Spring 2016: Volume 19, Issue 2

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Spring 2016: Volume 19, Issue 2 Clinical Science APA Society for the Science of Clinical Psychology III Section III of the Division of Clinical Psychology of Division12 the American Psychological Association Ψ Developing clinical psychology as an experimental-behavioral science Newsletter Spring 2016: Volume 19, Issue 2 SSCP Executive Board Table of Contents Presidential Column President: Steve Hollon, Ph.D. S. Hollon...............................................................................................................2 Vanderbilt University Financial Report Past-President: K. McLaughlin.......................................................................................................5 Mitch Prinstein, Ph.D. University of North Carolina at Cha- Diversity Corner pel Hill D. Rosmarin.........................................................................................................6 President-Elect: Scott Lilienfeld, Ph.D. Awards & RecoGnition...........................................................................................7 Emory University Updates from 2015 Varda Shoham Training Grant winners...............................15 Secretary/Treasurer: Kate McLaughlin, Ph.D. University of Washington Clinical Science Early Career Path C. Beard.............................................................................................................19 Division 12 Representative: David Smith, Ph.D. Clinical Science Early Career Path University of Notre Dame E. Ro..................................................................................................................21 Student Representatives: Andrea Niles Student Perspectives University of California, Los Angeles Lorenzo-Luaces, Lemmens, Cohen & Bos........................................................23 Jessica Hamilton Clinician Perspective Temple University M. Rouse.............................................................................................................26 At Large Members: Douglas Mennin, Ph.D. Update from Student Representatives Hunter College A. Niles & J. Hamilton.........................................................................................28 Leonard Simms, Ph.D. University at Buffalo Clinical Science Editor: Articles published in Clinical Science represent the views of the authors and not necessarily those Autumn Kujawa, Ph.D. of the Society for a Science of Clinical PsycholoGy, the Society of Clinical PsycholoGy, or the University of Illinois at Chicago American PsycholoGical Association. Submissions representinG differinG views, comments, and letters to the editor are welcome. Clinical Science Vol. 19 (2): Spring 2016 2 Presidential Column Psychosocial Interventions and Medications Steve Hollon, Ph.D., Vanderbilt University Earlier this spring I took part in a dialogue on the for psychosocial interventions (Driessen et al., 2010). relative contributions of psychosocial interventions I showed slides from Erick Turner’s classic study and medications in the treatment of depression. The that found that publication bias infated the apparent dialogue was sponsored by the McMaster University effcacy of antidepressant medications (Turner et Alumni Association and included presentations from al., 2008), but also showed evidence that the same Irving Kirsch, Associate Director of the Program in was true for psychosocial interventions (Driessen Placebo Studies at the Harvard Medical School, et al., 2015). While I would agree with Kirsch that author of the treatise “The Emperor’s New Drugs: nonspecifc placebo effects make up the largest Exploding the Antidepressant Myth”; Benoit Mulsant, portion of response to antidepressant medications, Professor and Chair of the Department of Psychiatry we also have meta-analytic data that suggest that at the University of Toronto and an expert in the the same is true with respect to nonspecifc “common pharmacological treatment of depression; and me. elements” for the psychosocial interventions (Cuijpers We each gave brief presentations then responded to et al., 2012). It is not that antidepressant medications questions posed by Paul Andrews, an evolutionary or empirically supported treatments like cognitive psychologist at McMaster University who organized behavior therapy do not work, but rather that they the dialogue and has some rather provocative things work for largely nonspecifc reasons among patients to say about the adaptive function of depression and with less severe depressions. Score one for Kirsch. the way antidepressant medications really work. The That being said, cognitive therapy does appear to audience posed questions as well. have an enduring effect that reduces risk for relapse following treatment termination (Cuijpers et al., 2013). Professor Kirsch went frst and presented meta- Medications also protect against subsequent relapse analytic evidence from controlled medication trials that and recurrence but only for so long as one stays on showed that the placebo effect was quite large and them. the pharmacological effect surprisingly small (Kirsch & Saperstein, 1998). He followed this up by using the Nonetheless, antidepressant medications do have Freedom of Information Act to obtain fles from the specifc effects that can be quite important for at Food and Drug Administration (FDA) containing the least some patients. Professor Mulsant focuses on data from all the trials (published and unpublished) “hard to treat” older patients with depression and co- that had been registered to win approval to take morbid physical illness, psychotic depression, bipolar various medications to market. What he found was disorder, schizophrenia, and dementia. He pointed that although differences between drug and placebo out that such patients often require more aggressive were signifcant, they were small in magnitude and medication treatment or somatic therapies like conditioned upon a signifcant treatment by severity electroconvulsive therapy (ECT) and tend to show far interaction such that only those patients with more more attenuated nonspecifc response. He also noted severe depressions passed the criteria for clinical that high quality psychosocial treatment of the kind signifcance established by the National Institute for delivered in my studies is largely unavailable in much Health and Clinical Excellence (NICE) in the United of the United States and Canada and he is right. In Kingdom (Kirsch et al., 2008). This led him to challenge the United Kingdom with its single payer system the the widely held view that depression was the result of government has invested over £700 million pounds a chemical imbalance in the brain and to emphasize to train therapists in the National Health Service to the role of nonspecifc factors (Kirsch, 2010). provide the kinds of psychosocial interventions that have fared well in controlled clinical trials (Layard My presentation came next. The bulk of my work has & Clark, 2015). We have nothing like that in North focused on comparisons between cognitive behavior America. More is the pity since, as Professor Mulsant therapy and antidepressant medications. Like pointed out, depression accounts for more misery and Kirsch, we have a meta-analytic study that indicates more deaths (by suicide) than many of the medical that “true” drug effects (drug-placebo differences) illnesses that attract more in the way of public only emerge among patients with more severe investment or charitable donations. depressions (Fournier et al., 2010), but we also have a meta-analysis that indicates that the same is true Now back to our host Professor Andrews. As an Clinical Science Vol. 19 (2): Spring 2016 3 evolutionary psychologist he asks whether depression of neurotransmitter in the synapse (which is what has an adaptive function and suggests that it promotes antidepressant medications frst do) but rather by the a tendency to dwell on the complex problems that subsequent reduction in the amount of neurotransmitter triggered the current episode, something he calls in the presynaptic neuron and sensitivity to it in the analytic rumination (Andrews & Thompson, 2009). post-synaptic neuron. It is like holding up a match to a Rather than being a problematic symptom (as I have thermostat to turn the furnace down. long believed) he views rumination as a search for a solution and suggests that this process may help Moreover, so long as the medication is in the system, account for the tendency of each episode to end on its the counter-regulatory homeostatic mechanisms are own even in the absence of treatment (spontaneous like a coiled spring, ready to spring back when the remission). Moreover, he views medications as medications are taken away. According to Andrews, it interfering with that process much as cold remedies is not that medications do not work, but that they do so suppress the symptoms of a cold while prolonging the by suppressing symptoms at the expense of prolonging infection. He suggests that medications work not so the underlying episode. The more the system is much by redressing a chemical imbalance in the brain perturbed, the greater the risk of relapse when the as by perturbing the balance of neurotransmitters in medications are taken away. If Andrews is correct, the synapse (Andrews et al., 2015). Consistent with then taking antidepressants virtually guarantees that this notion, the more a specifc medication perturbs you will become depressed again after you discontinue the neurotransmitters associated with depression (as them, the world’s most perfect mousetrap. measured in animals), the
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