Depression is an Anomaly (for Materialists)
J. Kenneth Arnette
Introduction: Anti-depressant (AD) medications appear not to work very well and present a sequence of puzzling problems: side effects, a long latency period before recovery, an uncertain theoretical foundation for psychopharmacology, the high relative efficacy of placebos, and the generally low efficacy of ADs. Behind these empirical and scientific problems lie a host of ethical issues within drug development: publication bias, conflicts of interest, ghost authorship, and informed consent.
Method: I reviewed the literature carefully, and used the following questions for my review: how are AD candidate drugs developed in the laboratory; how are the candidates tested on humans; what are the procedures for conducting clinical trials; what factors interfere with clinical trials; what are the typical results of such trials and how does the FDA evaluate trials; and how do these factors play out in routine use of the AD by the public?
Results: (1) there is no reason to believe that ADs should be effective for humans, given their origin in rodent research; (2) the placebo effect rivals the drug effect, showing that ADs are ineffective; (3) drug companies and doctors unethically continue to push the use of ADs; (4) analyses from science and the philosophy of science show that ADs are scientifically unsound; and (5) ethical analyses demonstrate that ADs are ethically intolerable.
Discussion: My analysis indicates that the monoamine (serotonin) hypothesis regarding the nature of depression is unsupported by the evidence. When such drugs seem to work, the improvements are, in fact due entirely to the placebo effect. The so-called active drug merely provides side effects, which ironically serve to convince the patient that the drug is actually doing something, thus producing the placebo effect. The side effects are mostly symptoms of depression itself because the drug is ineffective against depression. Thus, the latency period (around two months), after which the drug appears to begin working, is instead due to the cyclic nature of depression—after a serious bout, mood tends to move back in the direction of normal mood with no assistance from the AD.
Conclusion: There are deep implications for psychiatry, psychology, and philosophy. The primary implication is this: if one holds to the mind-brain identity thesis—that the mind is what the brain does—then how does one explain how a healthy brain generates a diseased mind? We can rule out the brain’s role in depression because no drug has succeeded in defeating it. The direct meaning of this is that depression is a disease of the mind, not of the brain, and thus the mind-brain identity thesis is refuted; with the same stroke, materialist explanations of consciousness are refuted. And for the materialist, depression becomes an anomaly because it cannot be explained in terms of material causation. This gives the mind an independent ontological status—it does not depend on the brain. This point of view is called interactive substance dualism, first proposed by Descartes, and forever thereafter hated by almost everyone.
Kenny Arnette is an academic wanderer. He began his journey with a BS in chemistry, which led him to earn a Ph.D. in Physical Chemistry. After a decade, in search of something more meaningful, he left chemistry and began studying psychology, ending in a Ph.D. in Clinical Psychology. Finding irreconcilable differences with psychology faculty members, he left the field and, in the third part of his life, pursued philosophy, earning an M.A. in 2020. He now works in a small group of researchers addressing death-related anomalous experiences and other problems related to consciousness.
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Published on February 9, 2024
