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Monday, February 4, 2013

Neural Plasticity and Error Management Theory



One of the ongoing themes of this blog is the nonsensical practice of some researchers in psychiatry of routinely labeling differences seen on brain scans between various diagnostic groups and control subjects as abnormalities

Just because there is more blood flow to one area of the brain during the performance of certain tasks or a difference in size between various subsections of the more primitive part of the brain, the limbic system, in a group of people who show similar behaviors and symptoms does not automatically mean that this demonstrates a disease process.

We know now that the neural structure of the brain is extremely plastic, and many of these differences merely reflect the fact that people who have certain habitual behavior patterns routinely show these differences. Disease processes can also certainly account for differences, but just the mere presence of a difference does not tell us which of the two possibilities - abnormality or normal difference – is the accurate explanation for the finding

As I pointed out on my post Neural Plasticity on March 14, 2010, after just three months of a vigorous exercise program in one study, the size of a brain structure called the hippocampus increased an average of 16% in normal people.

So how do we determine whether a difference is or is not an abnormality? Well, one line of evidence that may help tip the balance of evidence and help us to decide is the use of something called Error Management Theory (EM). This is an extensive theory of perception and cognitive biases that was created by David Buss and Martie Haselton (Haselton, M. G., & Buss, D. M.  Error management theory: A new perspective on biases in cross-sex mind reading. Journal of Personality and Social Psychology, 200078:81-91) and expanded upon in another article (Haselton MG, Nettle D. The paranoid optimist: an integrative evolutionary model of cognitive biases. Personality and Social Psychology Review. 2006; 10(1):47-66).


Martie Haselton, Ph.D.


The human species is highly adaptive to its environment, particularly its social environment. The survival of we human beings, and our ability to live long enough to have children and pass along our genes, depends on how well we can read and react to that environment. In particular, we need the ability to read the motives of other members of our species to determine whether or not we may be being deceived or endangered by them.

It making a determination about whether the environment is dangerous or friendly, it is often true that it is far better for long-term survival and procreation to err on one side or the other in making this judgment. A friendly situation might be misinterpreted as a dangerous one while a dangerous situation might be misinterpreted as a friendly one. 

Depending on the environment, a false negative or a false positive interpretation might prove fatal; hence, it is often best to err consistently in one of these directions.

The best illustration of this is the "unidentified animal in the woods" problem. If you are walking in a forrest and mistake a raccoon for a bear and run away, all you have lost is some needless expenditure of energy. If, on the other hand, you mistake a bear for a raccoon and don’t run away, you are dead.  So all other things being equal, if you cannot identify the animal for sure, it is always better to run.

So what does this have to do with neural plasticity? To illustrate, allow me return to the issue of my favorite “diagnostic” group, the patients who exhibit traits of borderline personality disorder (BPD). These folks can be extremely reactive to stress in the social environment. They tend to get more agitated that the average person in response to any perceived slight, and it takes them much longer to calm down. Their behavioral reactions tend to be sort of "shoot first and ask questions later, if at all."

It is also true that some but not all fMRI studies show that, on average, patients with BPD have slightly reduced volumes compared with normal controls in several brain areas including the frontal lobe, bilateral hippocampus, left orbito-frontal cortex, right anterior cingulated cortex, and right parietal cortex.  

Another recent study (Ruocco et. al., Biol Psychiatry, 2013;73:153–160) showed that BPD patients demonstrated greater activation within the insula and posterior cingulate cortex. Conversely, they showed less activation than control subjects in a network of regions that extended from the amygdala to the subgenual anterior cingulate and dorsolateral prefrontal cortex. 

Abnormalities, or just differences?

Well, these brain areas are involved in the body’s threat assessment as well as fight, flight or freeze reactions in response to potentially dangerous environmental situations.  Panic attacks and rage attacks, common in these patients, are also created in some of these brain areas.

Many studies have shown that the childhood family environment of patients who go on to develop BPD is often highly chaotic and unpredictable. Therefore, “normal” inhibition of fear and rage responses might be extremely maladaptive. The size and activity level of the amygdala and other limbic system structures might be gradually shaped through ongoing environmental interaction, so that on average they look different than "normal" control subjects.

Voila. If prospective (studies in which babies are followed for many years) studies showed this hypothesis to be true, this would be potential evidence that these differences are normal differences, not abnormalities. 

The borderline trait of hyper-reactivity often becomes maladaptive in non-family adult social situations because most other people do not react like the family members that produce offspring that show borderline traits.

Unfortunately, for reasons discussed elsewhere in this blog, patients with BPD usually look for people to hang out with that do in fact act like their family members, and, if the others do not act like that, often go out of their way to try to provoke them to react in these ways.

Error management theory may also explain something that psychologists call the fundamental attribution error. When observing the behavior of strangers, we are all more likely to attribute their behavior to the person’s underlying dispositions to a greater extent than is logically warranted. We all err on the side of thinking that their behavior is due to their innate tendencies rather than it being a reasonable reaction to the particular environmental situation in which they find themselves. This social judgment, wrong though it often is, helps us to avoid connecting with poor social partners.

So, is it better to be paranoid or to be optimistic? It all depends on our experiences over a lifetime. Due to natural selection, the truth of any particular judgment is far less important to us than its potential effects on our survival and reproductive success.

1 comment:

  1. Thanks for a well-thought post that centers on key aspects of the human condition.

    I particularly value how you remind us that observing anatomical differences in brains does not explain anything (especially from a monist perspective, it is expected that any learned behavior will translate into anatomically observable differences, as shown for instance in brain scans of London taxi drivers). And neural plasticity is still under-appreciated by many.

    I am uncertain whether the language of "abnormality versus normal differences" does not sometimes obscure rather than enlighten the debate by its ambiguity. Whether some abnormality or disability result from social processes rather than cellular-level mechanisms, or whether some symptom is only considered abnormal in a specific culture should not distract from considering the incapacitating consequences as center. And the potential of any method (whether pharmaceutical or psychosocial) to improve social functioning is not necessarily linked to the nature of the causes of the problem. A very common case might be a complex intertwining of gene-environment interactions where a combination of factors ends up badly, with few or none of those factors being bad or a risk by themselves (and with just a handful of factors, you can create a smooth multi-dimensional continuum where it becomes impossible to define a scientific boundary between abnormality and normality, and where the causality distinction between nurture and nature becomes only relevant in a small minority of cases).

    Finally, about the self-sabotaging behavior of some people (described as "BPD"), a lot of it can be explained by social dynamics out of their control: without having a formal system of cast in America, friends that are good for you are sometimes a bit like high-paying jobs, reaching for one does not mean you will be "hired", and you hang out with whoever is making themselves available to you. As you say yourself "This social judgment, [...], helps us to avoid connecting with poor social partners.". If anybody with a choice intentionally avoids "poor social" partners, we should no longer assume "BPD" have any choice in the quality of whoever they hang out with. A "social functioning" cast system is the direct result of most people considering "avoiding poor social partners" as a legitimate goal. That invidivual goal (often promoted by many mental health professionals) is fundamentally incompatible with the collective goal of eradicating or reducing the impact of mental illness in society at large.

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