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Home – Child Mental Health Blog

Vermont Center for Children, Youth and Families

Posted: September 30th, 2015 by David Rettew


Welcome to a new format to assist Vermont primary care clinicians and the general community to access new and quality information to help improve child mental health assessment and treatment.  We know the problem all too well:  emotional and behavioral problems are extremely common, affecting at least 1 in 5 children.  Vermont like every other state has a critical shortage of child psychiatrists, and primary care clinicians are often needed to deliver this important care.   Unfortunately, most pediatricians and family medicine physicians have had little formal training in mental health, and consequently are uncomfortable addressing emotional behavioral problems in their patients.

David Rettew, MD

This blog developed by the Vermont Center for Children, Youth and Families and supported by the Vermont Child Improvement Program (VCHIP) is designed to offer practical and easily assessable information related to child psychiatry.  The regularly updated information will offer the following.

  • Regular postings from VCCYF staff about the assessment and treatment of common child emotional behavioral challenges
  • Links to important local and national resources
  • An ability to send clinical questions to VCCYF faculty that will be responded to in a timely manner

The central model that will be used is the Vermont Family Based Approach – a strategy developed by Dr Jim Hudziak that expands the focus of assessment and treatment beyond the individual symptoms of the child and towards the entire family environment.


Bias Found for Depression Psychotherapy Trials

Posted: November 19th, 2015 by David Rettew

The medical community was disappointed, but perhaps not shocked, several years ago when it was revealed that the efficacy of antidepressant medications in the treatment of adolescent depression might not be as strong as we thought.  This bias was due to the fact that the clinical trials, most of which were funded by pharmaceutic companies, that showed a positive effect for theCounseling medication were published prominently in journals while negative trials got much less publicity and often were not published at all.   A deliberate effort to downplay unfavorable studies of antidepressants was generally suspected, although some people have argued that other factors may also be at work, such as journals being less enthusiastic to publish negative findings and researchers not wanting to devote lots of time and energy describing hypotheses that did not pan out.

With regard to depression, the publication bias for antidepressants made some clinicians think more strongly about recommending psychotherapy.  Now, however, a new study recently published in PLOS One, examines whether or not a similar bias may be present in psychotherapy studies of depression.

The authors looked back at grants awarded by the NIH for controlled psychotherapy studies for depression conducted between the years 1972 to 2008.  They found the publications for these studies and examined the effect size by which the therapy improved symptoms relative to placebo.  If they found a funded grant but no publication, the authors contacted the investigators and calculated the effect size for those studies.   Studies of children and adolescents, unfortunately, were excluded for these analyses.

Surprisingly, nearly a quarter (23.6%) of the 55 funded studies did not result in publication and two studies were never started at all. Most of the unpublished studies were never submitted for publication in the first place (rather than it being written up and rejected over and over by different journals).  Most notably, the effect size of unpublished trials was less than half that of published trials. When these unpublished studies were added to the published ones, the effect size for psychotherapy dropped by 25%.

The authors concluded that there is strong evidence to conclude that a publication bias exists for psychotherapy trials for depression and that our understanding of how effective psychotherapy is, at least for depression, may need to be adjusted somewhat.  That said, the evidence continues to show that psychotherapy generally works for depression and there is no reason to alter the general recommendation of psychotherapy as a first line treatment.

This study is useful in reminding us that bias can exist in many domains and for many reasons.  Most of us are now quite primed to recognize potential bias and conflict when it comes to the pharmaceutical industry, but we need to be vigilant about some of the less obvious sources as well.


Driessen E, et al.  Does Publication Bias Inflate the Apparent Efficacy of Psychological Treatment for Major Depressive Disorder? A Systematic Review and Meta-Analysis of US National Institutes of Health-Funded Trials.  PLOS One, epub ahead of print, 2015.

An Update on Concussion

Posted: November 4th, 2015 by David Rettew

(Editor’s Note:  I’m pleased to share this guest post by one of our first year child psychiatry fellows, Dr. Winston Chung.)

More recently, one of the hot topics in Pediatrics, Neurology, and Psychiatry is the impact of concussion(s) on the developing mind. It came into the public consciousness due to the highly publicized death of beloved NFL football players like Junior Seau, and the tragic accident of 13yo Zackery Lystedt who collapsed after a football game and later required neurosurgery to alleviate the pressure produced by the swelling in his brain.   Increasingly, we’re forced to confront the difficult decision of whether we should allow our kids to play football, hockey, or soccer, and the morality of supporting billion dollar industries that produced a product where men launch themselves at one another destroying their body and mind.

The American Academy of Neurology defines concussion as a biomechanically induced clinical syndrome leading to alteration of brain function, affecting memory, and orientation, and may involve loss of consciousness. Though definitions vary, many clinicians define concussion as a subset of mild Traumatic Brain Injury which is defined as Glasgow Coma Scale score of 13-15, loss of consciousness of less than 30 minutes (if present), and posttraumatic amnesia of 24 hours (if present). There are between 1.5-3.8 million sport-related TBIs in the US each year, the majority of which are mild TBI and concussions. Concussions lead to 100,000 Emergency Room visits each year for school-aged children and represents 9% of all high school sports injuries.

Concussions are produced by acceleration and deceleration forces on the brain, whether linear or rotational. When these forces act on the brain, it stretches and deforms, doing the same to the individual components that make up the brain such as neurons, and blood vessels. The axons that make up the white matter tracts are especially vulnerable to injury given their length. The disruption of the neuronal membranes leads to disruption of neurotransmitters and electrolytes that are neatly sequestered, causing the brain to go into a hypermetabolic state (thus requiring glucose) to return it to its former equilibrium. This leads to a widened gap between the increased energy needs of the neurons and the decreased blood flow to the brain, resulting in an energy crisis.

The result of this disruption are headaches, fatigue, dizziness, slowed mentation, drowsiness, difficulty concentrating, nausea, light sensitivity, noise sensitivity, forgetfulness, blurry vision, sleep disturbance, irritability, depression, vomiting, and tinnitus. Usually the symptoms are self-limiting and they resolve after 7-10 days. However, symptoms in children may resolve more slowly. The mean duration of post-concussion symptoms among patients age 8-23 years who were referred to a concussion clinic was 43+/- 55 days. A minority of the patients reports post-concussion symptoms that persist for months, sometimes years. Repeated head trauma appears to lead to one of two presentations. Mood and behavioral symptoms usually appearing in third decade of life, and cognitive impairment and memory loss developing in fifth decade of life. The majority of subjects who present initially with behavior or mood symptoms progress to have cognitive symptoms before passing away, whereas those who present with cognitive impairment less commonly develop mood symptoms.

One topic that hasn’t been discussed enough in the press is the potential health effects of subconcussive injuries. Subconcussive impact is defined as biomechanically induced injuries to the brain that do not result in clinical symptoms, but may have a cumulative effect leading to chronic traumatic brain injury in some adult patients. Recently, a small study showed white matter microstructure changes in professional soccer players who did not have a history of concussions when compared to age-matched swimmers. And it’s been reported that an offensive lineman in American football can experience over 1,000 subconcussive hits over the level of 10g in the course of a single collegiate season.

(Of note, for further information, please see an excellent presentation on the topic by Dr. Jim Hudziak who discussed concussions at a recent Community Medical School talk at the University of Vermont College of Medicine.  The video will soon be available and can be accessed here.)

Anxiety Risk with Stimulants Overstated

Posted: November 4th, 2015 by David Rettew

There is a widely held concern that psychostimulants when used to treat ADHD can induce or exacerbate anxiety.  This belief has led many clinicians to hesitate about using stimulants in patients who already suffer from high level of anxiety, prompting some prescribers to try, as first-line agents, nonstimulant medications that supposedly have less risk but may be less effective against core ADHD symptoms.  The actual data about stimulants and anxiety, are more mixed.  Recently, a meta-analysis was published with the hopes of coming to a more definitive answer on this questions.Stimulants and anxiety

The study reviewed 23 different placebo-controlled trails and encompassed nearly 3000 children and adolescents. Clinician rated side effect measures of anxiety, when available, was utilized to assess patient anxiety. Subgroup analyses and meta-regression techniques were carried out to examine differences between medication types and doses.

In terms of results, there was overall a decreased risk of anxiety in patients treated with stimulants versus controls.  This global finding, when analyzed more closely, held particularly with methylphenidate preparations (e.g. Ritalin, Concerta, etc) while amphetamine derivatives (e.g. Adderall) did not separate statistically from placebo. There was also some indication that short versus long-acting stimulants and higher versus lower doses were associated with this reduced anxiety risk. No evidence of publication bias was found, although a number of stimulant trials did not meet the authors’ inclusion criteria.

The authors concluded that, contrary to conventional wisdom and some FDA labelling, the risk of anxiety is actually lower compared to placebo in patients treated with stimulant medications.

In the Discussion section, the authors commented about the possible mechanism of their main finding and hypothesized that the reduced anxiety risk was likely not a direct antianxiety effect of the stimulant rather an indirect effect of improving ADHD symptoms.

While the study certainly doesn’t exclude the possibility of some patients experiencing worsening anxiety with stimulant treatment, the article should be somewhat reassuring to those who might otherwise be reluctant to prescribe stimulants to the large number of youth with ADHD who also experience significant anxiety.


Coughlin CG, Cohen SC, et al. Meta-Analysis: Reduced Risk of Anxiety with Psychostimulant Treatment in Children with Attention-Deficit/Hyperactivity Disorder. J Chi Adolesc Psychopharm. 2015;25:611-617.

Autism Diagnosis Made Later For Children with ADHD

Posted: October 21st, 2015 by David Rettew

Autism and ADHD can share many common features, and both disorders are being diagnosed more frequently compared to previous decades.  Making matters more complicated is the accumulating evidence that the two disorders may share some underlying genetics and neurobiology.  While autism is optimally diagnosed when children are around two years of age, many are not diagnosed until much later which represents a lost opportunity for early intervention.  Some preliminary evidence suggests that one factor that is related to a delayed diagnosis of autism is the presence of other psychiatric and developmental problems.  This study, recently published in Pediatrics, examines specifically the association between the age of autism diagnosis and presence of an ADHD diagnosis.

The data come from the National Survey of Children’s Health in the years 2011-2012.  This survey was conducted by randomly calling households in all 50 states. The response rate was 23%. From Autism age of DXan initial calling of over 85,000 households, a final sample of nearly 1500 autistic children between the ages of 2 and 17 was identified.  The main variable of interest was whether or not a child had also been given a diagnosis of ADHD and the specific ages that the two diagnoses were given.  Other factors such as illness severity were recorded an controlled for in some of the analyses.

A total of 42.9% of the autistic sample had also received an ADHD diagnosis, with slightly less than half of that number receiving the ADHD diagnosis first. In those cases in which ADHD was diagnosed first, the autism diagnosis was found to occur roughly 3 years later compared to children in which the ADHD diagnosis came at the same time or after the autism diagnosis, controlling for other variables. Examined another way, children in whom the ADHD diagnosis came first were found to be nearly 30 times more likely to have their autism diagnosis come after the age of 6. While an older age of diagnosis was found to be related to less severe autism, the delay in autism diagnosis among children first diagnosed with ADHD was found regardless of the severity of the autism or ADHD symptoms.

The authors concluded that the presence of ADHD symptoms could cause a delay in an autism diagnosis. They advise clinicians to consider autism in young children who present with ADHD symptoms.

This study raises an important issue in clinical practice, and supports the idea that clinicians may not be as vigilant about autism when a child has symptoms of ADHD.  I’ve tried to train myself (and teach others) that seeing a young child with OCD behaviors should trigger some additional investigation about autism, but thinking the same way for ADHD behaviors is new.

There was one aspect of the study that was puzzling to me and not well discussed.  From the Discussion section, one gets the impression is that the way this all works is that once a child receives a diagnosis of ADHD then subsequent behaviors are viewed through an “ADHD lens” which in turn causes less diligence to search for other potential diagnoses such as autism.  However, in reading the fine print (specifically Table 1) it appears that the mean age of a child receiving a diagnosis of ADHD was about 6, which is well beyond the period that autism screening and assessment is recommended.  Thus, it does not appear that the presence of the ADHD diagnosis itself is clouding judgements about an autism diagnosis but rather something else.  What could that be?  The article doesn’t really say.  Perhaps there is something about early emerging ADHD behaviors that are particularly salient and that may mask more subtle autistic symptoms.  More work needs to be done to figure out what really is going on here.


Miodovnik A, et al.  Timing of the Diagnosis of Attention-Deficit/Hyperactivity Disorder and Autism Spectrum Disorder.  Pediatrics 2015; epub ahead of print.

Antidepressants and Violent Crime in Youth

Posted: September 30th, 2015 by David Rettew

Antidepressants have carried a black box warning for years related to new or worsening suicidal behavior in children and young adults. A possible link, however, between SSRIs and other types of violent behavior has been more difficult to identify with studies finding inconsistent results. A recent large Swedish study, recently published in the journal PLOS One, now jumps into the debate.

The study used a somewhat novel approach in employing a “within subject” design by comparing individuals between periods someone was and was not taking a medication.  Records between

photo by patrisyu and freedigitalphotos.net

photo by patrisyu and freedigitalphotos.net

2006 and 2009 from a large national registry were used for this study and over 850,000 individuals were identified who were prescribed an SSRI medication (subjects who likely only took the medication very briefly were excluded). Another national registry was also used to identify individuals convicted of violent crimes, although other types of crimes were also investigated as a secondary outcome. The authors also tried to quantify the cumulative SSRI dose and divided subjects into groups of low, moderate, and high.

A total of 10.8% of the sample had been prescribed an SSRI with citalopram and sertraline being the most common. The main finding of the study, and the one that received the most press, was that for both males and females between the ages of 15 and 24 only, there was a statistically significant increase in the rate of violent crime during the period someone was taking the medication compared to the intervals that they weren’t. The “hazard ratio” for the 15-24 age group was 1.4 which roughly translates into a 40% increased likelihood. Described in the original study but not well reported by many press articles, however, was the important fact that this risk was increased only among youth with low SSRI doses and not those with moderate or high overall SSRI exposure. Some significant associations were also found between SSRI use and some non-violent crimes as well as non-fatal accidents. Regarding other types of antidepressants, a link was also found between violent crime and the antidepressant venlafaxine while, interestingly, the antidepressant mirtazapine was found to be related to a reduced risk of violent crime.

Sorting out what all of this means is challenging.  While it might be easy to jump to the conclusion that SSRIs cause violent behavior (and many have), the data can’t really support that claim.  In fact, the authors state in their discussion that one possibility is almost the opposite, namely that the finding of the link with violent crime only among those taking subtherapeutic doses suggests that undertreatment may be the mechanism behind this link.  That said, if antidepressants really worked wonders for young people, we should see that therapeutic SSRI usage was associated with a reduced risk of violent behavior, which it wasn’t.  These kinds of finer points have unfortunately been missing in much of the media coverage of this study.

While the within-subjects design is a clever way to reduce some potential confounding factors, it is important to remember also that the study is not randomized.   Therefore, another complicating issue is that individuals were probably more likely to be prescribed medications during times when they were feeling more depressed, anxious, and angry to start with, and thus at higher risk of acting violently. Another fact to keep in mind is that while a 40% increase in violent crime sounds scary, the absolute numbers remain low.  When taking SSRI medications, the conviction rate of violent crimes was 1.0% rate compared to 0.6% without medications.

It is certainly true that young people may become quite agitated when given SSRI antidepressants and it can be a tough call for clinicians to be able to distinguish between because a medication problem (requiring a drop or discontinuation of medication) and  a worsening of the primary condition (which might prompt the opposite response).

In the end, we need to be cautious when using SSRIs, like any class of prescription medication, and be open to the possibility that sometimes the medication is the problem and not the solution.  At the same time, it would be a shame if this study raises unnecessary panic that possibly could end up making the situation worse.


Molero Y, et al.  Selective Serotonin Reuptake Inhibitors and Violent Crime: A Cohort Study.  PLOS One.  Sept 2015, epub ahead of print.


Extreme Picky Eating Linked to Mental Health Problems

Posted: September 17th, 2015 by David Rettew

A parent’s concern about their young child’s picky eating is one of the most common presenting complaints to primary care clinicians.  Generally, if a child is growing and otherwise healthy, the most common response is reassurance and some helpful strategies for how to help kids slowly expand their food repertoire.  This strategy usually works well, and most kids do go on to eat a wider variety of foods with the tireless encouragement and cajoling from their parents.

For some, however, it is not so simple.  The current list of psychiatric disorders in DSM-5 now includes the term Avoidant/Restrictive Food Intake Disorder (ARFID). The diagnosis replaced the term Feeding Disorder of Infancy and Early Childhood which was rarely used and not well researched.  The definition includes the requirement that there is a “persistent failure to meet appropriate nutritional and/or energy needs.” Nevertheless, many medical professionals may be wondering whether ARFID represents a real problem worthy of clinical intervention or is an Picky eater 2example of the DSM over-pathologizing typical and transient child behavior.

To look at this question in more detail, researchers from the Duke Preschool Anxiety Study examined over 900 kids who on average were about 4 years old. They assessed the degree of selective eating through an interview and classified children into groups of “normal,” “moderate,” and “severe” levels of selective eating. Emotional-behavioral problems were was assessed with rating scales and a structured diagnostic interview to see if the children actually met criteria for certain psychiatric disorders.

Overall, at least moderate selective eating was present in 20% of the sample, while 3% were found to be in the severe range. Furthermore, severe selective eating was associated with higher rates of anxiety and depression both with regard to quantitative levels of symptoms and rates of some specific diagnoses (depressive disorder and social anxiety disorder). Investigating other domains, the authors also found that children with selective eating were also much more likely to be hypersensitive to smells, textures, or visual stimuli.

A subset of the sample was followed over time, and the high levels of anxiety were found to continue for many children when they were up to 8 years old.

The authors concluded that especially more severe levels of selective eating were related to other types of emotional-behavioral problems. Their hypothesis was that that the link was not causal (i.e. that selective eating caused anxiety and mood problems) but rather than an enhanced sensory sensitivity may underlie both the food selectivity and some of the associated emotional behavioral problems.

This study has some significant limitations.  While the authors do suggest that their data are relevant to the new ARFID diagnosis, they don’t directly assess ARFID in their study. Weight and weight trajectory were also not rigorously measured and indeed, the number of children with weight loss was not found to differ between the three groups of children (although 45% of the severe SE group had low growth). Finally, the number of 4-year-old children meeting DSM criteria for psychiatric illness in this study will strike many people as quite high. For example, 6% and 33% of the severe SE group met criteria for a depressive disorder and social anxiety disorder, respectively.  Of note, none of the subjects met criteria for autism.

Another practical issue is that an effective and well researched treatment for ARFID has yet to be determined, although it isn’t hard to find a multitude of recommendations for what to do about moderate and more severe selective eaters alike.

The take-away from this study is not to suddenly start treating every instance of picky eating as a mental health crisis, but perhaps to gather some additional information regarding the severity of the selective eating and the presence of other types of behavioral problems or sensory hypersensitivies that may deserve additional follow-up.


Zucker N.  Psychological and Psychosocial Impairment in Preschoolers With Selective Eating.  Pediatrics 2015; August, epub ahead of print.

Study Questions Reasons Behind the Rise in Autism Diagnoses

Posted: September 6th, 2015 by David Rettew

Autism rates - autism speaksThe question is no longer if the diagnosis of autism is rising but why.  Over the past 40 years, the rate has increased from around 1975 of 1 in about 5,000 children to, most recently in 2012, a rate of 1 in 68 , the CDC now estimates that 1 in 68.

The explanations for this surge can roughly be placed into one of two camps: 1)  that this increased prevalence is mostly due to an actual rise in the number of new cases, or 2) that at least the lion’s share of the increased numbers is really an artifact due to things like increased surveillance, a lower threshold for diagnosis, more public awareness, and shifts in diagnostic patterns.

This second explanation was recently investigated by Polyak and colleagues from Penn State University. Using the public IDEA Part B database,  they examined state-by-state enrollment statistics for school special education services from the years 2000 to 2010 for over 6 million children. Of primary interest were trends regarding the number of children who qualified for services due to having an autistic spectrum diagnosis versus qualifying due to other reasons such as intellectual disability or a specific learning disability.

The total number of children receiving special ed services was not found to change much from 2000 to 2010 (a result I found surprising, personally).  Not unexpectedly, the number of children in special ed because of autism rose a total of 331% during this time.  However, the number of children receiving services for what has labelled an intellectual disability dropped. Furthermore, the drop in cases of intellectual disability alone could numerically account for nearly two-thirds of the increase in children with autism.

Putting this all together, the authors concluded that their data support the idea that the often mentioned rise in autism is substantially due to a reclassification away from diagnoses of intellectual disability or a specific learning disability and toward autism.

A related finding was that there was significant variability from state to state for this inverse trend in the rate of autism versus intellectual disability.   Vermont, interestingly, showed this trend more than all other states with the exception of North Dakota, while states like California and Texas did not.  The authors speculated that the variability was related to differences in special education policy.   In another informative table, the authors summarize the rate of autism features among individuals with various known (and named) genetic conditions with the suggestion here being that there is quite of bit of subjectivity going into the decision to invoke autism as a primary diagnosis versus something else.

The evidence presented here is compelling but, of course, circumstantial.   A rise in actual autism cases has been linked to increased parental age, and many individuals and groups continue to contend that everything from environmental toxins to new infectious agents may be behind the rise.

Obviously there is room for some middle ground here. While this study cannot rule out the possibility that there are more “true” cases of autism than in the past, evidence does seem to be mounting that at least a significant portion of this increase is due to other factors.


Polyak A, et al.  Comorbidity of Intellectual Disability Confounds Ascertainment of Autism: Implications for Genetic
Diagnosis.  Am J Med Genetics 2015; epub ahead of print.

Eating Disorder Promoting Websites and Social Media: A 2015 Update

Posted: August 4th, 2015 by David Rettew

In the early 2000s, a great deal of concern was raised about so called pro-ana or pro-mia websites that to varying degrees seemed to endorse and even promote eating disorders such as anorexia and bulimia.  The alarm was loud enough to trigger an episode of the Oprah Winfrey Show in October 2001 on the subject. After that, however, public attention about this issue faded.

What has happened since?  Especially with all of the significant changes and development of social media over the last decade, it certainly seems worth a look.  Belgian researcher Kathleen Custers did just that in a recent review published in the European Journal of Pediatrics.

While the subject remains infrequently studied, several conclusions can be made. First, this content remains widely available and heavily accessed.   Rough estimates are that apPro-Ana siteproximately 13% of young female teens overall have visited pro-ED sites with the rate nearly tripling among those who manifest problematic eating disorder behaviors. One study reported that pro-ED content is searched on Google 13 million times per year.

Secondly, the sites have not changed drastically in terms of content or demographic. While social media has provided more of a venue for direct interaction among users of this content, the sites themselves continue frequently to display many of the same elements they have all along.  These include “thinspiration” photos of extremely thin women (sometimes photoshopped to make people look even thinner) in addition to tips and tricks that can be used to lose weight and evade detection.  A large percentage of these websites continue to be designed and run by adolescents and young women who struggle with eating disorders themselves.

Some controversy does exists about how destructive these sites are for people with eating disorders.  While the stereotype of the pro-ana sites is that they unequivocally try to get people to continue to starve themselves, the sites do vary quite a bit in how much ambivalence is expressed about seeking help and change.  Further, given the level of alienation that many individuals with eating disorders experience, some have argued that these sites provide a rare space for nonjudgmental support and reflection and thus may actually be providing a beneficial role.  Research data, however, tends to demonstrate more of the harmful effects. Survey studies have shown that those who visit these sites report more dissatisfaction with their appearance while in the process picking up new methods for losing weight and hiding their struggles from others. The chicken or egg question, however, can easily be raised here as it is likely that some of these attitudes are driving traffic to these sites rather than the other way around. More solid evidence comes from a few studies that have turned to more experimental models.  In these studies usually done with college age women, some are randomly assigned to viewing pro-eating disorder sites versus other type of content for a period of time and then their beliefs and behaviors are tracked. Some of these studies have found similar results as the surveys, and in a small percentage of subjects the viewing has prompted fairly drastic levels of calorie restriction.

The article concludes with some advice for both health professionals and parents. Clinicians are encouraged to become acquainted with pro-ED messages on the internet and to ask their patients  about it.  Custers suggests that patients keep a media diary while recording their feelings about themselves.   She does not advise clinicians to expressly forbid patient to go to those sites, especially for those who are not yet ready to consider changing their behavior.

For more informational and recovery oriented sites, she recommends that they use celebrities more to promote treatment and positive change since the pro-ED sites are often focused on celebrity issues.  Parents also are reminded to be aware of these sites, especially with how easily they can now be accessed with portable devices anytime and almost anywhere.

In reading this article, I worried a little that bringing up the topic might actually cause some youth to explore these kinds of sites even more. We’ve been taught for years that you can’t induce serious suicidal thinking in people by bringing up the subject, but here things feel a little different. On the other hand, it is difficult to think that most of us old timers would be ahead of our younger patients when it comes to knowledge about what is out there on the internet.  I currently try to bring up the subject with patients who currently have problem eating behaviors but not for all adolescents in general.  Please feel free to comment about your own thoughts and practices.

The article was a nice reminder that this topic has not disappeared with AOL but is taking different forms. While few would argue that culture and media are the sole drivers of eating disorders, their role is clearly important and deserving of this kind of investigation.


Custers K.  The urgent matter of online pro-eating disorder content and children: clinical practice.  Eur J Pediatrics 2015;174:429-433.

Exercise Linked to Reduced ADHD Behaviors

Posted: July 20th, 2015 by David Rettew

To many, ADHD treatment means using medications.  Yet while medications can play an important role, a number of other types of interventions have also been shown to be effective.  One area that has received some investigation is the role of physical activity and exercise in alleviating symptoms.  Parents and clinicians alike have naturally been drawn to activities that can “burn some of that energy,” but actual studies that have examined the role of exercise have often struggled to tease apart the direct contribution of physical activity from underlying genetic causes. A recent study attempted to examine the association between physical activity and ADHD symptoms by taking advantage of a twin design.

Photo by Photostock and freedigitalphotos.net

Photo by Photostock and freedigitalphotos.net

The data come from 232 monozygotic twins participating in the Swedish Twin Study of Child and Adolescent Development. Levels of physical activity were assessed when subjects were between 16 and 17 years old, based upon three multiple-choice questions, while ADHD symptoms were assessed at age 16 to 17 and again at 19 to 20. The statistical analyses tested the association between physical activity at age 16-17 with parent-rated ADHD symptoms at age 19-20 while controlling for initial ADHD symptoms and the shared genetic and environmental factors between each twin pair.

Results showed that more physical activity in late adolescence was associated with reduced ADHD symptoms in early adulthood even after controlling for ADHD symptoms at baseline, BMI, and most notably shared genetic and environmental factors. This reduction was found for both inattentive and hyperactive/impulsive symptoms, although the effect size was relatively small.  The authors concluded that their study added stronger evidence that reduced physical activity is indeed casually linked to more ADHD symptoms, albeit weakly.

It is worth noting that the sample was not a clinical one, so it remains to be seen whether or not the same results would have occurred with a group of individuals who have been diagnosed with ADHD.  The assessment of physical activity was also not particularly rigorous.  These limitations aside, the study does provide more compelling data that helping patients increase physical activity can be an important aspect of comprehensive multi-modal treatment.


Rommel AS, et al.  Is Physical Activity Causally Associated With Symptoms of Attention-Deficit/Hyperactivity Disorder? JAACAP 2015;54(7):565–570.

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