We first turn to Adolf Meyer, the most influential psychiatrist in the US over the first 3rd of the 20th century [27]. It should be recalled that until World War II, American psychiatry was a rather small profession, largely composed of superintendents of mental hospitals who largely had a biologically orientation to their work. In 1907, while the director of the New York Psychiatric Institute, Meyer wrote about his concerns of the narrow views that US physicians would typically take in their approach to psychiatric illness that likely reflected his views about the excesses of earlier authors like Meynert:
Instead of analyzing the facts in an unbiased way and using the great extension of our experience with mental efforts to get square with things … they pass at once to a one-sided consideration of the extra-psychological components of the situation, abandon the ground of controllable observation, translate what they see into a jargon of wholly uncontrollable brain-mythology, and all that with the conviction that this is the only admissible and scientific way [28] p. 172.
Next, we examine a text on a similar theme from a quite different source - the psychiatrist-philosopher Karl Jaspers. In his the introduction to the first (1913) edition of General Psychopathology [29], he writes:
The still widespread “somatic prejudice” is: everything mental cannot be examined as such, it is merely subjective. If it is to be discussed scientifically, it must be presented anatomically, physically, as a physical function; for this it is better to have a preliminary anatomical construction, which is considered heuristic, than a direct psychological investigation. Such anatomical constructions are quite fantastic (Meynert…) and are rightly called “brain mythologies.” Things that have no connection to one another, such as cortical cells and memory images, brain fibers and psychological associations, are brought together. There is also no basis for these mythologies insofar as not a single specific brain process is known that could be assigned to a specific mental process as a direct parallel phenomenon [29] p. 8 (KSK translation).
We might think that recent scientific developments over the rest of the 20th century eliminated the need for metaphorical brain talk. We provide three examples suggesting that this is not the case.
First, in a series of articles published over several decades, the distinguished psychologist Paul Meehl proposed a cognitively and psychometrically sophisticated genetic single-locus model for schizophrenia spectrum disorders. A core part of this theory was equating cognitive and neurobiological parts of his theory, as expressed here in 1962:
The cognitive slippage is here conceived as a direct molar consequence of synaptic slippage, potentiated by the disruptive effects of aversive control and inadequate development of interpersonal communication sets [30] p. 834.
His phrase, “synaptic slippage,” has commonly been repeated in the subsequent literature [31, 32].
Second, in 1985, a leading biological psychiatrist, Nancy Andreasen, published a widely-cited book whose title was a paradigmatic example of metaphorical brain talk: The Broken Brain [33]. She writes, for example, that recent advances in research have “taught us that many forms of mental illness are due to abnormalities in brain structure or chemistry. Psychiatry is moving from the study of the “troubled mind” to the “broken brain” [33] p. VIII. In a later section, she describes, using broad metaphors, the kinds of brain abnormalities that occur in psychiatric disorders.
The various forms of mental illness are due to many different types of brain abnormalities … sometimes the fault maybe in the pattern of the wiring or circuitry, sometimes in the command centers, and sometimes in the way messages move along the wires” [33] p. 221.
Third, in an important development in the history of neuroscience, in the early 1960s, cell bodies and neuronal pathways of the putative monoamine neurotransmitters dopamine, norepinephrine, and serotonin were demonstrated in mammalian brains [34,35,36]. Within a few years, prominent psychiatric researchers proposed that abnormalities of function in these neurotransmitters were the major cause of three of the most important of psychiatric disorders: schizophrenia, mania and depression [37,38,39,40]. I suggest that these theories reflect, in more subtle ways than prior examples, metaphorical brain talk. Or, perhaps these monoamine hypotheses could be seen as sitting somewhere on a continuum of naively enthusiastic scientific theories and metaphorical brain talk. They were grounded in solid basic neuroscience, and had support from pharmacologic studies of mechanisms of action of antipsychotic and antidepressant medication [41]. However, trying to clarify disease etiology through the mechanism of action of pharmacologic treatments is deeply problematic as illustrated by the now common phrase: “headache is not an aspirin-deficiency disease” [42]. Given the more than 100 neurotransmitters in the mammalian brain, the plausibility that dysfunctions in the first three to be traced in the brain caused the major psychiatric disorders strains to the breaking point any sense of credulity. Furthermore, these theories, for example, the serotonin hypothesis of depression [43,44,45,46,47], have not fared well over time. Large-sample, genome-wide association studies are now available on all three disorders, and none support a major role for genetic variants involved in the dopamine, norepinephrine, and serotonin systems for, respectively, schizophrenia [48], bipolar illness [49], and depression [50]. A recent widely-cited umbrella review concludes, “The main areas of serotonin research provide no consistent evidence of there being an association between serotonin and depression, and no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations” [46] p. 3243. While there remains substantial controversy about the precise etiological relationship between serotonin and depression [43, 51, 52], I do not seek to deny that serotonin may play some role in the complex pathophysiology of this syndrome. Rather, I suggest, less controversially, I hope, that the grand monocausal theory of depression resulting primarily from serotonin dysfunction (as I have argued earlier, regarding the dopamine hypothesis of schizophrenia [42]) is almost certainly false.
Importantly, these monoamine theories have had impacts outside of our research world. I recently heard the following story from friend of a friend, who knew I was a psychiatrist:
I was feeling really down and my family doctor referred me to a local psychiatrist, Dr. C. We talked for 30 min. He said I had what he called “major depression” and this was due to an imbalance in my brain serotonin. He said I should take the medicine he prescribed and it would correct that imbalance. Three weeks later I was feeling a lot better. I was really impressed.
While certainly more false than true, this example of metaphorical brain talk remains a common story in psychiatric culture. Some of us tell stories like this to our patients, in part because it may make them feel better and also perhaps because it is a story we like to tell. Metaphorical brain talk can be popular.
While my focus in this essay is the internal history of the psychiatric profession, there remains one elephant in the room that needs brief attention. When psychiatric research came to seek external financial support, simplistic metaphorical brain talk often appealed to prospective funders. This continues to the present day. Even more powerfully, advertising of psychopharmacological drugs, rising to prominence in the last third of the 20th century, often revolved centrally around metaphorical brain talk. While we like to claim that such advertising has no effect on us, this is naïve. An empirical review of this question, while far outside my remit, would, I suspect, find such advertisements have significantly increased the modern popularity of metaphorical brain.