Evolutionary Clinical Psychology at HBES 2012! (Part 1)

The Human Behavior and Evolution Society held its 24th annual meeting in Albuquerque, New Mexico from June 14th-17th. A staggering amount of knowledge was presented, and if you want to know more about it, see the conference page, program, or Google some of the many great blogs written about it.

Here, I’ll focus on the talks presented on the intersection of clinical and evolutionary psychology (if I have missed one, please notify me and I’ll add it)…see the full abstracts for more info.

Friday had an entire chunk of time devoted to “Darwinian Challenges to DSM and Treatment Paradigms.” Most of these talks involved suggestions that elements of mental disorder can be adaptive for various reasons.

“The relationship between anxiety and risk-taking propensity: An exploratory study,” presented by JeanMarie Bianchi from the University of Arizona, discussed the functional significance of anxiety, referencing a Yerkes-Dodson-type curve to show optimal arousal levels as those high enough to keep organisms from danger but not so high that they are debilitating. Their study showed anxiety to be negatively associated with self-reported risk taking, but interesting, there was no relationship found between anxiety and performance in behavioral risk, at least as measured by something called the Balloon Analogue Risk Task (BART)…participants can press a key to inflate an onscreen balloon more and more, for bigger monetary rewards (several cents, in this case), but the balloon could pop at any moment! More anxious individuals were expected to bow out sooner rather than risk having this digital balloon burst in their faces, but the experimenters didn’t find this. Maybe the task is just a safe way to manage anxiety, someone in the crowd suggested, and anxious people enjoy it.

Next, Paul Andrews from McMaster University, known for his work on adaptive explanations for depression, presented a host of facts about why anti-depressants are, in fact, dangerous! According to Andrews, most of the body’s seratonin receptors are not in the brain, but in the gut! Therefore, anti-depressants–which generally work via regulating seratonin reuptake–can change processes throughout the body as well as the brain, and create a host of serious health issues. Further, as anti-depressants result in more free seratonin, the body compensates by gradually producing less seratonin. This process, Andrews says, is why anti-depressants have decreasing efficacy as they are taken. When/if the anti-depressants are discontinued, of course, there is a serious dearth of seratonin in the brain, leading to a probable relapse of depressive symptoms. Andrews believes that this explains the maxim that major depressive episodes make future depressive episodes more likely (the so-called “kindling hypothesis”), and therefore one should predict that the kindling hypothesis would only hold true for patients who had taken antidepressants. Andrews’ message is that the danger of anti-depressants outweigh the benefits, and they should not be prescribed for depression.

His sometime colleague J. Anderson Thomson took a slightly less extreme position in his presentation–a followup to Andrews’–stating that antidepressants should be used sparingly, briefly, and only after a cost-benefit analysis taking the particular patient’s symptoms into account. Thomson reviewed the statistics about cardiac-related deaths which are supposedly the result of antidepressants; he further mentioned that these drugs can make a severely depressed person who is paralyzed with sadness feel just better enough to successfully act on suicidal intent, which is a chilling thought. His conclusion: that anti-depressants are not as safe as doctors think, and that treatment for depression should first attempt to identify and address the socioenvironmental triggers which precipitate depressed mood. It’s my understanding that some patients of major depression seem to have no identifiable triggering scenarios…they’re just hopeless and sad about everything. I can neither advance nor defend this position with any aptitude, having very little clinical experience, but I believe that someone like Thomson would say that many of these individuals do, in fact, have trigger issues upon further exploration–and in the case that a patient truly does not, then this would be a real case where an anti-depressant would, at least initially, be worth the risk.

Sacha Brown from the University of Arizona tested the hypothesis that anti-depressants may interfere with ruminative depressive processes that normally help individuals negotiate social problems–a somewhat controversial hypothesis (even as adaptive explanations for depression go) but one with a fair amount of theoretical literature behind it. The current study was an attempt to muster some empirical support. The experimenters attempted to induce low mood in participants (some of whom were on anti-depressants and some of whom were not), then compared their performance on social intelligence and social decision-making tasks. At this point I apologize profusely to Sacha Brown and her team, but I cannot remember–nor find in my notes–what the findings were. It is my faint recollection that the findings were mixed and the hypothesis was not supported, and the specific type of mood induction technique used was pointed to as a culprit. If anybody reading this remembers more, please let me know and I’ll make appropriate edits [EDIT: Sacha Brown has described, in the comments section, the results, conclusion, and implications better than I ever could have…see below!].

Finally, Ed Hagen from Washington State University presented some fascinating data to suggest that the human tendency to seek out and utilize substances such as tobacco and cannabis may be part of an unconscious behavioral immune system designed to protect our bodies from helminths (a kinder way to say “parasitic worms”). Nicotine is, after all, known to be harmful to these worms, and is, in fact, used to deworm livestock. Using a sample of Central American foragers, Hagen and colleagues tested this hypothesis in several different ways; ingestion of a nicotine-related substance smoked in this culture was higher in worm-infested individuals, and declined after de-worming treatment, relative to controls and individuals with less worm-load (what a gross word I’ve just used). This hypothesis may seem unlikely unless you know that behavioral immune responses–particularly, self-medication–in nonhuman animals have been observed for over forty years. Sick animals have been observed eating substances which can cure them, presumably without having sat through survivalist training sessions. In other words, some animals–possibly including us–have naturally selected behavioral drives to ingest certain substances, when infected or ill, which can ameloriate the problem (read this piece from the Economist for more info). What I’m saying is, this was an extremely neat talk.

In Part II, I cover the pertinent talks from the Mental Health and Personality session, including my own!


Daniel Glass

About Daniel Glass

Daniel Glass is a doctoral student at Suffolk University. He is interested in evolutionary approaches to clinical psychology. Evolved This Way explores this burgeoning field, which uses evolution to understand, classify, and treat mental disorders and other clinical phenomena.
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4 Responses to Evolutionary Clinical Psychology at HBES 2012! (Part 1)

  1. Pingback: Evolutionary Clinical Psych at HBES (The Lost Chapter)! | Welcome to the EvoS Consortium!

  2. Pingback: Evolutionary Clinical Psychology at HBES 2012! (Part 3) | Welcome to the EvoS Consortium!

  3. Avatar Sacha Brown says:

    JeanMarie found your blog and sent it to me. If you want the full talk I gave, including the script I was ostensibly following, drop me an email. I would be happy to provide it and answer any questions you might have.
    The basic point was that while our mood induction worked, none of the measured outcome variables behaved in the way they should of given a successful mood induction, even in a non-medicated sample. The favorite explanation for this among the audience members, particularly those whose theory we were testing, was that we needed a socially driven context specific mood induction for it to work. I (we) addressed this point in the conclusion of the talk we gave though it was picked up again during the open discussion period.
    We suggested that the problem might be bigger than the mood induction in that evolutionary theory that needs such a specific context to work is not necessarily compatible with our understanding of depression from a clinical perspective. This suggests that either a) evolutionary theory is incomplete AND/OR that the clinical perspective of depression is problematic. Regardless, there is a yet to be explored area between these two extremes that will need to be dealt with if we want to have a full understanding of this phenomena that describes and explains depression from the limited scope of a temporally limited single social event (current evo theory) out to depression as a dehabilitating collection of symptoms (current clinical conception) that impacts life across contexts.
    Sacha Brown (UA)

  4. Avatar Nick Armenti says:

    Thanks for these. Truly helpful to have shared the summaries and your reactions to them.

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