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 folksfrom all ends of the academic political spectrum, it’s easy to see how peoplebecome emotionally attached to certain ideas (for whatever internal reasons)and take the position that, “My mind is made up; don’t confuse with me withfacts."

Two of their tricks in arguing are:
  • To use aword that has several different senses or referents, and then subtly shift howthey are using the word as the argument progresses without admitting that thatis what they are doing.
  • Living their lives as if they really don’tbelieve a word they are saying. 

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

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

colleague from the Unified Psychotherapy Project, Gregg Henriques, quotes Ingram and Siegle, “The label depression hasbeen used to discuss a mood state, a symptom, a syndrome…a mood disorder, or adisease 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 thedebates.  Especially online, it’s verydifficult 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, whichmany 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 orwithout the “melancholic” specifier), dysthymia, adjustment disorder withdepression, and depression caused by a medical condition or an outsidesubstance 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 complicatedby the fact that the definitions of the syndromes overlap to some degree, but making aclinical decision is what medical education is supposed to be about – or atleast theoretically. 

The anti-antidepressant crowdloves to point out that recent "meta-studies" show that in mild tomoderate "depression," antidepressants are often no better thanplacebos.  They also conveniently love to ignore the fact that in theexact 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 twovery different syndromes, but no one mentions that!  
Even the president of theAmerican Psychiatric Association, John Oldham, was guilty of this confusion ofterms in a recent editorial in PsychiatricNews.

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

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

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

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

Neural plasticity means that the structureand function of the brain changes significantly in response to persistent environmentaldemands.  This happens in normals.  For example, the part of the brain that controls fingermovement is significantly larger in concert violinists than it is in averagecontrols.  So does this mean that being aconcert violinist is a disease?  I don’tthink so.

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

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

The epigenetic issue leads us to my second question: is ourbehavior predetermined or do we have free will?  Of course, people who take the determinist position do not agree amongthemselves 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 eventslike rewards and punishments. For family systems folk, it means determined bycollective forces, and for biological psychiatrists, it means determined bygenes.

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

But do any of these determinism types actually livetheir lives in a way consistent with their professed belief that when wethink we are freely and willfully making a choice as to how we are going tobehave in a given environment, it is nothing but an illusion?    If so, then their belief in thisproposition itself would have been predetermined by one or more of the fourfactors, 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 weighinginformation and anticipating the future in order to make behavioral choices inorder to meet their goals.  When theystop doing that, then we’ll talk.

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

Well, I believe in free will, althoughthere is no way to actually prove it one way or another.  The idea that may answer the question isactually provided by the radical Skinnerian behaviorists.  They start from the proposition that when arat is learning to run a maze, if it is rewarded (operantly given positive reinforcement), then the probability that it will behave in theway that was reinforced increases.  (Ofcourse, 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 positivereinforcement lead to a 100% chance that the rat will do anything.

In fact, when we look at all four factorsdescribed above, each one increases the oddsthat certain behavior will ensue.  Wecould express this probability mathematical as P = p + e + c + g, where P = theprobability 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 fourof 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 afifth factor.  Lets call this unknownfactor f.w.


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