Psychotherapy Brown Bag

Comparison of CBT and ACT in the treatment of depression and anxiety: Differences emerge at long-term follow-up

by Michael D. Anestis, Ph.D.

I absolutely LOVE it when impressive researchers compare two evidence-based treatments to one another in the same study.  Comparative efficacy is a wonderful thing and we don't get nearly enough of it.  I just came across a great example of this, as Evan Forman, Jena Shaw, Elizabeth Goetter, James Herbert, Jennie Park, and Erica Yuen just published a follow-up to an earlier comparision of cognitive behavioral therapy (CBT) and acceptance and commitment therapy (ACT) in Behavior Therapy, this time reporting results from an 18-month post-treatment assessment point.

In the earlier study, Forman and colleagues (2007) reported that there were no differences between ACT and CBT immediately post-treatment in a randomized controlled trial (RCT) examining a range of outcomes including depressive symptoms, anxiety symptoms, and overall functioning.  This was compelling evidence and supportive of the notion that ACT is a promising emerging treatment capable of producing results comparable to gold standard evidence-based psychotherapy for certain populations.  As the authors noted in this study, however, it is always important to ask not only how folks are doing right after treatment, but also whether or not treatment gains are maintained over time.

The total sample included 132 undergraduates seeking treatment at a counseling center.  Importantly, participants were not required to meet diagnostic criteria for a DSM-IV-TR disorder.  Rather, inclusion criteria centered around moderate levels of depression and/or anxiety as measured by the BDI-II and BAI (scores greater than 9).  In most healthy undergradaute samples I've collected, the mean for the BDI-II comes in around 7, with a standard deviation of 7, so I'm not entirely comfortable with considering 9 a measure of moderate depression symptoms (in fact, "moderate" for the BDI-II is typically defined by a score of 20-28 and the maximum score is 63).  The authors noted that the goal was to keep inclusion criteria broad in order to maximize external validity (e.g., the degree to which the sample and the results reflect what would typically be seen in the "real world").  That's a valid goal, but it is VERY important to keep the context of the sample in mind when interpreting the findings.

As far as diagnoses go, the authors used structured diagnostic interviews and reported that 49.2% met criteria for an anxiety disorder and 37.1%  met criteria for a depressive disorder.

On to the results.  91 participants provided follow-up data and were included in the analyses.  That being said, the authors used both intent-to-treat analyses and a second idetentical set of analyses that only considered the completers.  I'll present the ITT results here.

The authors found that the group of individuals receiving CBT reported greater maintenance of treatment effects for depression and general functioning than did individuals who received ACT.  There was a non-significant trend (p = .08) for quality of life favoring the CBT group and no between group differences on anxiety.  Putting these results in another context, the authors ran analyses considering clinical significance by comparing the percentage of individuals in each group (CBT vs ACT) who were "reliably recovered" on each outcome measure (see the original paper for a thorough description of the meaning of that phrase).  The found the following:

• Depression (BDI-II): 81.8% of CBT patients vs. 60.7% of ACT patients
• Anxiety (BAI): 72.7% of CBT patients vs. 56.0% of ACT patients
• General functioning: 46.4% of CBT patients vs. 22.6% of ACT patients
• Quality of life: 37.8% of CBT patients vs. 22.9% of ACT patients

So, on the whole, the results pain a rather plainly superior long-term outcome for CBT relative to ACT with this particular population, but it is VERY important to keep our understanding of those results within their context.  This is a strong study, but it's only one study.  This is a valid sample, but not a particularly severe one.  The authors used protocols specific to diagnosis, but not everyone had a diagnosis and results for specific diagnoses were not compared to one another here.  Also, the results do not mean that ACT does not work...they simply point towards CBT working better in the long haul.  It will be interesting to see if other studies like this emerge and, if so, whether these results will be replicated. If they are, confidence in their meaning will increase significantly.  In the meantime, this is something to keep in mind.

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Dr. Anestis is an incoming assistant professor in the Department of Psychology at the University of Southern Mississippi

Articles cited in this post:

Forman, E.M., Herbert, J.D., Moitra, E., Yeomans, P.D., & Geller, P.A. (2007).  A randomzied controlled effectiveness trial of acceptance and commitment therapy and cognitive therapy for anxiety and depression.  Behavior Modification, 31, 772-799.

Forman, E.M., Shaw, J.A., Goetter, E.M., Herbert, J.D., Park, J.A., & Yuen, E.K. (in press).  Long-term follow-up of a randomized controlled trial comparing acceptance and commitment therapy and standard cognitive behavior therapy for anxiety and depression.  Behavior Therapy.

Suicide, the NFL, and chronic traumatic encephalopathy

by Michael D. Anestis, Ph.D.

It's been a while since I last posted on PBB.  Back in mid-May, however, I wrote a piece about suicide in NFL players.  I was moved to write this after reading an article by a former NFL player discussing his own experiences and, towards the end of the post, I mentioned that chronic traumatic encephalopathy (CTE) has been the subject of significant recent research and is another important cause to consider with respect to deaths by suicide within this population.  I made this last point in large part due to substantial news coverage on the topic, which had reported that CTE - which can only be diagnosed post-mortum through an autopsy - had been found in a substantial number of professional athlete suicide decedents.  Now, my background in neuroscience is a bit lacking, so I want to preface this piece with a very clear statement that I have much to learn about the science underlying CTE and other medical conditions related to the brain; however, I felt compelled to write another piece today to share some surprising information I've come across in the past week or so.

In a casual conversation with a colleague, Joye heard about recent research presented by Dr.Christopher Randolph at the 2012 American Academy of Clincal Neuropsychology conference that called into question the validity of the CTE diagnosis.  I then emailed Dr.Randolph, who sent me the slides from his presentation and granted permission for me to discuss them here.  Dr.Randolph's presentation touched on a number of topics beyond CTE, but I want to focus this post specifically on this aspect of what he said.  Almost all of this information comes directly from his slides.

Dr.Randolph mentioned that the first reference he could find to CTE was in an article published by Omalu and colleagues in 2005 in which the authors discussed the results of an autopsy (physiological and psychological) that indicated that an NFL player who had died at age 50 from a heart attack had previously displayed symptoms consistent with dysthmia, memory and judgment deficits, and parkinsonian symptoms.  Most interestingly, however, the authors noted that the decedent's brain exhibited "diffuse amyloid plaques" and "sparse neurofibrillary tangles (NFT's)" but that his brain was otherwise quite normal.  The authors indicated that a diagnosis of CTE was warranted.

The authors did not present any specific criteria for CTE or any population-based comparisons that would enable a better understanding of the degree to which the abnormalities noted in the decedent's brain truly differed from the general population.  They did, however, list a number of possible symptoms of CTE, including mood disturbances, dysregulated behavior, difficulty concentrating, paranoia, and disturbances in movement.

Omalu and colleagues (2006) followed up that original study with another discussion of a former NFL player, in this case one who had died by suicide after intentionally ingesting antifreeze.  In this case, the decedent had experienced three prior psychiatric hospitalizations and an examination of his brain revealed no diffuse amyloid, but NFTs in "several regions." 

In 2009, McKee and colleagues presented three new cases, one a former NFL player (age 45) who died accidentally, one a retired boxer (age 80) who died of septic shock and had experienced progressive dementia (without formal diagnosis), and another retired boxer (age 73) who died of pneumonia after apparently suffering from progressive dementia.  Here again, the authors claimed to find evidence of CTE across all cases; however the only commonality across the decedents was the presence of NFTs.  Furthermore, the authors concluded that the total number of "neuropathologically verified" cases of CTE in the literature was now 51, including 48 other cases in the literature dating back to 1954 and including all deaths previously classified as dementia pugilistica. This is a surprisingly powerful statement given some fairly mixed results and a very limited sample across studies.

At this point in his presentation, Dr.Randolph noted that a diagnosis of CTE appears to only require the presence of NFTs somewhere in the brain.  As somebody with little background in neuroscience, I can look at a sentence like that and be completely unsure whether or not that constitutes a problem; however, Dr.Randolph clarified that quite well by presenting relevant findings from Bennett and colleagues (2006).  Using a sample of 134 individiduals who were examined prospectively and who were cognitively normal at the time of death, the authors found that 97% exhibited NFTs.  In other words, almost the entire sample had NFTs even though they exhibited no behavioral or cognitive difficulties at the time of death.

Now, does that mean that all NFTs are the same?  No.  Does it mean that the presence of NFTs can't serve as a vulnerability to particular outcomes (e.g., suicidal behavior) within the context of other risk factors?  Of course not.  But it does mean that finding NFTs in the brain of a deceased individual might not be enough to justify a diagnosis that can then be used to "explain" a behavioral outcome like death by suicide.

In my opinion, the most intriguing point raised by Randolph throughout this presentation (which is saying a lot, actually, as I found the entire thing rather enlightening) came from a reference to a study conducted by Baron and colleagues (2012).  Using a sample of 3,439 NFL players with at least 5 pension-credited seasons between 1959 and 1988, they found that fomer NFL players had a rate of death by suicide that was only 41% of that of the general population.  In other words, NFL players were significantly LESS likely to die by suicide than were individuals who did not play in the NFL.  Now, its entirely possible that the rate has changed in players with more recent careers or that deaths by suicide were classified as something else within that sample, but the evidence presented there in a rather large and representative sample directly contradicts the notion that suicide has become a near epidemic within the ranks of retired players.

I want to be very careful to ensure that I'm clear here.  I'm not saying that suicide within the NFL is not a problem or that brain injuries can not significantly impact behavior and mood.  In fact, I'm not saying the CTE doesn't exist (and I don't believe Dr.Randolph is either, necessarily).  In fact, Dr.Randolph has published plenty of data linking head injuries to dementia.  What I am saying, however, is that suicide is not an epidemic within the NFL.  It happens, and likely for the same reasons it happens elsewhere, with some differences that I outlined in my previous post on this topic.  Furthermore, I'm saying that research on CTE needs to result in greater specificity in terms of diagnostic criteria and there needs to be a greater degree of replication across studies before we place such a huge emphasis on using CTE as a blanket explanation for tragic outcomes that befall current and former professional athletes.

I would love to hear your thoughts on this, particularly if you have a neuroscience background.

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Dr.Anestis is an incoming assistant professor in the Department of Psychology at the University of Southern Mississppi

Articles cited in this post:

Baron, S.L., Hein, M.J., Lehman, E., & Gersic, C. (2012).  Body mass index, playing position, race, and the cardiovascular mortality of retired professional football players.  American Journal of Cardiology, 109, 889-896.

Bennett, D.A., Schneider, J.A., Arvanitakis, Z.Z., Kelly, J.F., Aggarwal, N.T., et al. (2006).  Neuropathology of older persons without cognitive impairment from two community-based studies.  Neurology, 66, 1837-1844.

McKee, A.C., Cantu, R.C., Nowinski, C.J., Hedley-Whyte, T., Gavett, B.E., et al. (2009).  Chronic traumatic encephalography in athletes: Progressive tauopathy after repetitive head injury.  Journal of Neuropathology and Experimental Neurology, 68, 709-735.

Omalu, B.I., DeKosky, S.T., Minster, R.L., Kamboh, M.I., Hamilton, R.L., et al. (2005).  Chronic traumatic encephalopathy in a National Football League player.  Neurosurgery, 57, 128-134.

Omalu, B.I., DeKosky, S.T., Hamilton, R.L., Minster, R.L., Kamboh, M.I., et al. (2006).  Chronic traumatic encaphalopathy in a National Football League player: Part II.  Neurosurgery, 59, 1086-1092.

Randolph, C. (2012).  Long-term consequences of sport-related concussion/repetitive head trauma.  Research presented at the American Academy of Clinical Neuropsychology annual conference.  Seattle, WA.