HERE IN THIS ISSUE I wish more kids could ride horses today . riding a horse isn’t what it looks like: it isn’t a person sitting in a saddle telling the horse what to do by yanking on the reins. Real riding is a lot like ballroom dancing or maybe figure skating in pairs. It’s a relationship. —Temple Grandin, Animals in Translation1
F
rom biomarkers to bridles, from telomeres to treatments, this month’s Journal features 3 articles about autism spectrum disorders (ASDs) and answers 2 important questions about pediatric psychopharmacology: What is the fate of treatment in preschoolers diagnosed with attention-deficit/hyperactivity disorder (ADHD) and what does a meta-analysis of selective serotonin reuptake inhibitor (SSRI) treatment of pediatric major depressive disorder (MDD) show? We first turn our attention to autism and biomarkers as discussed by Nelson and colleagues (p. 588). Telomeres, repeated nucleotide caps of chromatids, are longest early in life and slowly shorten over one’s lifespan. At a critical point, they no longer divide; this is associated with cell death. Decreasing telomere length has been linked not only to aging but also to stress and trauma. Further, shorter telomeres are associated with medical and psychiatric problems and have been shown to be highly heritable. Recognizing this, Nelson et al. examined telomere length as a marker of stress in mothers, fathers, and infant siblings in families who had a child with ASD (n ¼ 86) and in those who did not (n ¼ 118). Using DNA from saliva swabs, these researchers found that families of children with ASDs had shorter telomeres compared with those who did not. In their discussion, the investigators noted that telomere shortening can place entire families of children with ASDs at increased risk for poor health outcomes and, possibly, their infant siblings at greater risk for neurodevelopmental disorders as a variable independent of underlying genetic risk. They encourage close monitoring and support of families. Offering evidence about what might best support the development of young children with ASDs and their families, Estes and colleagues (p. 580) provide a follow-up on their early intervention study. From their original group of 48 children (18-30 months old) who were evenly divided between a group that received flexible intensive homebased treatment involving applied behavioral analysis
methods and parent coaching (Early Start Denver Model) and community treatment, these researchers were able to reassess 39 participants at 6 years of age. Compared with the community treatment group, the Early Start Denver Model group showed improved core symptoms, less restricted and repetitive behaviors, more adaptive behavior, and better peer relationships. Although myriad books and Web sites tout unconventional interventions for youth with ASDs, there is little evidence about many nontraditional therapies. Luckily, the hoof beats of this month’s Journal signal a 127-participant randomized trial of a 10-week therapeutic horseback riding intervention for children (6-16 years old) diagnosed with ASDs. Gabriels and colleagues (p. 541) found that their therapeutic horseback riding group versus a control group, which had a barn-based activity, exhibited significant improvements in irritability and hyperactivity and on measurements of social cognition and communication. In terms of pharmacologic treatment studies, in Vitiello and colleagues’ follow-up of the Preschool ADHD Treatment Study (PATS), we learn which, if any, pharmacologic agents 206 of the original 303 PATS participants were taking 3 years after the original study and which 179 were taking at year 6 (p. 550). PATS was a controlled trial that demonstrated the utility of methylphenidate in decreasing ADHD symptoms in children 3.5 to 5 years of age. Researchers followed up on the original study to look at treatment stability and long-term pharmacotherapy course. The findings of Vitiello’s research group showed that 65% were still on some ADHD medication at year 3, whereas 70.9% were on some medication at year 6. The researchers noted that 13.4% of children from the original study were on antipsychotic treatment at year 6; this treatment was associated with more comorbidities. In their meta-analytic effort, Varigonda and colleagues (p. 557) found 13 studies involving SSRI treatment of pediatric MDD, with a total of 3,004 participants. In their discussion, they list some interesting findings vital to our field, among them that the benefit of SSRIs in pediatric depression is statistically significant within 2 weeks of starting treatment; the greatest incremental benefits of SSRIs for pediatric depression are observed early in treatment; there is no evidence of increased benefit with higher maximum doses of SSRIs used in pediatric depression trials; and pediatric patients compared with adults with MDD exhibited a smaller treatment benefit from SSRIs.
REFERENCE 1. Grandin T. Animals in Translation: Using the Mysteries of Autism to Decode Animal Behavior. Orlando: Harcourt; 2006.
JOURNAL OF THE AMERICAN ACADEMY OF C HILD & ADOLESCENT PSYCHIATRY VOLUME 54 NUMBER 7 JULY 2015
www.jaacap.org
525
THERE ABSTRACT THINKING Child Psychiatry in the (Mis)Information Age We have to be there at the birth of ideas, the bursting outward of their force: not in books expressing them, but in events manifesting this force, in struggles carried on around ideas, for or against them. —Michel Foucault1
B
y now, most Journal readers know the story well. In 1998, a case series was published in a prominent medical journal sounding an alarm: autism might be caused by vaccines!2 In the aftermath, politicians accused the Centers for Disease Control and Prevention of hiding data, and celebrities cautioned parents about the dangers of vaccines.3 Despite the emergence of sound evidence refuting causality and the retraction of the original article, many parents chose not to vaccinate their children.4 Although there has been consistent concern about the public health risks, it was not until recent measles outbreaks—particularly one at Disneyland—that a vocal outcry against the “antivax” movement emerged. It is against this backdrop that many people wonder: How can scientific misinformation be so easily propagated and persistent? To begin to answer this question, Bessi et al.5 from the Institute for Advanced Study in Pavia in Italy tracked 1.2 million Facebook users. Focusing on 73 pages, 34 featuring science news and 39 containing conspiracy or “alternative news,” these social scientists found that the communities surrounding these 2 groups of social media pages were highly polarized and apt to “like” (in Facebook parlance), comment on, and share news within their own range of beliefs. Specifically, when looking at comments made on scientifically grounded articles, they found that 90.29% of comments came from typical consumers of scientific news. Moreover, they showed that 99.08% of comments on alternative news came from typical consumers of alternative news. With these data, one discovers that it is much less likely that a conspiracy theory—which the investigators noted “tend to reduce the complexity of reality by explaining social or political aspects as plots conceived by powerful individuals or organizations”—is met with direct opposition. Among the like-minded, these notions sustain internal momentum. The Italian researchers took their study a step further by tracking what occurs with intentionally misleading memes
(media that are copied and widely disseminated) posted on Facebook. They found that consumers of alternative news were far more likely to like and comment on these patently false news items—with the information being passed along to their friends, unchecked—absurdities masquerading as truth. It is in this climate of marked polarity and in an Internet age of rapid proliferation of untruths that our field operates. There is no doubt—and this month’s article by Nelson et al.6 on shortened telomere length and autism demonstrates this—that having a child with a neurodevelopmental disorder is stressful. The toll of stress on individuals and family members of those with psychiatric or neurodevelopmental disorders clearly fuels a search for answers about causality and best treatments. Furthermore, there is little doubt that our field lacks many answers. We do well to offer studies outlining the neurobiological underpinnings, phenomenology, and treatment of psychiatric disorders and to humbly acknowledge the ways our science falls short of ideal understanding and treatment offerings. The latter is beautifully demonstrated by the title of Brent’s commentary on the Treatment of Adolescent Depression Study (TADS): “Glad for What TADS Adds, but Many TADS Grads Still Sad.”7 The climate of headline-grabbing sensationalism challenges us to read and disseminate high-quality information with our patients, colleagues, friends, and wider community, sharing the nuanced findings of our field. Further, polarities such as those described by Bessi et al. urge us to respond early, often, and in a kind manner to misinformation. To do this is to help contemporary society eschew reductionism and protect the wider community against false claims— those with potentially deleterious effects on young people and families. Craigan Usher,
MD
[email protected] Oregon Health and Science University Portland, OR
The author acknowledges Samuele Cortese, MD, PhD, Cambridge University Hospitals, University of Nottingham for his help in preparing this article. Disclosure: Dr. Usher reports no biomedical financial interests or potential conflicts of interest. http://dx.doi.org/10.1016/j.jaac.2015.04.008
REFERENCES 1. Eribon D. Michel Foucault. Cambridge, MA: Harvard University Press; 1991. 2. Wakefield AJ, Murch SH, Anthony A, et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet. 1998;351:637-641. 3. Willingham E. Is the CDC hiding data about mercury, vaccines, and autism? Forbes. http://www.forbes.com/sites/emilywillingham/2014/ 02/22/is-the-cdc-hiding-data-about-mercury-vaccines-and-autism/. Published February 22, 2014. Accessed April 17, 2015. 4. Fombonne E. Thimerosal disappears but autism remains. Arch Gen Psychiatry. 2008;65:15-16.
5. Bessi A, Coletto M, Davidescu GA, Scala A, Caldarelli G, Quattrociocchi W. Science vs conspiracy: collective narratives in the age of misinformation. PLoS One. 2015;10:e0118093. 6. Nelson CA, Varcin KJ, Coman NK, DeVivo I, Tager-Flusberg H. Shortened telomeres in families with a propensity to autism. J Am Acad Child Adolesc Psychiatry. 2015;54:588-594. 7. Brent DA. Glad for what TADS adds, but many TADS grads still sad. J Am Acad Child Adolesc Psychiatry. 2006;45:1461-1464.
JOURNAL 526
www.jaacap.org
OF THE
AMERICAN ACADEMY OF C HILD & ADOLESCENT PSYCHIATRY VOLUME 54 NUMBER 7 JULY 2015
F
rom biomarkers to bridles, from telomeres to treatments, this month’s Journal features 3 articles about autism spectrum disorders (ASDs) and answers 2 important questions about pediatric psychopharmacology: What is the fate of treatment in preschoolers diagnosed with attention-deficit/hyperactivity disorder (ADHD) and what does a meta-analysis of selective serotonin reuptake inhibitor (SSRI) treatment of pediatric major depressive disorder (MDD) show? We first turn our attention to autism and biomarkers as discussed by Nelson and colleagues (p. 588). Telomeres, repeated nucleotide caps of chromatids, are longest early in life and slowly shorten over one’s lifespan. At a critical point, they no longer divide; this is associated with cell death. Decreasing telomere length has been linked not only to aging but also to stress and trauma. Further, shorter telomeres are associated with medical and psychiatric problems and have been shown to be highly heritable. Recognizing this, Nelson et al. examined telomere length as a marker of stress in mothers, fathers, and infant siblings in families who had a child with ASD (n ¼ 86) and in those who did not (n ¼ 118). Using DNA from saliva swabs, these researchers found that families of children with ASDs had shorter telomeres compared with those who did not. In their discussion, the investigators noted that telomere shortening can place entire families of children with ASDs at increased risk for poor health outcomes and, possibly, their infant siblings at greater risk for neurodevelopmental disorders as a variable independent of underlying genetic risk. They encourage close monitoring and support of families. Offering evidence about what might best support the development of young children with ASDs and their families, Estes and colleagues (p. 580) provide a follow-up on their early intervention study. From their original group of 48 children (18-30 months old) who were evenly divided between a group that received flexible intensive homebased treatment involving applied behavioral analysis
methods and parent coaching (Early Start Denver Model) and community treatment, these researchers were able to reassess 39 participants at 6 years of age. Compared with the community treatment group, the Early Start Denver Model group showed improved core symptoms, less restricted and repetitive behaviors, more adaptive behavior, and better peer relationships. Although myriad books and Web sites tout unconventional interventions for youth with ASDs, there is little evidence about many nontraditional therapies. Luckily, the hoof beats of this month’s Journal signal a 127-participant randomized trial of a 10-week therapeutic horseback riding intervention for children (6-16 years old) diagnosed with ASDs. Gabriels and colleagues (p. 541) found that their therapeutic horseback riding group versus a control group, which had a barn-based activity, exhibited significant improvements in irritability and hyperactivity and on measurements of social cognition and communication. In terms of pharmacologic treatment studies, in Vitiello and colleagues’ follow-up of the Preschool ADHD Treatment Study (PATS), we learn which, if any, pharmacologic agents 206 of the original 303 PATS participants were taking 3 years after the original study and which 179 were taking at year 6 (p. 550). PATS was a controlled trial that demonstrated the utility of methylphenidate in decreasing ADHD symptoms in children 3.5 to 5 years of age. Researchers followed up on the original study to look at treatment stability and long-term pharmacotherapy course. The findings of Vitiello’s research group showed that 65% were still on some ADHD medication at year 3, whereas 70.9% were on some medication at year 6. The researchers noted that 13.4% of children from the original study were on antipsychotic treatment at year 6; this treatment was associated with more comorbidities. In their meta-analytic effort, Varigonda and colleagues (p. 557) found 13 studies involving SSRI treatment of pediatric MDD, with a total of 3,004 participants. In their discussion, they list some interesting findings vital to our field, among them that the benefit of SSRIs in pediatric depression is statistically significant within 2 weeks of starting treatment; the greatest incremental benefits of SSRIs for pediatric depression are observed early in treatment; there is no evidence of increased benefit with higher maximum doses of SSRIs used in pediatric depression trials; and pediatric patients compared with adults with MDD exhibited a smaller treatment benefit from SSRIs.
REFERENCE 1. Grandin T. Animals in Translation: Using the Mysteries of Autism to Decode Animal Behavior. Orlando: Harcourt; 2006.
JOURNAL OF THE AMERICAN ACADEMY OF C HILD & ADOLESCENT PSYCHIATRY VOLUME 54 NUMBER 7 JULY 2015
www.jaacap.org
525
THERE ABSTRACT THINKING Child Psychiatry in the (Mis)Information Age We have to be there at the birth of ideas, the bursting outward of their force: not in books expressing them, but in events manifesting this force, in struggles carried on around ideas, for or against them. —Michel Foucault1
B
y now, most Journal readers know the story well. In 1998, a case series was published in a prominent medical journal sounding an alarm: autism might be caused by vaccines!2 In the aftermath, politicians accused the Centers for Disease Control and Prevention of hiding data, and celebrities cautioned parents about the dangers of vaccines.3 Despite the emergence of sound evidence refuting causality and the retraction of the original article, many parents chose not to vaccinate their children.4 Although there has been consistent concern about the public health risks, it was not until recent measles outbreaks—particularly one at Disneyland—that a vocal outcry against the “antivax” movement emerged. It is against this backdrop that many people wonder: How can scientific misinformation be so easily propagated and persistent? To begin to answer this question, Bessi et al.5 from the Institute for Advanced Study in Pavia in Italy tracked 1.2 million Facebook users. Focusing on 73 pages, 34 featuring science news and 39 containing conspiracy or “alternative news,” these social scientists found that the communities surrounding these 2 groups of social media pages were highly polarized and apt to “like” (in Facebook parlance), comment on, and share news within their own range of beliefs. Specifically, when looking at comments made on scientifically grounded articles, they found that 90.29% of comments came from typical consumers of scientific news. Moreover, they showed that 99.08% of comments on alternative news came from typical consumers of alternative news. With these data, one discovers that it is much less likely that a conspiracy theory—which the investigators noted “tend to reduce the complexity of reality by explaining social or political aspects as plots conceived by powerful individuals or organizations”—is met with direct opposition. Among the like-minded, these notions sustain internal momentum. The Italian researchers took their study a step further by tracking what occurs with intentionally misleading memes
(media that are copied and widely disseminated) posted on Facebook. They found that consumers of alternative news were far more likely to like and comment on these patently false news items—with the information being passed along to their friends, unchecked—absurdities masquerading as truth. It is in this climate of marked polarity and in an Internet age of rapid proliferation of untruths that our field operates. There is no doubt—and this month’s article by Nelson et al.6 on shortened telomere length and autism demonstrates this—that having a child with a neurodevelopmental disorder is stressful. The toll of stress on individuals and family members of those with psychiatric or neurodevelopmental disorders clearly fuels a search for answers about causality and best treatments. Furthermore, there is little doubt that our field lacks many answers. We do well to offer studies outlining the neurobiological underpinnings, phenomenology, and treatment of psychiatric disorders and to humbly acknowledge the ways our science falls short of ideal understanding and treatment offerings. The latter is beautifully demonstrated by the title of Brent’s commentary on the Treatment of Adolescent Depression Study (TADS): “Glad for What TADS Adds, but Many TADS Grads Still Sad.”7 The climate of headline-grabbing sensationalism challenges us to read and disseminate high-quality information with our patients, colleagues, friends, and wider community, sharing the nuanced findings of our field. Further, polarities such as those described by Bessi et al. urge us to respond early, often, and in a kind manner to misinformation. To do this is to help contemporary society eschew reductionism and protect the wider community against false claims— those with potentially deleterious effects on young people and families. Craigan Usher,
MD
[email protected] Oregon Health and Science University Portland, OR
The author acknowledges Samuele Cortese, MD, PhD, Cambridge University Hospitals, University of Nottingham for his help in preparing this article. Disclosure: Dr. Usher reports no biomedical financial interests or potential conflicts of interest. http://dx.doi.org/10.1016/j.jaac.2015.04.008
REFERENCES 1. Eribon D. Michel Foucault. Cambridge, MA: Harvard University Press; 1991. 2. Wakefield AJ, Murch SH, Anthony A, et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet. 1998;351:637-641. 3. Willingham E. Is the CDC hiding data about mercury, vaccines, and autism? Forbes. http://www.forbes.com/sites/emilywillingham/2014/ 02/22/is-the-cdc-hiding-data-about-mercury-vaccines-and-autism/. Published February 22, 2014. Accessed April 17, 2015. 4. Fombonne E. Thimerosal disappears but autism remains. Arch Gen Psychiatry. 2008;65:15-16.
5. Bessi A, Coletto M, Davidescu GA, Scala A, Caldarelli G, Quattrociocchi W. Science vs conspiracy: collective narratives in the age of misinformation. PLoS One. 2015;10:e0118093. 6. Nelson CA, Varcin KJ, Coman NK, DeVivo I, Tager-Flusberg H. Shortened telomeres in families with a propensity to autism. J Am Acad Child Adolesc Psychiatry. 2015;54:588-594. 7. Brent DA. Glad for what TADS adds, but many TADS grads still sad. J Am Acad Child Adolesc Psychiatry. 2006;45:1461-1464.
JOURNAL 526
www.jaacap.org
OF THE
AMERICAN ACADEMY OF C HILD & ADOLESCENT PSYCHIATRY VOLUME 54 NUMBER 7 JULY 2015
