Abstract
Medical interventions that cure or prevent medical conditions are central to medicine; and thus, understanding them is central to our understanding of medicine. My purpose in this paper is to explore the conceptual foundations of medicine by providing a singular analysis of the concept of a ‘preventive or curative medical intervention’. Borrowing a general account of prevention from Phil Dowe, I provide an analysis of prevention, cure, risk reduction, and a preventive or curative intervention, before turning to preventive and curative medical interventions. The resulting counterfactual-mechanistic account holds that preventive and curative medical interventions reduce the probability of a medical condition in an actual population compared to their counterfactual omission, commonly by disrupting an etiological or constitutive mechanism for the condition.
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Notes
For instance, we could understand the counterfactual in P2 through a non-backtracking miracle (Lewis, 1973) or an ideal intervention (Woodward, 2003). If the causal claim in the consequent of P2 is itself to be understood counterfactually, our solution must also make sense of nested counterfactual claims.
Broadbent (2019) similarly argues that cure and prevention are part of the same goal in that they have the same result, the absence of the disease. The main difference is when the intervention is implemented.
Elsewhere, I argue that medicine conceives of individual risks as something like a propensity; however, there are significant problems with inferring an individual risk as a patient-level propensity from a population risk as an aggregate propensity that is measured in an epidemiologic study (Fuller, 2020).
Consequently, defining a preventive or curative intervention through risk reduction in a population makes no assumptions about how its effect is distributed among individuals, assumptions which typically are not supported by the results of a population comparison alone. INTERVENTION is thus well suited to interventions that are studied in a clinical trial or other epidemiologic study (as most contemporary medical interventions are).
In characterizing disease mechanisms, we may need to depart from Dowe’s (2000) account of a causal process, which involves transfers of conserved quantities. Woodward (2002) notes that biological mechanisms commonly include components engaged in ‘double prevention’ (Hall 2004) or ‘causation by disconnection’ (Schaffer 2000), in which A inhibits B, stopping B from inhibiting C. In these cases, there may be no transfer of a conserved quantity between A and C because A and C never come into physical contact, yet we may still want to say that A causes C. Rather than using conserved quantities, Woodward (2002) understands the causal interactions among the components of a mechanism according to his manipulability theory of causation (Woodward, 2003).
A disease’s etiological mechanism includes the pathogenesis of the disease—the bodily process generating the disease—and can also be thought to include causes external to the body that initiate pathogenesis (Damman, 2020). The relationship between a disease and its constitutive mechanism is more variable, as we will see momentarily. Static diseases such as osteoarthritis that depend entirely on structural derangements may not have a constitutive mechanism.
Steel (2008) articulates this intuitive idea as a ‘disruption principle’: “The disruption principle asserts that interventions on a cause make a difference to the probability of the effect if and only if there is an undisrupted mechanism running from the cause to the effect” (2008, p. 7), where a mechanism is the causal structure generating probability distributions involving such variables as the cause and the effect. Steel argues that the forward conditional (‘if’) is a consequence of the faithfulness condition, while the reverse conditional (‘only if’) is a consequence of the principle of the common cause. Steel further argues that the faithfulness condition is only sometimes reasonable in biological contexts, while the principle of the common cause is “on very firm ground” in biological contexts (p. 66). I cannot assess Steel’s argument here. But if Steel is right, then our assumption that there must be a mechanism running from our indirect etiological factor to the disease is “on very firm ground” because it amounts to the idea that a preventive intervention can prevent the disease only if there is a connecting mechanism.
In contrast, Sara Moghaddam-Taaheri (2011) conceptualizes medical interventions as targeting the malfunctioning stage of a broken-normal mechanism in order to restore the mechanism’s normal physiological counterpart.
Krueger (2017) objects to Stegenga’s account partly on the grounds that a curative intervention on this view may be less effective at preventing death than a non-curative intervention (e.g. antibiotics, which target the constitutive basis for cholera, may be less effective at preventing death from cholera compared to oral rehydration therapy, which does not target the constitutive basis). Krueger instead proposes that a curative intervention is “[a]n intervention that, on its own, is able to reduce patient mortality”, while noting that his definition is limited in its application (p. 233). However, Krueger’s objection and his definition are not compelling unless we require that a medical cure prevents death, which would fail to capture the paradigm case of a curative antibiotic for a typically benign infection like strep throat.
It also suggests that one promising way to develop medical interventions is to research etiological and constitutive mechanisms for medical conditions and the ways that they can be disrupted.
For example, analytic restrictions could be placed on the kinds of interventions that are ‘medical’ or on the kinds of etiologic factors that can be the target of ‘medical’ intervention.
These inferences about preventive and curative interventions assume both that (i) the etiological mechanism’s parts are not all contained within the system (the body) exhibiting phenomenon D (the medical condition), and (ii) most or all of the constitutive mechanism’s parts are contained within the system. I cannot defend these assumptions here, but on this topic see (Craver, 2007; Kaiser & Krickel, 2017; Kastner & Andersen, 2018).
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Acknowledgements
Thanks to the audience at the 2020 Conceptual and Methodological Aspects of Biomedical Research conference for helpful feedback and discussion of some of the ideas in this article. Thanks also to Olaf Dammann and to an anonymous reviewer for providing comments that helped improve the article.
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Fuller, J. Preventive and curative medical interventions. Synthese 200, 61 (2022). https://doi.org/10.1007/s11229-022-03579-0
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DOI: https://doi.org/10.1007/s11229-022-03579-0