in general – keep us rooted in the daily joys of clinical practice.

Some handy influenza facts:

1. In well-matched years, the number needed to treat (NNT) to prevent one flu-like illness is 33.

2. In unmatched years, the NNT is 100.

We should be adding to this discussion some information about the observed association between the influenza vaccine and acute myocardial infarction (AMI). If compelling arguments about preventing flu-like symptoms don’t carry the day, maybe preventing heart attack will.

Dr. Michelle Barnes and her colleagues at UNSW Australia, Sydney, published the results of a systematic review of case-control studies evaluating the association between the influenza vaccine and AMI (Heart, 2015 Aug. 26. doi:10.1136/heartjnl-2015-307691). In this study, the investigators identified 16 studies on AMI and influenza vaccination or influenza infection.

The odds of influenza infection, influenza-like illness, or respiratory infection were significantly greater in patients with AMI (odds ratio, 2.01; 95% confidence interval: 1.47-2.76). Influenza vaccine was associated with a lower risk of AMI (OR, 0.71; 95% CI: 0.56-0.91).

This is the first meta-analysis compiling all case-control data on the relationship between AMI and the influenza vaccine. Overall, cases had double the risk of influenza or respiratory tract infection, compared with controls.

Influenza has been hypothesized to cause coronary artery occlusion through stenosis of subcritical atherosclerotic plaque, and it has been shown to promote atherogenesis in animal models. The connection between AMI and influenza was first observed in the 1930s during the flu season.

But medicine has a short memory, and our patients sometimes do as well. So, it is time we remind them about this link and encourage them to get their flu shots.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

As we head into influenza season, we are likely steeling our nerves for the inevitable debate with some of our patients about receiving the influenza vaccination.

We are used to hearing patients say, “I have never had it, and I have never gotten the flu,” or (my favorite), “Last time I got the shot, I got the flu.” Arguments that – while defying chance, logic, and science in general – keep us rooted in the daily joys of clinical practice.

Some handy influenza facts:

1. In well-matched years, the number needed to treat (NNT) to prevent one flu-like illness is 33.

2. In unmatched years, the NNT is 100.

We should be adding to this discussion some information about the observed association between the influenza vaccine and acute myocardial infarction (AMI). If compelling arguments about preventing flu-like symptoms don’t carry the day, maybe preventing heart attack will.

Dr. Michelle Barnes and her colleagues at UNSW Australia, Sydney, published the results of a systematic review of case-control studies evaluating the association between the influenza vaccine and AMI (Heart, 2015 Aug. 26. doi:10.1136/heartjnl-2015-307691). In this study, the investigators identified 16 studies on AMI and influenza vaccination or influenza infection.

The odds of influenza infection, influenza-like illness, or respiratory infection were significantly greater in patients with AMI (odds ratio, 2.01; 95% confidence interval: 1.47-2.76). Influenza vaccine was associated with a lower risk of AMI (OR, 0.71; 95% CI: 0.56-0.91).

This is the first meta-analysis compiling all case-control data on the relationship between AMI and the influenza vaccine. Overall, cases had double the risk of influenza or respiratory tract infection, compared with controls.

Influenza has been hypothesized to cause coronary artery occlusion through stenosis of subcritical atherosclerotic plaque, and it has been shown to promote atherogenesis in animal models. The connection between AMI and influenza was first observed in the 1930s during the flu season.

But medicine has a short memory, and our patients sometimes do as well. So, it is time we remind them about this link and encourage them to get their flu shots.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

At one time or another, insomnia afflicts nearly one-half of U.S. adults, half of whom have a clinically diagnosable disorder. This presents perpetual challenges in the face of patient populations that have been told to “ask your doctor about” sleeping medications or have received them already.

We know that the Z-drugs (zolpidem, zaleplon, and eszopiclone), some of the most widely used pharmacologics for insomnia, are benzodiazepine receptor agonists. As such, tolerance develops, and this tolerance leads to escalating doses, increased side effects, and sleepier patients.

Cognitive-behavioral therapy has been shown to be effective for insomnia, but this clinical service is not widely available. For busy clinicians trying to help these patients, we need a simple tool that can be easily explained to patients, giving them a project on which to work.

This tool is sleep restriction. The goal of sleep restriction is to consolidate fragmented sleep to increase the intrinsic sleep drive.

You might have heard your patients describe their bedroom as a “torture chamber.” Some of this torture relates to sleepless staring at the ceiling for hours on end. Sleep restriction gets them out of the chamber.

Karen Falloon, Ph.D., of the University of Auckland (New Zealand), and her colleagues conducted a randomized trial in New Zealand investigating the impact of simplified sleep restriction (SSR) for patients with primary insomnia (Br J Gen Pract. 2015 Aug;65(637):e508-15).

A total of 97 patients were randomized. All patients received sleep hygiene advice, including avoiding caffeine and developing a consistent bedtime routine. Patients in the SSR arm received a verbal and written sleep prescription establishing bedtime and wake-up times informed by a baseline 2-week daily sleep diary.

The sleep prescription was average total sleep duration plus 50% of the total time spent awake in bed. The minimum time in bed was 5 hours. If participants were sleeping less than 85% of the time in bed, the time allowed in bed was reduced to total sleep time plus 30 minutes. Sleepy patients could spend 30 more minutes in bed. All changes were made at bedtime, with wake-up time held constant.

At 6 months, the SSR group had improved perceived sleep quality and fatigue, and improved sleep efficiency as measured by actigraphy. A total of 67% of patients responded to SSR, compared with 41% of controls (number needed to treat = 4).

The efficacy of this intervention is extremely impressive. Importantly, it was delivered by a general practitioner without specialized training during two “slightly extended” visits.

Potential participants were excluded if they were on a sleeping medication, which does not imply that this would not work in a population already on Z-drugs. Consideration should to be given to possible risks when implementing sleep restriction with patients taking Z-drugs with longer half-lives (for example, eszopiclone is 6 hours, zolpidem is 3 hours, and zaleplon is 1 hour), because of higher serum concentrations upon waking.

But when these medications fail, or you have Z-drug–naive patients with insomnia, have this intervention ready.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

At one time or another, insomnia afflicts nearly one-half of U.S. adults, half of whom have a clinically diagnosable disorder. This presents perpetual challenges in the face of patient populations that have been told to “ask your doctor about” sleeping medications or have received them already.

We know that the Z-drugs (zolpidem, zaleplon, and eszopiclone), some of the most widely used pharmacologics for insomnia, are benzodiazepine receptor agonists. As such, tolerance develops, and this tolerance leads to escalating doses, increased side effects, and sleepier patients.

Cognitive-behavioral therapy has been shown to be effective for insomnia, but this clinical service is not widely available. For busy clinicians trying to help these patients, we need a simple tool that can be easily explained to patients, giving them a project on which to work.

This tool is sleep restriction. The goal of sleep restriction is to consolidate fragmented sleep to increase the intrinsic sleep drive.

You might have heard your patients describe their bedroom as a “torture chamber.” Some of this torture relates to sleepless staring at the ceiling for hours on end. Sleep restriction gets them out of the chamber.

Karen Falloon, Ph.D., of the University of Auckland (New Zealand), and her colleagues conducted a randomized trial in New Zealand investigating the impact of simplified sleep restriction (SSR) for patients with primary insomnia (Br J Gen Pract. 2015 Aug;65(637):e508-15).

A total of 97 patients were randomized. All patients received sleep hygiene advice, including avoiding caffeine and developing a consistent bedtime routine. Patients in the SSR arm received a verbal and written sleep prescription establishing bedtime and wake-up times informed by a baseline 2-week daily sleep diary.

The sleep prescription was average total sleep duration plus 50% of the total time spent awake in bed. The minimum time in bed was 5 hours. If participants were sleeping less than 85% of the time in bed, the time allowed in bed was reduced to total sleep time plus 30 minutes. Sleepy patients could spend 30 more minutes in bed. All changes were made at bedtime, with wake-up time held constant.

At 6 months, the SSR group had improved perceived sleep quality and fatigue, and improved sleep efficiency as measured by actigraphy. A total of 67% of patients responded to SSR, compared with 41% of controls (number needed to treat = 4).

The efficacy of this intervention is extremely impressive. Importantly, it was delivered by a general practitioner without specialized training during two “slightly extended” visits.

Potential participants were excluded if they were on a sleeping medication, which does not imply that this would not work in a population already on Z-drugs. Consideration should to be given to possible risks when implementing sleep restriction with patients taking Z-drugs with longer half-lives (for example, eszopiclone is 6 hours, zolpidem is 3 hours, and zaleplon is 1 hour), because of higher serum concentrations upon waking.

But when these medications fail, or you have Z-drug–naive patients with insomnia, have this intervention ready.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

At one time or another, insomnia afflicts nearly one-half of U.S. adults, half of whom have a clinically diagnosable disorder. This presents perpetual challenges in the face of patient populations that have been told to “ask your doctor about” sleeping medications or have received them already.

We know that the Z-drugs (zolpidem, zaleplon, and eszopiclone), some of the most widely used pharmacologics for insomnia, are benzodiazepine receptor agonists. As such, tolerance develops, and this tolerance leads to escalating doses, increased side effects, and sleepier patients.

Cognitive-behavioral therapy has been shown to be effective for insomnia, but this clinical service is not widely available. For busy clinicians trying to help these patients, we need a simple tool that can be easily explained to patients, giving them a project on which to work.

This tool is sleep restriction. The goal of sleep restriction is to consolidate fragmented sleep to increase the intrinsic sleep drive.

You might have heard your patients describe their bedroom as a “torture chamber.” Some of this torture relates to sleepless staring at the ceiling for hours on end. Sleep restriction gets them out of the chamber.

Karen Falloon, Ph.D., of the University of Auckland (New Zealand), and her colleagues conducted a randomized trial in New Zealand investigating the impact of simplified sleep restriction (SSR) for patients with primary insomnia (Br J Gen Pract. 2015 Aug;65(637):e508-15).

A total of 97 patients were randomized. All patients received sleep hygiene advice, including avoiding caffeine and developing a consistent bedtime routine. Patients in the SSR arm received a verbal and written sleep prescription establishing bedtime and wake-up times informed by a baseline 2-week daily sleep diary.

The sleep prescription was average total sleep duration plus 50% of the total time spent awake in bed. The minimum time in bed was 5 hours. If participants were sleeping less than 85% of the time in bed, the time allowed in bed was reduced to total sleep time plus 30 minutes. Sleepy patients could spend 30 more minutes in bed. All changes were made at bedtime, with wake-up time held constant.

At 6 months, the SSR group had improved perceived sleep quality and fatigue, and improved sleep efficiency as measured by actigraphy. A total of 67% of patients responded to SSR, compared with 41% of controls (number needed to treat = 4).

The efficacy of this intervention is extremely impressive. Importantly, it was delivered by a general practitioner without specialized training during two “slightly extended” visits.

Potential participants were excluded if they were on a sleeping medication, which does not imply that this would not work in a population already on Z-drugs. Consideration should to be given to possible risks when implementing sleep restriction with patients taking Z-drugs with longer half-lives (for example, eszopiclone is 6 hours, zolpidem is 3 hours, and zaleplon is 1 hour), because of higher serum concentrations upon waking.

But when these medications fail, or you have Z-drug–naive patients with insomnia, have this intervention ready.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

My 27-year-old patient with a body mass index of 64 kg/m² presented to my clinic with back and leg pain. Unfortunately, I was not the least bit surprised.

When bending over, he developed acute onset of back pain, with radiating pain down the lateral side of his right leg to his foot. Exam and history were consistent with lumbar radiculopathy.

©Ingram Publishing/Thinkstock.com

Over the next several months, the patient had intractable pain in the presence of escalating opioids. The neurosurgeons said that his weight created too high a risk for intraoperative and postoperative complications, with which I agreed.

And so began the work of titrating his pain-modulating agents, along with the significantly less glamorous and substantially more challenging task of helping him lose weight.

He was staunchly opposed to bariatric surgery and could not afford weight loss medications, presenting a bit of an impasse. To me, the fact that his insurance company would have covered his spinal surgery but not his FDA-approved weight loss medications embodies one of the great medical mysteries of modern times.

His mother accompanied him on one of his several visits and chimed in, “He needs to eat bread, doesn’t he?”

One of my common weight loss counseling mantras is “no whites for breakfast, lunch, or dinner.” These whites would include rice, bread, pasta, and potatoes. The airwaves have been crackling for a while with calls to decrease carbohydrate consumption to combat the obesity epidemic and to eat bread only if you’re a duck. As a result, bread consumption has declined worldwide.

So how bad is bread? Are all breads the same?

Luis Serra-Majem and Inmaculada Bautista-Castano of the University of Las Palmas de Gran Canaria, Spain, conducted a systematic review of the impact of bread consumption on obesity and abdominal adiposity (Br. J. Nutr. 2015;113:S29-S35). The authors concluded that white (refined grain) bread, but not whole-grain bread, may be associated with excess abdominal fat.

Proposed hypotheses for how breads impact adiposity differently are:

1. Whole-grain bread increases satiety more than white bread;

2. Whole-grain bread results in lower plasma glucose and insulin responses than white bread;

3. Higher fiber content of whole-grain bread limits glucose absorption more than white bread; and

4. Whole-grain bread may positively influence gut microbiota through a probiotic effect.

My advice to the patient was to restrict calories, avoid carbohydrates, and if bread must be consumed, then it must be whole grain. Baby steps.

But he found religion in this (and in walking) and lost 200 pounds over the next 5 years. Miracles are still possible.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

My 27-year-old patient with a body mass index of 64 kg/m² presented to my clinic with back and leg pain. Unfortunately, I was not the least bit surprised.

When bending over, he developed acute onset of back pain, with radiating pain down the lateral side of his right leg to his foot. Exam and history were consistent with lumbar radiculopathy.

©Ingram Publishing/Thinkstock.com

Over the next several months, the patient had intractable pain in the presence of escalating opioids. The neurosurgeons said that his weight created too high a risk for intraoperative and postoperative complications, with which I agreed.

And so began the work of titrating his pain-modulating agents, along with the significantly less glamorous and substantially more challenging task of helping him lose weight.

He was staunchly opposed to bariatric surgery and could not afford weight loss medications, presenting a bit of an impasse. To me, the fact that his insurance company would have covered his spinal surgery but not his FDA-approved weight loss medications embodies one of the great medical mysteries of modern times.

His mother accompanied him on one of his several visits and chimed in, “He needs to eat bread, doesn’t he?”

One of my common weight loss counseling mantras is “no whites for breakfast, lunch, or dinner.” These whites would include rice, bread, pasta, and potatoes. The airwaves have been crackling for a while with calls to decrease carbohydrate consumption to combat the obesity epidemic and to eat bread only if you’re a duck. As a result, bread consumption has declined worldwide.

So how bad is bread? Are all breads the same?

Luis Serra-Majem and Inmaculada Bautista-Castano of the University of Las Palmas de Gran Canaria, Spain, conducted a systematic review of the impact of bread consumption on obesity and abdominal adiposity (Br. J. Nutr. 2015;113:S29-S35). The authors concluded that white (refined grain) bread, but not whole-grain bread, may be associated with excess abdominal fat.

Proposed hypotheses for how breads impact adiposity differently are:

1. Whole-grain bread increases satiety more than white bread;

2. Whole-grain bread results in lower plasma glucose and insulin responses than white bread;

3. Higher fiber content of whole-grain bread limits glucose absorption more than white bread; and

4. Whole-grain bread may positively influence gut microbiota through a probiotic effect.

My advice to the patient was to restrict calories, avoid carbohydrates, and if bread must be consumed, then it must be whole grain. Baby steps.

But he found religion in this (and in walking) and lost 200 pounds over the next 5 years. Miracles are still possible.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

My 27-year-old patient with a body mass index of 64 kg/m² presented to my clinic with back and leg pain. Unfortunately, I was not the least bit surprised.

When bending over, he developed acute onset of back pain, with radiating pain down the lateral side of his right leg to his foot. Exam and history were consistent with lumbar radiculopathy.

©Ingram Publishing/Thinkstock.com

Over the next several months, the patient had intractable pain in the presence of escalating opioids. The neurosurgeons said that his weight created too high a risk for intraoperative and postoperative complications, with which I agreed.

And so began the work of titrating his pain-modulating agents, along with the significantly less glamorous and substantially more challenging task of helping him lose weight.

He was staunchly opposed to bariatric surgery and could not afford weight loss medications, presenting a bit of an impasse. To me, the fact that his insurance company would have covered his spinal surgery but not his FDA-approved weight loss medications embodies one of the great medical mysteries of modern times.

His mother accompanied him on one of his several visits and chimed in, “He needs to eat bread, doesn’t he?”

One of my common weight loss counseling mantras is “no whites for breakfast, lunch, or dinner.” These whites would include rice, bread, pasta, and potatoes. The airwaves have been crackling for a while with calls to decrease carbohydrate consumption to combat the obesity epidemic and to eat bread only if you’re a duck. As a result, bread consumption has declined worldwide.

So how bad is bread? Are all breads the same?

Luis Serra-Majem and Inmaculada Bautista-Castano of the University of Las Palmas de Gran Canaria, Spain, conducted a systematic review of the impact of bread consumption on obesity and abdominal adiposity (Br. J. Nutr. 2015;113:S29-S35). The authors concluded that white (refined grain) bread, but not whole-grain bread, may be associated with excess abdominal fat.

Proposed hypotheses for how breads impact adiposity differently are:

1. Whole-grain bread increases satiety more than white bread;

2. Whole-grain bread results in lower plasma glucose and insulin responses than white bread;

3. Higher fiber content of whole-grain bread limits glucose absorption more than white bread; and

4. Whole-grain bread may positively influence gut microbiota through a probiotic effect.

My advice to the patient was to restrict calories, avoid carbohydrates, and if bread must be consumed, then it must be whole grain. Baby steps.

But he found religion in this (and in walking) and lost 200 pounds over the next 5 years. Miracles are still possible.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

Navigating the world of autism treatments and staying abreast of the evolving evidence base of a wide array of interventions spanning diverse modalities can be overwhelming for even well-trained clinicians. Parents and caregivers for children with an autism spectrum disorder (ASD) equally face troubles reconciling treatment information often obtained not only from their health care providers, but from family members, friends, and the Internet (where thousands of websites promise “cures” or improvements for ASD/ASD-related symptoms). In this context, families are commonly seeking complementary and alternative treatments for their children. Although some of these treatments are relatively benign, key safety and efficacy issues remain, and parents often act with little to no guidance from their child’s primary care provider. With the increasing prevalence of the use of nontraditional treatments used both with and in place of conventional treatments, you should be prepared to counsel families in making the most informed decisions in the best interest of their child.

Case Summary

Adam is a 15-year-old boy who carries a diagnosis of an ASD accompanied by enduring gastrointestinal troubles (constipation), auditory and tactile sensitivities, and episodes of aggression towards himself and others. Adam is essentially nonverbal and enjoys watching children’s videos repeatedly (Thomas the Train); he attends school in an alternative classroom as his hyperactivity, impulsivity, and susceptibility to behaving in an unpredictable physical manner limits his ability to successfully engage with peers without one-on-one supervision.

In an attempt to address Adam’s challenging behaviors (that haven’t responded significantly to a variety of conventional medications and behavioral strategies), his well-meaning and highly educated parents seek advice. They admit they’ve come across websites that offer treatments with a promise to cure their son’s autism symptoms. Adam’s mother has always preferred “a more natural” approach to her son’s treatment, and she still has vivid memories of the side effects her son experienced on past medications, such as akathisia with risperidone.

Discussion

Adam’s case is not an uncommon scenario encountered by many families who may be experiencing increasing desperation to address their child’s autism-related struggles while being disappointed by conventional treatments. Autism is a complex neurobiologic disorder with a heterogeneous presentation for which there are no well-established pharmacologic treatments to address its core symptoms of social-communication impairments and restricted, repetitive behaviors/interests. With this in mind, it’s not surprising that studies indicate that at least 50% of families with an autistic child have tried complementary and alternative medicine (CAM) treatments. Notably, the higher the child-related stress, the more likely the families are to try CAM interventions (J. Child Neurology 2014;29:360-7) and higher use of CAM is associated with coexisting gastrointestinal problems, seizure disorders, and behavioral problems in youth with autism (Pediatrics 2012;130:S77-S82).

CAM treatments are defined by the National Center for Complementary and Integrative Health (nccih.nih.gov) as “a group of diverse medical and health care systems, practices, and products that are not presently considered to be a part of conventional medicine.” They may include biologically based therapies (dietary supplements, chelation, immune-modulating agents, special diets), mind-body medicine (acupuncture, biofeedback), energy medicine, and manipulative and body-based treatments (massage, chiropractic manipulation). Families who choose CAM interventions for their children with autism tend to try natural products, special diets, and/or mind and body practices.

Reviewing the literature surrounding CAM, there are few randomized controlled trials published, and you should be aware that evidence for most of these interventions is insufficient to make strong recommendations for or against their use. Certainly, some treatments considered as CAM can be effective in treating specific target symptoms that often co-occur in individuals with autism (using melatonin to address sleep difficulties) without major safety issues, but others are potentially dangerous and likely ineffective (chelation therapy, hyperbaric oxygen, mineral solutions). The National Autism Center has published a comprehensive analysis of autism interventions (www.nationalautismcenter.org) that can be helpful for parents and practitioners to make informed treatment decisions; their most recent 2015 review categorizes some CAM treatments as having “emerging” evidence for favorable outcomes (music therapy, massage therapy, exercise) and labels some CAM interventions as having little to no evidence to support their efficacy. Interestingly, gluten-free and casein free diets are included in this latter category. Families are frequently curious about such elimination diets, especially given the buzz in both the popular and scientific press about the gut-brain connection. Although these diets do not have strong evidence to support their use in managing core features of autism, investigators are examining whether there may be a subgroup of children with autism (those with gastrointestinal problems) who may achieve potential benefits. All in all, there’s a need for more robust research on this particular set of treatments. Families should be aware that if they chose to pursue an elimination diet, adherence for children who are inherently picky eaters may be challenging. Furthermore, although commonly labeled as safe, these diets could be linked with potentially harmful adverse effects such as nutritional deficits.

To help guide clinical decision making, it may be helpful for you to first consult the American Academy of Pediatrics 2001 policy statement, “Counseling families who choose complementary and alternative medicine for their child with chronic illness or disability” (Pediatrics 2001;107:598-601) and then consider a range of variables when discussing the use of CAM treatments with families. Some authors classify treatments as being safe, easy, cheap, and sensible (SECS) versus being risky, unrealistic, difficult, and expensive (RUDE) (Contemporary Pediatrics 2004;21:61-72), and using these terms when engaging parents in treatment decisions can be instructive for all parties. For example, there is limited high-quality evidence that omega-3 fatty acid supplementation is effective in treating autism symptoms, but the fact that this can be easy, inexpensive, and relatively safe for families to use may ultimately inform your decision to support a family’s trial of this with close monitoring. Additionally, it is important to explore whether families are seeking to replace other therapies with something novel and new, or are they looking for something to complement existing treatments/services? You should always, while being mindful of a family’s needs, values, and resources, consider first and foremost the use of treatments with established efficacy. Certainly CAM treatments – particularly those that are nonbiologic (pet therapy) – may positively augment standard interventions without potential significant harm.

Clinical Pearl

With the increasing number of parents turning to CAM treatments for their children with autism (particularly when the parents themselves use CAM), you should be prepared to talk with families about their decision making and actively ask families if this is something that they’ve considered. Given that the research on many CAM treatments is in early stages, it’s not unique to perhaps feel ill prepared to make CAM recommendations to families. Often it’s helpful to share this “CAM illiteracy” with families and aim to work together in a nonjudgmental manner to evaluate and select individualized treatment programs based on factors of potential efficacy, safety, cost, and family values. Regardless of the intervention, you should establish, with all patients, reliable methods for documenting past trials of all treatments, evaluating target symptoms, monitoring clinical outcomes, and measuring adverse events.

You should work to provide realistic hope to families and acknowledge that some CAM treatments may work better for some children, but we often don’t have a great sense, from the current state-of-the-science of ASD treatment, as to who these kids may be.

Dr. Dickerson, a child and adolescent psychiatrist, is an assistant professor of psychiatry at the University of Vermont. He is the director of the university’s autism diagnostic clinic. Dr. Dickerson said he had no relevant financial disclosures. Contact Dr. Dickerson at [email protected].

Navigating the world of autism treatments and staying abreast of the evolving evidence base of a wide array of interventions spanning diverse modalities can be overwhelming for even well-trained clinicians. Parents and caregivers for children with an autism spectrum disorder (ASD) equally face troubles reconciling treatment information often obtained not only from their health care providers, but from family members, friends, and the Internet (where thousands of websites promise “cures” or improvements for ASD/ASD-related symptoms). In this context, families are commonly seeking complementary and alternative treatments for their children. Although some of these treatments are relatively benign, key safety and efficacy issues remain, and parents often act with little to no guidance from their child’s primary care provider. With the increasing prevalence of the use of nontraditional treatments used both with and in place of conventional treatments, you should be prepared to counsel families in making the most informed decisions in the best interest of their child.

Case Summary

Adam is a 15-year-old boy who carries a diagnosis of an ASD accompanied by enduring gastrointestinal troubles (constipation), auditory and tactile sensitivities, and episodes of aggression towards himself and others. Adam is essentially nonverbal and enjoys watching children’s videos repeatedly (Thomas the Train); he attends school in an alternative classroom as his hyperactivity, impulsivity, and susceptibility to behaving in an unpredictable physical manner limits his ability to successfully engage with peers without one-on-one supervision.

In an attempt to address Adam’s challenging behaviors (that haven’t responded significantly to a variety of conventional medications and behavioral strategies), his well-meaning and highly educated parents seek advice. They admit they’ve come across websites that offer treatments with a promise to cure their son’s autism symptoms. Adam’s mother has always preferred “a more natural” approach to her son’s treatment, and she still has vivid memories of the side effects her son experienced on past medications, such as akathisia with risperidone.

Discussion

Adam’s case is not an uncommon scenario encountered by many families who may be experiencing increasing desperation to address their child’s autism-related struggles while being disappointed by conventional treatments. Autism is a complex neurobiologic disorder with a heterogeneous presentation for which there are no well-established pharmacologic treatments to address its core symptoms of social-communication impairments and restricted, repetitive behaviors/interests. With this in mind, it’s not surprising that studies indicate that at least 50% of families with an autistic child have tried complementary and alternative medicine (CAM) treatments. Notably, the higher the child-related stress, the more likely the families are to try CAM interventions (J. Child Neurology 2014;29:360-7) and higher use of CAM is associated with coexisting gastrointestinal problems, seizure disorders, and behavioral problems in youth with autism (Pediatrics 2012;130:S77-S82).

CAM treatments are defined by the National Center for Complementary and Integrative Health (nccih.nih.gov) as “a group of diverse medical and health care systems, practices, and products that are not presently considered to be a part of conventional medicine.” They may include biologically based therapies (dietary supplements, chelation, immune-modulating agents, special diets), mind-body medicine (acupuncture, biofeedback), energy medicine, and manipulative and body-based treatments (massage, chiropractic manipulation). Families who choose CAM interventions for their children with autism tend to try natural products, special diets, and/or mind and body practices.

Reviewing the literature surrounding CAM, there are few randomized controlled trials published, and you should be aware that evidence for most of these interventions is insufficient to make strong recommendations for or against their use. Certainly, some treatments considered as CAM can be effective in treating specific target symptoms that often co-occur in individuals with autism (using melatonin to address sleep difficulties) without major safety issues, but others are potentially dangerous and likely ineffective (chelation therapy, hyperbaric oxygen, mineral solutions). The National Autism Center has published a comprehensive analysis of autism interventions (www.nationalautismcenter.org) that can be helpful for parents and practitioners to make informed treatment decisions; their most recent 2015 review categorizes some CAM treatments as having “emerging” evidence for favorable outcomes (music therapy, massage therapy, exercise) and labels some CAM interventions as having little to no evidence to support their efficacy. Interestingly, gluten-free and casein free diets are included in this latter category. Families are frequently curious about such elimination diets, especially given the buzz in both the popular and scientific press about the gut-brain connection. Although these diets do not have strong evidence to support their use in managing core features of autism, investigators are examining whether there may be a subgroup of children with autism (those with gastrointestinal problems) who may achieve potential benefits. All in all, there’s a need for more robust research on this particular set of treatments. Families should be aware that if they chose to pursue an elimination diet, adherence for children who are inherently picky eaters may be challenging. Furthermore, although commonly labeled as safe, these diets could be linked with potentially harmful adverse effects such as nutritional deficits.

To help guide clinical decision making, it may be helpful for you to first consult the American Academy of Pediatrics 2001 policy statement, “Counseling families who choose complementary and alternative medicine for their child with chronic illness or disability” (Pediatrics 2001;107:598-601) and then consider a range of variables when discussing the use of CAM treatments with families. Some authors classify treatments as being safe, easy, cheap, and sensible (SECS) versus being risky, unrealistic, difficult, and expensive (RUDE) (Contemporary Pediatrics 2004;21:61-72), and using these terms when engaging parents in treatment decisions can be instructive for all parties. For example, there is limited high-quality evidence that omega-3 fatty acid supplementation is effective in treating autism symptoms, but the fact that this can be easy, inexpensive, and relatively safe for families to use may ultimately inform your decision to support a family’s trial of this with close monitoring. Additionally, it is important to explore whether families are seeking to replace other therapies with something novel and new, or are they looking for something to complement existing treatments/services? You should always, while being mindful of a family’s needs, values, and resources, consider first and foremost the use of treatments with established efficacy. Certainly CAM treatments – particularly those that are nonbiologic (pet therapy) – may positively augment standard interventions without potential significant harm.

Clinical Pearl

With the increasing number of parents turning to CAM treatments for their children with autism (particularly when the parents themselves use CAM), you should be prepared to talk with families about their decision making and actively ask families if this is something that they’ve considered. Given that the research on many CAM treatments is in early stages, it’s not unique to perhaps feel ill prepared to make CAM recommendations to families. Often it’s helpful to share this “CAM illiteracy” with families and aim to work together in a nonjudgmental manner to evaluate and select individualized treatment programs based on factors of potential efficacy, safety, cost, and family values. Regardless of the intervention, you should establish, with all patients, reliable methods for documenting past trials of all treatments, evaluating target symptoms, monitoring clinical outcomes, and measuring adverse events.

You should work to provide realistic hope to families and acknowledge that some CAM treatments may work better for some children, but we often don’t have a great sense, from the current state-of-the-science of ASD treatment, as to who these kids may be.

Dr. Dickerson, a child and adolescent psychiatrist, is an assistant professor of psychiatry at the University of Vermont. He is the director of the university’s autism diagnostic clinic. Dr. Dickerson said he had no relevant financial disclosures. Contact Dr. Dickerson at [email protected].

Navigating the world of autism treatments and staying abreast of the evolving evidence base of a wide array of interventions spanning diverse modalities can be overwhelming for even well-trained clinicians. Parents and caregivers for children with an autism spectrum disorder (ASD) equally face troubles reconciling treatment information often obtained not only from their health care providers, but from family members, friends, and the Internet (where thousands of websites promise “cures” or improvements for ASD/ASD-related symptoms). In this context, families are commonly seeking complementary and alternative treatments for their children. Although some of these treatments are relatively benign, key safety and efficacy issues remain, and parents often act with little to no guidance from their child’s primary care provider. With the increasing prevalence of the use of nontraditional treatments used both with and in place of conventional treatments, you should be prepared to counsel families in making the most informed decisions in the best interest of their child.

Case Summary

Adam is a 15-year-old boy who carries a diagnosis of an ASD accompanied by enduring gastrointestinal troubles (constipation), auditory and tactile sensitivities, and episodes of aggression towards himself and others. Adam is essentially nonverbal and enjoys watching children’s videos repeatedly (Thomas the Train); he attends school in an alternative classroom as his hyperactivity, impulsivity, and susceptibility to behaving in an unpredictable physical manner limits his ability to successfully engage with peers without one-on-one supervision.

In an attempt to address Adam’s challenging behaviors (that haven’t responded significantly to a variety of conventional medications and behavioral strategies), his well-meaning and highly educated parents seek advice. They admit they’ve come across websites that offer treatments with a promise to cure their son’s autism symptoms. Adam’s mother has always preferred “a more natural” approach to her son’s treatment, and she still has vivid memories of the side effects her son experienced on past medications, such as akathisia with risperidone.

Discussion

Adam’s case is not an uncommon scenario encountered by many families who may be experiencing increasing desperation to address their child’s autism-related struggles while being disappointed by conventional treatments. Autism is a complex neurobiologic disorder with a heterogeneous presentation for which there are no well-established pharmacologic treatments to address its core symptoms of social-communication impairments and restricted, repetitive behaviors/interests. With this in mind, it’s not surprising that studies indicate that at least 50% of families with an autistic child have tried complementary and alternative medicine (CAM) treatments. Notably, the higher the child-related stress, the more likely the families are to try CAM interventions (J. Child Neurology 2014;29:360-7) and higher use of CAM is associated with coexisting gastrointestinal problems, seizure disorders, and behavioral problems in youth with autism (Pediatrics 2012;130:S77-S82).

CAM treatments are defined by the National Center for Complementary and Integrative Health (nccih.nih.gov) as “a group of diverse medical and health care systems, practices, and products that are not presently considered to be a part of conventional medicine.” They may include biologically based therapies (dietary supplements, chelation, immune-modulating agents, special diets), mind-body medicine (acupuncture, biofeedback), energy medicine, and manipulative and body-based treatments (massage, chiropractic manipulation). Families who choose CAM interventions for their children with autism tend to try natural products, special diets, and/or mind and body practices.

Reviewing the literature surrounding CAM, there are few randomized controlled trials published, and you should be aware that evidence for most of these interventions is insufficient to make strong recommendations for or against their use. Certainly, some treatments considered as CAM can be effective in treating specific target symptoms that often co-occur in individuals with autism (using melatonin to address sleep difficulties) without major safety issues, but others are potentially dangerous and likely ineffective (chelation therapy, hyperbaric oxygen, mineral solutions). The National Autism Center has published a comprehensive analysis of autism interventions (www.nationalautismcenter.org) that can be helpful for parents and practitioners to make informed treatment decisions; their most recent 2015 review categorizes some CAM treatments as having “emerging” evidence for favorable outcomes (music therapy, massage therapy, exercise) and labels some CAM interventions as having little to no evidence to support their efficacy. Interestingly, gluten-free and casein free diets are included in this latter category. Families are frequently curious about such elimination diets, especially given the buzz in both the popular and scientific press about the gut-brain connection. Although these diets do not have strong evidence to support their use in managing core features of autism, investigators are examining whether there may be a subgroup of children with autism (those with gastrointestinal problems) who may achieve potential benefits. All in all, there’s a need for more robust research on this particular set of treatments. Families should be aware that if they chose to pursue an elimination diet, adherence for children who are inherently picky eaters may be challenging. Furthermore, although commonly labeled as safe, these diets could be linked with potentially harmful adverse effects such as nutritional deficits.

To help guide clinical decision making, it may be helpful for you to first consult the American Academy of Pediatrics 2001 policy statement, “Counseling families who choose complementary and alternative medicine for their child with chronic illness or disability” (Pediatrics 2001;107:598-601) and then consider a range of variables when discussing the use of CAM treatments with families. Some authors classify treatments as being safe, easy, cheap, and sensible (SECS) versus being risky, unrealistic, difficult, and expensive (RUDE) (Contemporary Pediatrics 2004;21:61-72), and using these terms when engaging parents in treatment decisions can be instructive for all parties. For example, there is limited high-quality evidence that omega-3 fatty acid supplementation is effective in treating autism symptoms, but the fact that this can be easy, inexpensive, and relatively safe for families to use may ultimately inform your decision to support a family’s trial of this with close monitoring. Additionally, it is important to explore whether families are seeking to replace other therapies with something novel and new, or are they looking for something to complement existing treatments/services? You should always, while being mindful of a family’s needs, values, and resources, consider first and foremost the use of treatments with established efficacy. Certainly CAM treatments – particularly those that are nonbiologic (pet therapy) – may positively augment standard interventions without potential significant harm.

Clinical Pearl

With the increasing number of parents turning to CAM treatments for their children with autism (particularly when the parents themselves use CAM), you should be prepared to talk with families about their decision making and actively ask families if this is something that they’ve considered. Given that the research on many CAM treatments is in early stages, it’s not unique to perhaps feel ill prepared to make CAM recommendations to families. Often it’s helpful to share this “CAM illiteracy” with families and aim to work together in a nonjudgmental manner to evaluate and select individualized treatment programs based on factors of potential efficacy, safety, cost, and family values. Regardless of the intervention, you should establish, with all patients, reliable methods for documenting past trials of all treatments, evaluating target symptoms, monitoring clinical outcomes, and measuring adverse events.

You should work to provide realistic hope to families and acknowledge that some CAM treatments may work better for some children, but we often don’t have a great sense, from the current state-of-the-science of ASD treatment, as to who these kids may be.

Dr. Dickerson, a child and adolescent psychiatrist, is an assistant professor of psychiatry at the University of Vermont. He is the director of the university’s autism diagnostic clinic. Dr. Dickerson said he had no relevant financial disclosures. Contact Dr. Dickerson at [email protected].