Debating Tricks in Arguments about Psychiatry

“Arguing with some true believers is like playing chess with a pigeon.  No matter how good you are at chess, the pigeon is just going to knock over the pieces, crap on the board, and strut around as if it were victorious.” ~ Anonymous

When arguing points in psychology and psychiatry with folks from all ends of the academic political spectrum, it’s easy to see how people become emotionally attached to certain ideas (for whatever internal reasons) and take the position that, “My mind is made up; don’t confuse with me with facts."

Two of their tricks in arguing are:

• To use a word that has several different senses or referents, and then subtly shift how they are using the word as the argument progresses without admitting that that is what they are doing.
• Living their lives as if they really don’t believe a word they are saying. 

In today’s post, I would like to illustrate this by discussing two questions:  “What is depression?” and “Is our behavior pre-determined by our past, or do we have free will?”

First, what is depression?  In his great new book, A New Unified Theory of Psychology, my 

colleague from the Unified Psychotherapy Project, Gregg Henriques, quotes Ingram and Siegle, “The label depression has been used to discuss a mood state, a symptom, a syndrome…a mood disorder, or a disease associated with structural abnormalities.” 

Gregg Henriques

[A syndrome is a group of symptoms and/or behaviors that seem to cluster together in many individuals, creates distress or dysfunction, does not include certain other symptoms or behaviors, and has a definitive epidemiology (the incidence and distribution of a disorder in a population, and the sum of the factors controlling its presence or absence].  

These alternate definitions of depression are highly relevant to the question currently being batted around so fervently by all sides, “Do antidepressants work for depression?”  


The answer to the question depends on which definition is being used in the debates.  Especially online, it’s very difficult to tell.  Obviously, if by “depression” we mean a mood state, then of course antidepressants do not always “work.”  If you are merely unhappy about living in a bad situation, taking an antidepressant will in most cases be a colossal waste of your time and money.

Well, what if it’s a syndrome?  Well, at least according to the DSM, which many people seem to use when it suits their purpose but disparage when it does not, there are, at the very minimum, at least four completely different “syndromes” of depression:  Major Depression (with or without the “melancholic” specifier), dysthymia, adjustment disorder with depression, and depression caused by a medical condition or an outside substance like a drug.  So in a “debate,” which one are we talking about here?


In discussions of studies of the effects of antidepressants, this question is often fudged.  Rather than using the names for the two different syndromes major depression and dysthymia, debaters tend to use the terms "mild to moderate depression" and "severe depression."  The "mild to moderate" depression seen in studies is actually much more likely to be dysthymia, while the severe ones are more likely to be major depression.

Clinically, major depression is more likely to respond to antidepressants, while dysthymia is less likely to.  This is complicated by the fact that the definitions of the syndromes overlap to some degree, but making a clinical decision is what medical education is supposed to be about – or at least theoretically. 


The anti-antidepressant crowd loves to point out that recent "meta-studies" show that in mild to moderate "depression," antidepressants are often no better than placebos.  They also conveniently love to ignore the fact that in the exact same meta-studies, the drugs are shown to be highly effective for severe "depression."  

Actually, the use of the word depression is being used here to describe two very different syndromes, but no one mentions that!  

Even the president of the American Psychiatric Association, John Oldham, was guilty of this confusion of terms in a recent editorial in Psychiatric News.

By the way, if you don’t think defining syndromes based on symptomatic and other variables is a valid way to identify diseases, then ask yourself  how people could tell infectious diseases apart before we knew about the existence of germs.

These debates also revolve around another question - whether the syndromes that do tend to respond to drugs are loosely defined mental disorders, or are actually a “disease associated with structural [brain] abnormalities.”

When this question comes up, the people who think that psychiatric drugs have to either be “all good for all people” or “all bad for all people” with nothing in between (you “splitters” know who you are), tend to presume that we have a scientific understanding of the neurochemical microarchitecture of the brain that we are not even close to actually having.  Since that is the relevant science needed to answer this question, at present we are unable to definitively answer it, so we can only make judgments based on a variety of indirect evidence.

The scientific task is made particularly complicated by the existence of neural plasticity and epigenetics.  


Neural plasticity means that the structure and function of the brain changes significantly in response to persistent environmental demands.  This happens in normals.  For example, the part of the brain that controls finger movement is significantly larger in concert violinists than it is in average controls.  So does this mean that being a concert violinist is a disease?  I don’t think so.

Epigenetic influences, loosely translated, means that most genes in any given cell have a switch that turns them off or on – a switch which is also activated in response to environmental contingencies. So, if the average brain of someone with a given psychiatric syndrome seems to be significantly different than the average brain of someone who does not, does this mean that the syndrome is a normal variant caused by a conditioned response, or evidence of a diseased brain?  With our current knowledge of neurochemical brain microarchitecture being so minimal, we cannot answer that question for certain. 

If there are a very large number of brain differences that are unique to a disorder, and some of the differences do not seem to be directly related to the syndrome in question (such as significant differences in eye movements in schizophrenia), then I lean heavily towards the “disease” model for that syndrome. If not, then I lean towards the “normal variant” model.  But I am at least willing to admit that we can’t possibly know for sure given our current knowledge base.  Major Depression is somewhere near schizophrenia in this regard, whereas dysthymia is not.

The epigenetic issue leads us to my second question: is our behavior predetermined or do we have free will?  Of course, people who take the determinist position do not agree among themselves as to exactly what factors are making the determination.  “Determinism” when used by an psychoanalyst means determined by prior psychological events; when used by a radical behaviorist it means determined by prior external events like rewards and punishments. For family systems folk, it means determined by collective forces, and for biological psychiatrists, it means determined by genes.

That so-called doctors and scientists could each completely discount three out of four variables which clearly and undoubtedly affect human behavior is bizarre in and by itself. 

But do any of these determinism types actually live their lives in a way consistent with their professed belief that when we think we are freely and willfully making a choice as to how we are going to behave in a given environment, it is nothing but an illusion?    If so, then their belief in this proposition itself would have been predetermined by one or more of the four factors, and not by the actual scientific merits of their position!  They do not seem to be saying that, do they?

In fact, they live their lives weighing information and anticipating the future in order to make behavioral choices in order to meet their goals.  When they stop doing that, then we’ll talk.

Of course, this admittedly still leaves open the question of the existence of free will.  What do I think?

Well, I believe in free will, although there is no way to actually prove it one way or another.  The idea that may answer the question is actually provided by the radical Skinnerian behaviorists.  They start from the proposition that when a rat is learning to run a maze, if it is rewarded (operantly given positive reinforcement), then the probability that it will behave in the way that was reinforced increases.  (Of course, if food is used as a reinforcer the rat has to be hungry or else this does not work, but that’s a different issue).

In no case does the provision of positive reinforcement lead to a 100% chance that the rat will do anything.

In fact, when we look at all four factors described above, each one increases the odds that certain behavior will ensue.  We could express this probability mathematically as P = p + e + c + g, where P = the probability of a certain human behavior taking place at a given point in time, p = prior psychological experiences, e = external reinforcement by environmental factors, c = collective or social forces impinging on the person, and g = their genome.

I submit that when we add together all four of these factors, P will still not ever reach 100% - there is no certainty or absolute predictability.  If this is true, there would have to be a fifth factor.  Lets call this unknown factor f.w.