“Hypocritical Oath”

Lilienfeld, 2007

Of this week’s five articles, I found the by far the most compelling one to be (the always controversial) Scott Lilienfeld’s manifesto on Potentially Harmful Therapies (PHTs). Taking on quackery, DARE, and experiential therapies in one fell swoop, Lilienfeld sets forth a powerful argument for the real and present urgency of addressing PHTs in clinical psychology ­now – before, even, taking another step towards establishing firm ESTs. This is a powerful idea of which, I admit, I was quite skeptical at the outset. However, having walked Lilienfeld’s path of logic (sic) with him, I am largely compelled by his claim of importance in addressing PHTs

To catalogue the interesting and/or contentious ideas discussed in this article would be both overlong and boring. So, I will touch on some of what I see to be the most intriguing ideas:

-I have not before heard a more damning portrayal of the impact of the “file-drawer effect” and its brother, “Type III error” (p.57). That all finding should be somehow reported is, of course, prescriptively wonderful, but awfully hard to make happen, especially given the (necessary) rigors of the peer-review process. That the lack of reporting of Type III error may very well be masking a body of research demonstrating iatrogenic (at least) effects of various treatments is just downright scary. Though the International Journal of Non-Significant Results represents a step in the right direction towards resolving this mishap, the notion of “enrolling all intervention studies in a centralized data bank that is publicly accessible” (p. 57) is probably a better idea.

-I was particularly heartened to see Facilitated Communication (FC) listed on the provisional list of PHTs. Having seen firsthand the amount of false hope that such interventions can provide to families that are desperately seeking real hope, it is worrisome to me that its prevalence has not diminished at all over time. I find it telling, too, that, in additional to FC, several of therapies listed in the article are directed towards children with autism (chelation, hyperbaric chambers, etc). Perhaps this population is a good starting point from which to address this pressing concern, as most information-providing agencies for families are proscribed from providing preferential treatment information – except in the case of conclusive demonstration of harmful effects. To my knowledge, no treatment has been sufficiently widely accepted to meet this criterion.

-Most notably, there is a logical flaw in Lilienfeld’s paper when he claims, “the literature here suggests that it would be erroneous to presume that these [untested] treatments are safe prior to subjecting them to adequate tests.” (p. 62; italics mine) In contrast to the Dodo Verdict, Lilienfeld is proposing an “inverse treatment specificity” effect. As a result, he proclaims that we should indeed be wary of untested treatments, as they may, in fact, prove more harm than good. However, he may be committing a sort of Type I error, here, by too hastily rejecting his null hypothesis of treatment equivalence. Given this formulation, though, it seems we are stuck with trying to impose a 3-factor logic on a binary set of choices: though in principle we would like to presume a priori that a treatment is either efficacious, negligible, or iatrogenic, in practice one must either offer a treatment option to a patient or not.

As such, from a practical standpoint, it may behoove us to no longer view the large body of untested treatments as either “probably ok” or “maybe harmful,” but to use the existing body of research to make solid evidence for use in clinical practice prior to subjecting them to rigorous research. To wit: we have a body of literature speaking to “common factors” (such as positive treatment alliance) for efficacious treatments. It seems, then, that Lilienfeld’s list of potential “underlying principles of negative change, such as premature termination of exposure, vicarious exposure to negative role models, and induction of false traumatic memories, that cut across numerous specific techniques,” (p. 65) could be seen as “common factors” of PHTs (indeed, Lilienfeld calls them “mediators”). Of course, research would be needed to ensure that these are appropriately-defined constructs, but it seems that, as Lilienfeld notes, undertaking this line of research would be “more informative and parsimonious than a catalogue of PHTs” (p. 65). This, then, brings me to my point: using both sets of positive and negative “common factors,” one could evaluate an untested treatment as being at risk for being a PHT or as having a protective factor against such risk. Treatments, for instance, that hinge on the generation of “suppressed memories,” could be seen as at risk treatments, while those that adhered centrally to principles of exposure for phobia treatment could be seen as somewhat protected against the potential likelihood of being iatrogenic. This rather easy and straightforward process of evaluating the prima facie characteristics of treatments could provide the useful direction needed for those researchers hoping to heed the urgent call of this paper to begin to determine a more comprehensive list of PHTs.

Standing on Shaky Ground

Linehan, 1993

Marsha Linehan takes us through the first of our two (14 year old…) trips across the shaky ground of personality disorder. When Jim told us in class today that it is a “mess,” I figured the thicket of conflicting ideas, incomplete theories, and constructs that fell apart upon scrutiny. Though this may be the case broadly, I was actually fairly impressed with how Linehan was able to make a strong case for her position on one of the most contentious of disorders.

I should insert a bit of personal disclosure before I continue: I have, in recent years, had much direct contact with (and consequent from) an individual with BPD. Indeed, she was treated by the selfsame Dr. Gunderson -- using DBT -- who is cited throughout the article (e.g. p. 8) during the time I knew her. As such, many of the positions I hold on this matter are strongly influenced by this experience (as is the case, it seems, for many people who have had close relationships with people with BPD), and I may therefore make statements stemming from my n of 1 that may not otherwise generalize.

A quick note on the interpersonal relationships section (p. 9): yes, I know what they mean by the various criteria, but it seems these should be awfully difficult ideas to get good interrater reliability on, since almost everyone who has been in serious or complex relationships has experienced “intolerance of aloneness,” “stormy relationships,” “abandonment concerns,” or some confluence of them. The criterion I am most concerned about, though, is the “treatment regressions” one. I understanding this to be byproduct of BPD as we understand it now, but to include it as an inclusion criterion for the disorder seems to belie the whole notion of trying to come up with good treatments for it in the first place! What if DBT or its successors end up minimizing regression in the vast majority of cases? Does this mean they’ve “cures” a symptom of BPD?

One thing I appreciate about Marsh Linehan is her perspective on individuals with BPD. While many clinical psychologists view the disorders they treat or research through a clinical (in the sterile or… pejorative… sense) lens, it seems that this approach is a double-edged sword. On the one hand, you maintain scientific objectivity and appropriate distance. On the other hand, one may lose sight of the actual issues facing individuals with the disorder; to cite Allison’s quote in her Blog of the child who spoke at the Autism: the Musical Q&A “A person with autism can't tell you what it's like to not have autism and a person without autism can't tell you what it's like to have autism. It's part of me, I don't know what it's like.” This is problematic in a practical, and, perhaps, ethical sense. Linehan, however, seems to have no qualms playing the role of advocate and empath for her patients (and this is reflected in her treatment methodology). Her sympathy for them is particularly evident in her damning of the “pejorative” terminology that’s often associated with the diagnostic criteria for BPD (see pp. 17-18). Though I’m not sure all clinical researchers need hold such a sympathetic position (though, perhaps they do?), it does seem to be an important position to exist to keep us from going so far down the pure science route that we lose sight of who we’re working for in the first place.

Given Linehan’s position, I must say that my biggest concern stems from an unlikely source. Again, this is coming largely from my subjective experience with one individual who met criteria for BPD, but it seems that the goal of DBT doesn’t seem to address the underlying distress of individuals with the disorder. Indeed, this seems to be a natural position for many CBT-derived treatments to take (“we’re not trying to eliminate the unwanted thoughts you have, just how you react to them”). Though this makes sense functionally, I believe it is important to see it as a starting point, not a conclusion, for treatment targets. Even Linehan’s own studies bear out somewhat the phenomenon I’m addressing, when she finds “no differences between groups in self-reported depression” and that “DBT was not more effective… in raising subjects’ rating of their own success in accepting and tolerating both themselves and reality.” (p. 24) These self-report measures (read: subjective) haven’t changed much under treatment. This is precisely what I saw with my friend, whose dangerous behaviors declined, but still came home daily reporting on a slew of upsetting interpersonal interactions which where often based upon “unusual perceptual experiences” (DIB-R term). It was, of course, wonderful to see her living more safely; I also hoped that DBT might begin to help her intervene in her own head to decrease her distress. Though I know this is, of course, a latent construct I’m pointing to, it certainly isn’t one for her (and, I imagine, others with BPD). Is there any hope, when the research is populated by observational measures and practice is slowly being engulfed by EST-CBT, for treatment of these symptoms to emerge as a target – if only an incremental one?

Speaking of increments, the value of the “face” of DBT is perhaps an interesting one. By this, I am speaking of the Zen basis for DBT, and its consequent “hippie-dippy” and decidedly unscientific presentation when examined by a casual observer. It is evident after reading Linehan’s introduction that these facades are, for the most part, a mask for sound, integrative behavioral and cognitive-behavioral approaches. Even the purported exceptions to this -- e.g. “emphasis on the therapeutic relationship as essential to treatment” (p. 20) -- are dubious at best. How, then, do we reconcile this with the scientific goal of parsimony? Perhaps, it is on the grounds of what might be called incremental utility. While it may be that behavioral principles have tremendous therapeutic power, if people are typically wary of them (gasps of fear and horror!), is it not incumbent upon the purveyors of treatment technology to consider this in the design process? Perhaps Linehan is on to something when she couches DBT in her “Eastern” terms. If doing so will increase the willingness of individuals to enter treatment, and their receptivity once they get there, has she not then increased the value – the utility – of the treatment, even if it had already existed in some form before? This is an idea I’ve been batting about for some time now (Jim & Allison, my apologies if I unduly exposed you to it in several of our past interactions), but one about which I’m curious as to others’ thoughts.

Hello Muddah, Hello Faddah

Barlow, 2000

Barlow provides us a thorough examination of the state of the most prominent models of anxiety. Though his findings are, not surprisingly, quite compelling, it is interesting to think of them in light of our previous readings. For instance, his framing of the relationship of anxiety & depression (p. 1252) follows from the model presented in the Cuellar et al. article. Just as there is an intersecting track between depression & mania, it seems like, likewise, it may be the same for anxiety and depression. I’m not sure what the implications of this may be for diagnosis (is it useful to reframe our terminology to accept this, or can this model be effectively implemented under the current terminological paradigm?), it does seem useful for better approximating etiology and treatment.

Additionally, Barlow speaks frequently of the role of parenting and early development in contributing to anxiety. Specifically, he seems to allude to a uniquely important role in this case. Though he does this in the context of something like a largely interactional model of anxiety, I wonder of Coyne would consider this an example of what Coyne calls “neocryptopsychoanalytic” thinking? Inasmuch as early psychology blamed parents for quite nearly everything, I can sympathize with Coyne’s aversion to this kind of formulation. However, is it incumbent upon David Barlow to know and address this in his presentation of findings, or is it up to us – the academic readership – to take these findings with a historical grain of salt, and to translate them with care and caution to our … anxious… clients?

Mineka & Zinbarg, 2006

So, here we are again, deep in the throes of classical conditioning and its offspring. It seems to turn out that these principles may underlie – every major disorder thus far? I’m increasingly unsure of whether I am heartened by the flexibility inherent in each person’s psyche to be able to adapt, learn, and insulate himself or herself against disorder – or scared stiff by the notion that our innate biological defenses may be largely helpless against the unwavering assault of conditioning. Aside from some mildly-influential genetic predisposition to the contrary, it seems I could very easily – and unpredictably – find myself afflicted with an anxiety disorder. Perhaps only Tony Soprano knows my newfound fear more fully than I.

Be that as it may, there were some interesting – and not totally discouraging – parts of this article. Most notably, the sections on “vicarious conditioning of fears and phobias” (p. 11) under “specific phobia,” and “social learning and social phobia” (p. 14) seem to point to a neurological phenomenon about which I (admittedly) know little, but nonetheless find fascinating: mirror neurons. These little bundles of cells in our brains (examined, of late, for their role in the development of Theory of Mind and empathy) simulate the experience of doing or feeling whatever it is you are watching someone else do. Implicated in such dubious human activity as the vast success of the porn industry, it seems to me that they may prove to be the best place to look for the neurological proof vicariously acquired fears and phobias. If “simply observing others experiencing a trauma or behaving fearfully could be sufficient for some phobias to develop,” (p.11) and “simply observing another being ridiculed or humiliated… may be sufficient to make the observer develop social phobia,” (p. 14) then it seems a fruitful place to look for proof of concept may be the very part of our brain that may be responsible for vicarious sensation and emotion. Then again, in light of the anxiety that all this anxiety research has provoked in me … maybe I don’t want to know.

Isn't it neurotic? Don't you think?

Kendler, Kuhn, Prescott, 2004

This was a very powerful (experientially and statistically) analysis of the role of neuroticism, gender, and stressful events in predicting depressive episodes. I was impressed, frankly, that such analyses have been undertaken at all, and I couldn’t help but wonder what other goodies could be plumbed from the amazing data set (the Mid-Atlantic Twin Registry) that was used. I was also curious about the construct the authors used for “stressful life events.” It seems that their criteria (lasting more than 10-14 days, self-reported, recent relative to the interview date) are neither the most conservative nor the most exploratory of the options that could have been used. I guess that, given the size of the sample, one could argue for the normality of the distribution of adverse life events, leaving this middling choice to be at least representative enough to capture a real phenomenon – but still! What about acute life events NOT captured in the time window? What about more persistent life events? What about the possibility of cyclical or random emergence of depressive episodes and the possibility of those with more primarily neurochemically-induced depression (I now know better than to make a distinction between neurochemically- and non-neurochemically-based, though)? These are the types of questions one might expect to see (or at least see discussed) in an analysis such as this (especially given the advantages of having a large sample of MZ twins), but they were nowhere to be found.

Even more perplexing was the lack of any meaningful discussion of the implication of the findings. The authors speak about the implications as they relate to the modification of a model depression of etiology (an important area of inquiry in its own right), but they say nothing about the implications for individuals who might be at risk for such disorders, and they make no effort to speculate as to why their unexpected findings might have occurs. Specifically, why are females (regardless of rates of neuroticism) so much more likely to have a major depressive episode following a “minor” stressful life event? Does the model of “minor” life events not map appropriately onto the stress-management systems of differing genders? Do women have defense mechanisms against depression that don’t “kick in” until higher levels of distress are experienced? What, if anything, are the implications for targeted treatments for women at risk for depression (e.g. with high neuroticism)? The lack of (apparent) interest in addressing these sorts of “real world” implications for findings seems to be the downside of doing research with an n of 7517.

Rabbit Holes, Rest, and Relapse: that was Groucho, this is Karl

Bootzin & Epstein, 2000, Stimulus Control

I must say, though I already knew that behavioral treatment for Insomnia were apparently effective, these findings still really wowed me. Seeing the incremental effectiveness Stimulus Control (both on its own and as part of a larger treatment package) has over pharmacological interventions (and, in some cases, even over combined behavioral/pharmacological treatments) makes me wonder about the already-suspect motives of drug companies in pushing these meds. Is the book essentially closed on treatments for sleep disorders – the problem already largely solved? Do articles in the journal SLEEP about treatments amount to the academic equivalent of the very Nick-at-Nite reruns their subjects were once ensnared by in the wee hours? I find it telling, though, that such strong effectiveness findings for behavioral treatments seem to present themselves in the arena of more unitary, nomothetic, reactive, and instrumental disorders, while they are more contentious (at best) with regard to more potentially complex, behaviorally aggregate, usually ipsatively-deduced disorders (such depression, autism, personality disorders, etc).

That said, there were a few areas of the Bootzin and Epstein paper that caught my interest and led to several questions:

-On the first page of the article, the authors note that in the 60’s and 70’s, “programs for weight reduction that focused on SC were found to be highly effective” (p. 168). What happened to these “highly effective” programs, though? Were they overtaken by more cognitively-based approaches, discarded for some methodological reason, or simply lost to history for no good reason?

-The authors note that their preferred method, the “small-group format,” (p.171) had some evidence for its specific effectiveness (although, near the end of the article, they seemed to note that there was some evidence to the contrary). I’m wondering, then, if there has been any mechanisms of change work examining the potential “common factor” in this condition. Specifically, what, if anything, might the role of normalizing sleep disturbances be in reducing the stigma (and consequent anxiety) surrounding them? I imagine there might be a differential effect (that could be easily testable with an intervention group, plus wait-list control and a support-group control conditions), though I’d be curious to find out if such a thing exists.

-On p. 177, the authors note that “older adults usually take longer to fall asleep than younger persons.” Though I’ve certainly seen this phenomenon in action, it seems counter-intuitive to me. Young, spry individuals seem more likely to have an excess of wakeful energy to keep them up at night. Is this not the case?

-Finally, among the treatment instructions, Bootzin & Epstein note that “SC should be followed at the time of the final awakening.” However, they don’t say what to do in the event of finding oneself very sick with a cold or flu. In these situations, staying in bed can be healthy and necessarily (not to mention medically indicated), and could certainly circumvent the effectiveness of a SC protocol. I imagine that the authors would allow for this as an exceptional circumstance, though I wonder what their preferred method of response might be (e.g. get up and be sick on the couch instead). Additionally, does this response change when a mental illness such as depression is involved? Are there intermediary interventions to break the cycle of exhaustion and depression that can be so self-reinforcing in depressed individuals?

Sleep Hygiene Handout

I guess my main reaction to the Sleep Hygiene handout was simple: how, if at all, does Sleep Hygiene (programmatically) differentiate itself from the Stimulus Control method outlined by Bootzin & Epstein? It seems to just incorporate it as the manualized component of a larger battery of recommendations around, well, healthy sleep. Is that all?

-Also, is the nightmare component of sleep Hygiene simply a variant on systematic desensitization? If so, I wonder if augmenting the “change” component of it with humor or absurdity (e.g. “put a bow on the snake,” or “you fall… into a big pile of tapioca pudding”) might increase its reliable effectiveness.

Witkiewitz & Marlatt, 2004, Relapse Prevention for Alcohol & Drug Problems: That was Zen, this is Tao

I found myself perplexed by my response to this article. Though the model and systems (and, importantly, the article’s subtitle) should have been fascinating to me, I had a lot of trouble getting into it. In any case, I came up with a couple of thoughts:

-After much ado, on p. 229-230, Witkiewitz & Marlatt present their Dynamic Model of Relapse. This model is fascinating in its complexity, modernity (it’s awfully hip), and comprehensiveness. Not being extremely well-versed in the literature, I don’t really feel qualified to take serious issue with any component of it, though, importantly, the authors themselves do note that the model “needs to be empirically tested and replicated across drug classes and with a variety of distinct substance-using populations” (p. 232). An interesting factor that they touch upon only briefly is the role of neural mechanisms & correlates of additions. Specifically, I’m curious as to whether the authors would conceptualize them as more “phasic” or “tonic,” as the implications for “hard-wiring” learning and thereby neurologically protecting relapse seem to be great.

-Also, I’m not entirely clear how the Dynamic Model of Relapse directly speaks to treatment. Though it “depends on clinicians’ ability to gather detailed information about an individual’s background, substance use history, personality, coping skills, self-efficacy, and affective states,” (p. 231) I’m not sure how, given the necessarily immense complexity of the relationship of these factors as they relate to the Dynamic Model, it can give direction to a clinician. Put simply: it’s just too much information to effectively synthesize; indeed, the comparison to chaos & catastrophe theories, whose models can only be analyzed and plotted using the most cutting-edge computing hardware, seems apt. If a clinician is to use the model, it should inform either a) how s/he should intervene, or b) when is the most optimal time to apply specific interventions. As it stands now, the Dynamic Model seems to provide meaningful direction for either of these questions, but it certainly does hold immense promise.

Voelker, 2006, Stress, Sleep Loss, and Substance Abuse Create Potent Recipe for College Depression

The findings reported in Voelker’s article are striking indeed! It is really quite amazing to see how mutable the brain and its structures are. That socially-activated adrenocorticotropic hormones “have the potential to remodel the brain” (p. 2177) at the genetic level says a tremendous amount about the importance of our ability to process and regulate social information – and about the fragility of the brain’s architecture in the first place. Though I don’t believe that anyone really thinks of humans as nothing more than walking bags of blood & neurons & hormones that just bump into different environmental factors (or, as Greenberg put it more eloquently in our first reading, we are beings “orchestrated by ion channels and neural pathways and axonal projections… deep in the grips of [our] chemicals”), the findings reported in this article are pretty persuasive in that direction. Though the finding the “brain change that defines addiction” may take us beyond the “metaphor of the frying pan,” I daresay that it may take is into the fire. If we find that all this neurobiological information is knowable, and all that we are is changeable, then the only field with more infinite promise than psycho(pharmaco)therapy is… bio-psycho-totalitarianism.

FIN

The New Behaviorism: Perfect Grammar or Poor Poetry?

Hayes, et. al 2004, DBT, FAP, and ACT: How Empirically Oriented are the New Behavior Therapy Technologies?

Several things excited me about this article. Specifically, it was very helpful to see how well-reasoned and promising some of the “new behavior therapies” may be, and how much they may, indeed, not just be “old wine in a new bottle,” due to a renewed focus on non-observable behaviors, in vivo practice/training methods, transportability methods, and clearer models of change. To wit:

-In the description of more comprehensive treatment packages such as DBT, it is exciting to hear about the sequential focus beginning with behavioral training and continuing through “living skills” such as employment and education. One of the biggest problems in the long-term effectiveness of any treatment is the lack of explicit tools to apply it to functional settings in an ongoing way. It seems to me that the addition of such functional modules to existing treatments would be an interesting imperative to put before practitioners of existing ESTs to see how their therapeutic principles apply.

-There were some interesting methods of ensuring agreeable treatment fidelity mentioned in this article. For instance, in comparing CBT to ACT, “the same primary therapist was trained both by Beck and Hayes in their particular form of intervention.” (p. 45) This is a good idea (to have the treatment originators of the competing treatments BOTH be involved in the training process), and, when feasible, can go a long way towards resolving some of the recursive arguing from both sides that can emerge in a comparison study.

-More personally, I was excited to see some of the principles employed in my Spotlight Program reflected (and deemed important) by these new behavior therapies. For instance, the value of in vivo examination (and reframing) because “it is easier to deal with actual relevant behavior within session than with a mere description of the behavior.” (p. 44) is a fundamental approach I’ve been espousing for years, and it is nice to see that others have been adopting it as well. In general, the notion that these approaches are “often more experiential than didactic,” (p. 36) is an exciting discovery for me in light of my experience with other purported behavioral approaches.

An important theme implicit in this article is the connection of the theoretical model of change in a given treatment to the specific disorder it is intend to treat and the consequent projected outcomes. In many of the meta-analyses we’ve read, there have been awfully impressive outcomes reported about effectiveness with a range of disorders. However, there is often not a clear picture of why the researchers figured their treatment might work with these disorders in the first place, and, concurrently, why certain specific outcome measures were chosen. A good instance of where this issue is addressed is Hayes’ et. al’s recount of how ACT was used for patients with positive psychotic symptoms. This particular treatment “targeted acceptance of the private experience of symptoms, defusion from these symptoms, the importance of distinguishing one’s self from the content of one’s thoughts, and the role of … action.” (p. 46) The authors then report that the best outcome in this case was lower levels of rehospitalization at follow-up, but say that, “paradoxically,” more ACT participants admitted to symptoms than TAU controls, and ACT participants showed lower levels of believability. In light of the purported goals of ACT in this case, this is not paradoxical at all. It seems that part of the proposed treatment mechanism is about accepting and owning up to such symptoms (while simultaneously disassociating from them personally), and, importantly, is not trying to extinguish them from existing altogether. As such, it is completely in line with the theory of change underlying ACT in this case that such patients would be happy to report their symptoms if asked, but would not be sufficiently perturbed by them to require subsequent hospitalization. Though the question remains as to whether extinguishing the underlying symptoms might be an important therapeutic adjunct (or alternative), it is important to note the clear relationship here between the theorized change mechanism in ACT, the chosen disordered population, and the subsequent measured (and, in this case, achieved) outcome. This seems a far superior (and more scientifically valid) method of approaching treatment research than that of haphazardly applying a treatment to a disorder and hoping that it sticks, somehow.

Jacobson, Martell, & Dimidjian, 2001, Behavioral Activation Treatment for Depression: Returning to Contextual Roots

It is also consistent with the very approach that, according to Jacobson et. al, 2001, led to the rise of Behavior Activation (in the second article we read) in the first place. This radical behavioral intervention is predicated on the notion that the cognitive components of cognitive therapy for depression are extraneous, and that comparable results can be obtained from focusing primarily on the adaptive behaviors that CT prescribes. Much is compelling to me about BA, despite myself. For instance, I am very partial to the notion of what Jacobson et. al call “focused activation.” Also known as “person-specific motivators” (as used in the Spotlight Program) this idea of using non-generic reinforces is – given its commonsense value -- surprisingly spare in much of the behavioral literature to which I’ve been exposed. That BA embraces it is further evidence of the evolution in thinking that the “new behavior therapies” demonstrate. The contextual approach (which is very much like an environmental or narrativist approach) is very much “old wine,” but is nonetheless compelling in its own right.

That said, I had a few problems with the sort of radical behaviorism espoused by the authors. First of all, the “distinctly behavioral model of depression” (p. 258) that is presented is somewhat problematic. Certainly, there are individuals and circumstances for whom contextual factors are a cause and support of depression. For such individuals (who, it could strongly be argued, may be the majority of those afflicted with major depressive disorder), getting at the events that have led to the particular episode(s) of depression can be fruitful, and doing so in the sophisticated way that BA employs can be valuable for many. However, there are those for whom even a diathesis-stress model of depression is tenuous – for whom a clear-cut cause of the specific depressive cycle is elusive at best. For these individuals, the notions upon which BA is predicated may be more frustrating than helpful – at least at first. This, indeed, may be the problem: for such people, the later steps of BA could be useful, but getting to them in the first place may be quite insurmountable.

Second, it seems ironic that an approach so grounded in visible behavioral processes can be so contingent upon a relational component. Specifically, the authors note that “establishing a collaborative foundation is a critical part of effectively presenting the model and conducting effective BA in general.” (260) This idea is present throughout much of the article, and is a circuitous way of saying: therapeutic alliance really matters here. That this is the case is fairly straightforward and evident: you can’t get a patient to buy into a model that requires so much of them (in terms of both belief and action) without getting them to trust you and want to work collaboratively with you as the therapist. However, this idea (very much relating to the content of the patients thoughts and feelings about the therapist) seems to run counter to the behavioral underpinnings of BA (that it is all context over content). This discrepancy is never reconciled through the article.

Finally, my largest concern emerges from the overall feeling I have about radical behavioral treatments in general. My position is this: they are not inherently wrong; there is certainly (and necessarily, a priori) a behavioral component to both disorders and the capacity to change them. This is true of the psychological condition in general. However, to borrow from my old mentor and esteemed colleague Dr. Karen Levine, to say this is much akin to saying that all sentences have grammar in them. It is definitely true, but it may be beside the point. I can write many sentences about old men in boats, lecherous gentlemen, and obscure neurological conditions, but this does not mean those sentences will be comparable to those written by Hemingway, Nabokov, or Sacks. Emotional content, form, artistry, word choice, and a host of other factors differentiate my sentences from theirs, even though one could properly say that both our form (grammatical structure) and content (topic) were identical. So it goes for behaviorism: I am not convinced that, in getting at the form that necessarily underlies psychological being and action, we have stumbled upon the best or even truest model of change, even if it is the most universal. This, I guess, is what comparative outcome and mechanism studies are all about: does one form of therapeutic prose outstrip another? Do the different forms of form perform differentially – just as Faulkner resonates more with some than Fitzgerald, does Rogers do likewise relative to Beck? Or, for that matter, is all we need the therapeutic equivalent of Strunk & White to cure what ails us?

cognitiverationalemotivebehaviorism -- and why it's so great.

What are CBT Psychotherapies?

This article highlights one of the greatest concerns I’ve had as we move through our review of the empirical foundations underlying clinical psychology at present: its disconnect with the views of so many practitioners in the field. While many of the academic articles we’ve read have tried to cautiously circumscribe their positions in terms of support for specific interventions, clearly the British Association for Behavioural and Cognitive Psychotherapies has no such imperative. Bald-faced claims such as CBT being “based on concepts and principles derived from psychological models of human emotion and behaviour,” and involving therapists who only work “once a therapeutic alliance has been formed,” ‘treatment interventions are predicated on a robust evidence base derived from studies utilising randomised controlled and single-case methodologies that have demonstrated the efficacy and effectiveness of cognitive and behavioural psychotherapies” are proudly put forth with little or no citation. Such claims, of course, and ones much worse, are the norm amongst organizations like this one, much to the detriment of a field desperately clamoring to come out from the pall of practices like phrenology and tarot cards.

Though organizational self-promotion is a fact of life in a free market society, it occurs to me that even bare-bones regulations could reasonably be put in place for psychotherapy organizations mandating a more balanced perspective. In particular, the BABCP site espouses the various strengths of CBT (populations it’s been proved effective for, skills CBT therapists apparent must possess), but nowhere does it make mention of its limitations. I know of few who would advocate that symptoms of MR could be effectively addressed by CBT, and, as mentioned in class, CBT could certainly be shown to be nominally effective at best as a unitary treatment for severe schizophrenia, though such disclaimers (necessary in medicine as regulated by the FDA) are nowhere to be found in this field. Perhaps this would be a good role for a new APA task force.

Butler, et. al, 2006, Empirical status of CBT: review of meta-analyses

Where the BABCP article/site was unapologetically overzealous, the Butler et. al article is surprisingly evenhanded. Though clearly written by proponents of the CBT model (Beck himself is a co-author), this meta-meta analysis (a it is proudly defined in Kazrin, 1978) does an impressive job of delineating the limitations of its findings by being very careful to not compare apples-to-oranges in review of meta-analytic design, and to address such effects as researcher allegiance on outcomes. More importantly, the authors expressly address the critical issue of the persistence of treatment effects after treatment cessation. Some of these efforts seem to come up a bit short -- for instance, I’m not sure I buy the “possible explanation for the difference in findings… that researcher allegiance influences study outcomes when a new treatment is first tested, but its influence fades over time” (p. 20) – but, on the whole the findings are impressive. Most impressive, I thought, was the comparisons with psychopharmacological conditions, in which CBT (or its variant) outperformed pharmacological treatment and combination treatment for panic disorder, and outperformed medication for Bulimia. This seems to be powerful supporting evidence for treatment specificity for these disorders.

The one caveat I might offer is one the authors attempt to address. Specifically, I’m speaking of the differential effects offered by the unfortunately wide array of heterogeneous treatments being offered under the title of “CBT.” Though Butler, et. al attempt valiantly to address this (they clarify differences in modality, such as CT, CBT, Cognitive-behavioral Marital Therapy, Trauma-focused CBT, etc), for there to be truly sufficient internal validity (not my favorite axe to grind, but so be it) to ensure real equivalence, it might behoove the authors to ensure that similar methodologies (in additional to similar modality) are being appropriately compared.

Engels, et. al, 1993, Efficacy of RET: a Quant. Analysis

… and just when I thought that such an approach to treatment research might be hard to find, along comes an article from 1993 that is up to the task. In painstaking detail, Engels, Garnefski, and Diekstra provide a useful meta-analysis of RET that (in my mind) more than adequately breaks down the treatments being aggregated using a useful coding system which accounts for methodological treatment variance (i.e. types of interventions “said to be used”), allegiance effects, and other relevant variables. That such a system was devised more than 15 years ago (with little follow-up as far as I can see) is a little disheartening, but I digress. Addressing all these relevant variables, Engels et. al tentatively conclude that RET does, in fact, seem to demonstrate effects above and beyond wait-list control and placebo. Interestingly, though, it seems that a major theme of the findings in this article is that these effects are “mainly due to the therapeutic effects of rational thinking” (p. 1086). That is, rational thinking seems to have a differential effect above and beyond behavioral components – a very different finding than many studies on CBT-related interventions. I would be curious to find out more about follow-ups in RET meta-analyses since 1993 to see if such findings (as well as findings for non-YAVIS populations, as Engels et. al ask for) bear out.

Ellis, 1999, Why RET to REBT?

Our readings this week conclude with a funny little article from Ellis that, at first, seems to cast his RE(B)T as an aspiring also-ran in the emergent world of empirically-supported behavior therapies. This initially struck me as rather odd, and I wasn’t entirely dissuaded of this conception as the article progressed. However, I was certainly struck by the astonishing amount of versatility Ellis packs into (his conception of) RE(B)T. In particular, I found his framing of the empowerment of human agency (and its consequent relating of human choice to human behavior) rather compelling as a therapeutic foundation – though, admittedly, it certainly seems well-tailored to the YAVIS set. By and large, though, I had trouble distinguishing the characteristics Ellis describes as endemic to good RE(B)T specifically, from those qualities one might use to describe good therapy in general.