Abstract
Causal mediation mechanisms are well supported by available experimental evidence and provide a practicable way to reductive physicalism. According to the causal mediation account of mechanistic explanation, descriptions as diverse as ‘black-box’ phenomena, mechanistic sketches and schemas mixing physically interpreted and operationalized biological, psychological and social variables, and detailed descriptions of mechanisms refer to the same causal structure circumscribed within the spatiotemporal boundaries of a replicable experimental setup. The coreference of coarser- and finer-grained descriptions of causal structures opens new possibilities for testing the reductive physicalism conjecture. I discuss experimental designs supporting the causal mediation account and show how recent studies demonstrating the biological mediation of mind-mind causal processes can provide evidence for reductive physicalism.
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Notes
For a nonreductive proposal, see Krickel (2018).
This explanatory standard corresponds to what Seth (2021, Ch. 1) calls the ‘real problem of consciousness,’ the goal of which is “to explain, predict, and control the phenomenological properties of conscious experience.”
If (i)-(iii) are construed as necessary and sufficient conditions for mechanistic constitution, the trio defines the set of relationships in the world that simultaneously behave like material composition and reciprocal manipulability, where manipulability is causation as understood by interventionist accounts. Since the properties of composition and causation are mutually exclusive (e.g., one is synchronic, the other diachronic), their simultaneous conjunction stipulates a counterintuitive mode of existence analogous to the wave-particle duality. Following Craver and Bechtel (2007), the more intuitive interpretation adopted in this paper is that mechanistic constitution is a type of material composition, but not all material composition is mechanistic composition.
In the above scenarios, there is no mechanistic constitution relationship behaving both like identity/composition and causality (manipulability). Instead, identity and composition relationships merely appear to be causal due to experimental artefacts.
Rod (and cone) cells are ‘on’ in the dark (i.e., depolarized at -40 mV, corresponding to the ‘dark current’ discovered Hagins and coworkers) and ‘off’ when stimulated by light (hyperpolarized to a potential of -60mV, as indicated by Tomita). It was subsequently discovered that cGMP levels are high in the dark and keep cGMP-gated sodium channels open, hence the inward dark current resulting in the inhibitory neurotransmitter glutamate being released in the synaptic cleft. Light results in the activation of a phosphodiesterase, which hydrolyzes cGMP, reducing its the intracellular concentration. cGMP-gated sodium channels close, causing a hyperpolarization of the cell due to a continuous efflux of potassium ions. Hyperpolarization causes voltage-gated calcium channels to close and therefore of calcium levels in the cell to drop. This reduces the amount of inhibitory glutamate released in the synaptic cleft, causing the depolarization (excitation) of bipolar neurons (Fu, 2020). Note also that this explanation too is strictly about causal mediation, not mechanistic constitution.
‘Dark permeability’ refers to the inward Na+ dark current explained in note 5. Methylene ATP analogs are resistant to hydrolytic attack by nucleotide phosphohydrolases and are thought to act as competitive inhibitors of nucleotide cyclases.
Mechanisms are described as causal pathways doesn’t entail that they are linear. For example, in the absence of measurements of intermediary stages, a cyclical metabolic pathway, such as Krebs’ cycle, appears as a linear input-output phenomenon (2 acetyl-CoA, 6 NAD+, 2 FAD, 2 ADP + Pi→ 4 CO2, 6 NADH, 6 H+, 2 FADH2, 2 ATP, 2 CoA).
Some authors argue that the empirical justification of antireductionism rests primarily on the notion that causal inference from controlled experiments is indifferent to the nature of the variables manipulated in the experiment (Baetu, 2019b; Campbell, 2008; Kendler & Campbell, 2009; Woodward, 2008). For instance, if we agree that ibuprofen, a drug known to target the molecular mechanisms of inflammation, has a measurable analgesic effect on pain (as measured by verbal reports) because randomized controlled trials demonstrate a statistically significant difference in pain ratings between test patients exposed to ibuprofen and comparable control patients (Rainsford, 2011), then we must concede that hypnotic suggestion targeting expectations must also have a real analgesic effect, since methodologically equivalent randomized trials likewise demonstrate a statistically significant difference in reported pain between test patients exposed to hypnotic suggestion and comparable control patients (Rainville, 2008).
The biopsychosocial consensus is also reflected in the IASP (2020) definition of pain.
Haxby (2012, 853) explains the technique as follows: “The idea was straightforward and based on a concept from conventional statistics, namely split-sample cross-validation. If a given stimulus category evoked a distinct pattern of activity, then independent observations of the response to that category should be more similar to each other than to responses to different categories. Correlation of patterns was the chosen measure of similarity, and I made independent observations by dividing the data for each subject into two halves–even-numbered and odd-numbered runs. Thus, I predicted that within-category correlations would be higher than between-category correlations.”
In the absence of experimental techniques selectively interfering with the activity of specific brain areas in humans, causal mediation was assessed by statistical methods. Psychological manipulations (conditioning individuals to associate auditory cues or options denoted by abstract symbols with high- and low-intensity noxious heat) were the independent variable, trial-by-trial pain ratings the dependent variable, and trial-by-trial SIIPS1 and NPS responses during pain were the mediating variables transmitting the influence of the independent variable to the dependent variable.
Reference may hold true only locally–that is, only as far as pain modulating effects are concerned, without being generalizable to other experimental setups or phenomena involving measurements or manipulations of the variable expectation. If so, this would suggest that psychological function is underpinned by a variety of related or unrelated biological mechanisms [e.g. (Corns, 2012; Hardcastle, 1999)]. This is certainly true of many biological functions (e.g., gene expression regulation, immune responses, metabolic pathways) and dysfunctions (e.g., types of diabetes, genetic disorders), a situation often reflecting an evolutionary process of duplication and coopting of mechanistic components. It is also worth emphasizing that the fact that an operationally defined measured/manipulated variable expectation is shown to have a biological referent does not automatically entail the elimination of a theoretically defined construct expectation associated with this variable. The theoretical construct may survive, although it is now associated with a biological activity.
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Baetu, T.M. A mechanistic guide to reductive physicalism. Euro Jnl Phil Sci 12, 62 (2022). https://doi.org/10.1007/s13194-022-00489-3
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DOI: https://doi.org/10.1007/s13194-022-00489-3