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On Anti Humeanism and Medical Singular Causation

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Abstract

In this paper I offer an anti-Humean interpretation of the causal interactions in somatic medicine. I focus on life-threatening pathological states and show how Nancy Cartwright’s capacities can offer a plausible epistemology for medical processes and the singular causal claims advanced in medical diagnoses. I argue that the capacities manifested in the emergence of symptoms and signs could be tracked down if healthy organisms are construed as nomological machines and suggest that the causal reasoning from current medical practice bears a tacit adherence to anti-Humean assumptions.

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Notes

  1. See for instance Lipton and Ødegaard (2005)

  2. See Whitbeck (1977), Parascandola and Weed (2001), Lagiou et al. (2005)

  3. See Russo and Williamson (2007) in which the two authors put forward a Humean view of causation, appealing to Williamson’s own account of ‘epistemic causality’. Williamson and Russo develop a coherent, sophisticated and clear argumentation. They conclude however that ‘an epistemic account of causality is required to capture the full complexity of [medical] causal evidence’ (Russo and Williamson, 2007, 13, italics added) without a treatment of the other, anti-Humean side of the discussion. I provide a criticism of their approach, insofar as medical mechanisms are concerned, in Dragulinescu (2011).

  4. Cartwright has often been accused, quite rightly I think, of drawing unnecessarily strong conclusions, from the actual methodology and epistemology of science, to a metaphysical picture that rejects altogether the Humean interpretation; see Papineau (1991), Steel (2008).

  5. See Ashcroft (2004) and Parascandola and Weed (2001) for instance.

  6. See for instance Ellis (2000, 329-330, 348-349).

  7. One obvious connection here is with the counterfactual analysis of dispositions. For some anti-Humeans, dispositions are indeed modal properties, or features of modal properties, in the sense in which dispositional subjunctive conditionals are not just a way to set out what having a disposition represents, but to underlie the range of possible causal interactions in which the bearers of dispositions can engage, due to their properties, as such (Bird 1998, 233). These counterfactuals are made true by the dispositional properties at hand and not by some sort of regularity (Mumford 1998, 87-91). What I have designated above as ‘circumstances C’ are reckoned with, in the counterfactual analysis, by way of also mentioning (beside disposition- and manifestation-properties) stimulus properties and by specifying either that the analysis holds in ‘ideal conditions’ (Mumford, 1998, 87–91) in which finks and antidotes should be absent (Bird 2007, 60) or in a certain range of situations that can be indexically circumscribed and referred to (Bird 1998, 234).

  8. Different authors employ different terms in order to designate the causal powers and underline certain aspects of them. ‘Potency’ is a term used by Bird in his (2007), which I think captures nicely the modal level of the properties in question. Cartwright’s preferred term is ‘capacity’ (Cartwright, 1999). Other terminologies include propensity, tendency, etc.

  9. Schaffer (2008, 4) and Ellis (2000, 329), Psillos (2007, 139).

  10. I should note that what specifically are the characteristics of modal properties, as opposed to non-modal ones, is a rather unsettled issue, which has to do with the related, problematic distinction between dispositional and categorical properties (the latter distinction having been often cashed out in terms of the relational/intrinsic dichotomy, or unobservable/observable, or non-measurable/measurable, etc.) and ultimately, with the very Humean/anti-Humean dispute; see Schaffer 2008, 4 and Ellis 2000, 329. I have assumed above the simplest approach according to which the actual instantiation of a modal property says something about the real of possibilia. For Bird, this merely means that modal properties (or potencies, in his terminology) make true certain subjunctive conditionals, Cf. Bird (2005, 438). For Molnar, to take another example, it means modal properties (powers, in his idiom) bear the mark of intentionality: they have a direction to particular manifestations, even when they are not exercised, as such; Cf. apud Psillos (2007, 139).

  11. The direction of ontological dependency is thus from the ‘bottom’ level (singular causal interactions) to the ‘top’ (regularities exhibited by particulars bearing the relevant properties). It is for this reason that Ellis characterises his anti-Humeanism as a ‘bottom-up sort of theory, rather than top-down, [which] depends on taking a realist, non-reductionist, view of causal powers, capacities and propensities’ (Ellis, 2000, 330). Ellis retains however the ‘top’ level of laws, just as Bird for instance. Their position amounts to what Wilson calls ‘general’ (as opposed to ‘singularist’) anti-Humeanism (Cf. Wilson 2006), position criticised by Mumford (2004).

  12. In Ellis and Bird’s cases, this more sophisticated ‘general’ expression is underlined by a metaphysics of universals whose identity is linked with their associated powers/potencies. Laws are portrayed using first order quantified, universal statements (just as the Humean laws are expressed); see Ellis (2000, 345-46), Bird (2005, 441-2)

  13. Bird 2004, 268-9

  14. Bird 2007,60

  15. Bird 2005,441-2

  16. Ellis, 2000, 345

  17. See Schrenk (2006).

  18. See for instance Armstrong and Heathcote (1991, 63-64) where this view is nicely summarised, and also Nagel (1961) Lewis (1973) Papineau (1991) for a more extensive exposition. In this sub-section I discuss only the Humean strategy appealing to deterministic regularities; the probabilistic regularities will be discussed in the next sub-section, in direct relation to Cartwright’s views.

  19. For Hempel, just as for Nagel and Mackie, these non-accidental regularities are the scientific laws, where no definite indication is given as to why the laws in question back up counterfactuals; see for instance Hempel (1966) and also van Fraassen (1980) for a critique. For Lewis, the non-accidental regularities are the axioms of a deductive system which organizes all facts with the ideal combination of strength (scope of application) and simplicity (coherence of axiomatixation); Cf. Lewis (1973, 73).

  20. See Armstrong and Heathcote (1991, 63-64) Cartwright (1999, 144) Bird (2005, 440). The conditions C are not usually mentioned in the classical Humean analysis and they represent in fact a great problem for the Humean strategy. One of Cartwright’s main arguments against this strategy, as we shall see, is that in nature we find no universal regularities and that the respective conditions C can be reckoned with only in an anti-Humean framework. See, however, Papineau (1991) where a response to Cartwright’s contention vis-à-vis the conditions C is framed in Humean terms.

  21. Lewis is sometimes referred to as theorist of “counterfactual” causality, which is correct, insofar as one also bears in mind that the metaphysical burden of his account lies in what are intended to be the truth-makers of his counterfactuals, and these truth makers are regularities; indeed the first criterion of the similarity between the actual world and the worlds in which both the antecedent and consequent of subjunctive conditionals are true is that the regularities of the Best System analysis are violated as little as possible; see Lewis (1973) Psillos (2007, 81-106) Psillos (2009) Armstrong and Heathcote (1991, 63-64) Cartwright (1999, 144).

  22. See Lewis (1986, 223).

  23. Hence the Humean Supervenience thesis espoused by Lewis: all the modal features of the world supervene on the non-modal ones; see Lewis (1986, ix). Ellis (2000, 329) gives a general characterisation of this stance on the modal features of the world, which is not limited to Lewis’s views. There are classical criticisms of this position, see for instance Armstrong and Heathcote (1991),- that underlie a central difficulty of the Humean program: if regularities are to dissolve any modal feature of the world, why certain regularities are non-accidental cannot be justified in non-modal terms only.

  24. See for instance Cartwright (2007a, 8). Menzies also proposed that capacities could be taken as truth-makers of counterfactuals (see Menzies 2002), a move rejected by Cartwright however, for un-specified reasons (Cartwright, 2002). In her (2007a) such a counterfactual-based feature is I think adopted tacitly though - see (2007a, 24-5) and the discussed difference between the exercise and the manifestation of a capacity.

  25. It should be noted that Cartwright is not always clear about the precise metaphysics that underlies her account of causation; for instance the bearers of capacities are sometimes considered to be properties, other times natural kinds or systems; see Paul (2002) who note this lack of clarity. My employment of the category of property in the above presentation of her views is in a sense just a way of cutting the Gordian knot.

  26. Cartwright (1989).

  27. Cartwright (1999, 25-27, 148).

  28. Cartwright (1999, 65-66, 71, 139-143).

  29. Cartwright (1999, 59, 66, 138) (1989, 142-145, 154).

  30. ‘[capacities-claims]1. are claims about what systems with the cited features…can cause 2. the effect described may not occur but only ‘contribute’ in some appropriate way to the actual outcome in any given case 3. the effect or even the successful ‘contribution’ will only occur ceteris paribus…[the] prescriptions for filling in the ceteris paribus clauses…involve a whole range of categories from the ontology of capacities that are abhorrent to the Humean: triggering, shielding, enhancing, interfering and the like’.

  31. Cartwright (2002b, 3-4).

  32. See Cartwright (2005, 2) and the discussion of ‘background knowledge. See also Cartwright (2002a, 12-16), (2007, 58).

  33. Cartwright (2007b, 220).

  34. When discussing exceptionless, deterministic regularities (which are usually referred to in connection with ‘experimental settings’), Cartwright has in mind both the regularities of classical physics, for instance, and at the same time the regularities established on a microstructural level in the special sciences; see Cartwright (1999). When discussing the probabilistic regularities, Cartwright usually refers to the population-level assessments from the special sciences; see Cartwright (1989).

  35. Cartwright (1989, 142) (1999, 24-27) (2007a, 58).

  36. Cartwright (1989, 11) Cartwright and Dupre (1988, 521,522). Some Humean theorists, like Patrick Suppes, stress that their probabilistic approach is a departure from Hume’s idea of ‘constant conjunction’, while still denying the existence of causal powers (Suppes 1970, 10). At the same time, there is a striking parallel between the deterministic and indeterministic regularities, within the common program of reducing powers to higher level patterns; the parallel is nicely developed by Wolfgang Spohn, a Humean theorist himself, in Spohn (1983, 70,74,75).

  37. I shall be using ‘A’, ‘B’ (and ‘F’) as standing either for a property or a causal factor (the causal factor that instantiates the property in question) depending on the context of the discussion.

  38. This principle is to be found in all population-level techniques of ‘hunting down’ causes. In the causal path modelling, it is expressed in the condition that the error terms of the recursive equations are independent, in Bayesian nets by the Markov condition, in the Geiger causality by the condition that populations should be stratified such that all the other causes of the effect in question should be present or absent; see Cartwright (1989), (2007b).

  39. Cartwright (1989, 142-145).

  40. Cartwright (1989, 142-145); the argument is extended for randomised controlled trials in Cartwright (2007a), (2010). Note that even in the test population T itself one can raise doubts as to whether the probabilistic pattern resulting from stratification gives the correct causal relations. That is because, given a probabilistic common cause producing an effect and a side effect via a certain pattern of ‘firing’, the effect and the side effect could still be correlated, even after reckoning with the common cause and calculating the partial conditional probability. That is to say, not all probabilities’ dependencies indicate causal relations (see Cartwright’s comments against the Markov condition used in Bayesian nets, in her 1999, 107-111). On the other hand, probabilistic independencies do not entail that no causal relations are in place; that is, not all causal relations manifest as probabilistic dependencies (against the Faithfulness condition in Bayesian nets techniques; see her 1999, 117-118). For instance, a factor (cause) might produce an effect via two pathways, an enhancing and a preventative one, such that the overall influence of one over the other is cancelled and appears invisible in the statistical evaluation. The case discussed by Cartwright in her (1989) is Hesslow’s birth control pills, with their dual effects on thrombosis.

  41. Cartwright nourishes herself some of these questions in Cartwright and Dupre (1988).

  42. See Cartwright’s discussion of ‘background knowledge’ in her (2005, 2) and the comments in her (1999) on the information needed to built up experimental settings. The respective information ‘is not itself a report of any regular association – neither a real regular association (one that occurs) nor a counterfactual association (one that might occur)’ (Cartwright 1999, 143). See also her discussion of ‘rules of thumb’ in Cartwright (2007a, 62-64).

  43. This is not always true however, in that on the one hand the epidemiological results might be interpreted as incomplete data for what are otherwise exceptionless causal laws whereas, on the other, the results of many laboratory assessments are framed in probabilistic terms.

  44. See Whitbeck (1977), Parascandola and Weed (2001), Lagiou et al. (2005).

  45. Cartwright and Dupre (1988, 526-527), Cartwright (2007a, 58, 65). Of course, a hypothetical mechanism for the improvement of function could be postulated: e.g. in some people, it may be that smoking inhibits the operation of some other factor even more deleterious for lung function.

  46. Cartwright criticises in her (1999) the fact that huge financial resources are allotted to breast cancer research investigating its genetic bases, while much less (financial) attention is paid to the research into the causal influence of the endogenous oestrogen levels on breast cancer, simply because 'the genetic programme is our best shot right now at a theory of everything' (Cf. Cartwright, 1999, 17).

  47. Cartwright (1999, 72).

  48. In the case of the microstructural assessments we might have two sources of ‘causal context’ variation. One would be the different sets of causal factors showing up from one context to another, as different ‘backgrounds’ for the cause and effect under study; this is a sort of variation that these assessments share with the probabilistic, population level evidence. The other source would be the difference between the laboratory settings and the real life organisms. The medical laboratory conditions operate, of course, on grounds of a ‘shielding’ that eliminates (what an anti-Humean would call) a whole range of causal factors, interferences and stimuli. This latter sources of variation could evidently be invoked when questioning not only the Humean approach to medical ‘causal laws’ but also the move from ‘causal laws’ to singular causal claims. I shall return to this issue in Section 4.

  49. Cartwright 2005, italics original, underlines added.

  50. Cartwright (1989, 39).

  51. The rationale would be the same as the one I framed in Section 2.3. It would cite the variation in the causal contexts given for instance different arrays of causal factors showing up from one population to another, the difference between laboratory setting and the real-life organisms, etc. The series of ‘questions’ that the anti-Humean could throw at the Humean strategy and ‘causal laws’ are also of the same type: does the decreased cardiac output produce the increased tonus of the sympathetic system and hence tachycardia? Well, we could have a population in which the sympathetic tonus is decreased by lowered cardiac output. Does the increased pressure in pulmonary capillaries, given the rates of filtration, reabsorbtion and lymph flow, produce the extravasation of proteins in the alveoli? Well, we might have a singular organism in which the congestion of the pulmonary capillaries helps the alveoli remain intact.

  52. ….and their laborious construction requires singular causal ‘information’, knowledge of stimuli, interferences, etc., which needs much experience but is in the end, says Cartwright (following Anscombe at this point) acquired because we can perceive natural necessity; see Cartwright (2002b).

  53. In the solar system, the interferences represented by all the other causal influences different from the gravitational one are naturally negligible; see Cartwright (1999).

  54. Whereas the Humean looks for regularities to reduce and ground ontologically the modal features of causation—recall capacities/powers are to be viewed as ‘bestowed upon’ by a certain type of constant conjunction—the anti-Humean looks for regularities in order to know about capacities. This is indeed a very special sense of ‘path parallelism’. For the anti-Humean, the regularities from the ‘inside’ are local and not universal regularities. Moreover, when nomological machines are of the ‘man-made’ type, singular causal information about stimuli, interferences, etc. is essential in constructing them. In other words, that in a special sense the metaphysical path of the Humean is the epistemic one for the anti-Humean does not trivialise at all the Humean/anti-Humean distinction.

  55. Note that by “abnormal” stimuli and interferences I mean simply the circumstances that in present-day medicine are recognized as conducive to life-threatening conditions in somatic medicine, which, as mentioned in the Introduction, are the main target of the present paper. In other words, I do not wish to enter into the dispute over the exact distinction between disease and non-disease in borderline cases, e.g. attention deficit disorder or infertility (see also Dragulinescu, 2010). If anything, life-threatening conditions in somatic medicine are diseases, and if we assume that physicians have in this respect a basic knowledge of the distinction between physiology and physiopathology, the “abnormal” stimuli are those that figure in their description of the physiopathological context.

  56. Recall that the crucial point of determining the capacities inside nomological machines is that regularities (resulting from their systematic manifestations) cannot be justifiably projected ‘outside’ nomological machines (and indeed this is the entire significance of Cartwright’s insistence on modal inference tickets, which are different from the occurent ones). In the backdrop of our discussion, it seems evident that the regularities of physiology cannot be projected to the level of the pathological. This does not entail however that ‘outside’ there are no regularities: there might be, or there might not be (and Cartwright offers examples that cover both possibilities; think of the cathedral banknote situation vs. the example of charges in a specially framed magnetic field, both offered in her 1999, 27, 60). Indeed, in the medical realm there are certain diseases (especially the chronic ones) that exhibit a somewhat regular behaviour. In my scheme, this regular pathological behaviour occurs in an ‘outside’ context in which the abnormal stimuli and interferences, being present long enough and affecting the physiological capacities in a certain sense, produce regular manifestations. Thus, the causal laws of medicine should be taken to emerge out of such pathological regularities (construed as an epistemic and not metaphysical source). Insofar as causes per se are concerned, however, my primary interest is in singular causation in medical contexts. I shall not insist upon the general causal claims and their interpretation.

  57. Cartwright (1989).

  58. See Cartwright and Dupre (1988).

  59. Even if Canguilhem was not concerned with the causation aspects I deal with in the present paper.

  60. See Lote (2000).

  61. See Arnold (2010).

  62. See Tanser (2007), Arnold (2010), Sharpe and Swedberg (1996).

  63. In point of fact, this is a variant of AoI, the variant in which the displacement of the aortic valve is large enough to quickl bring abouty the cardiac insufficiency stage, in the context in which the volume of blood ejected through the aortic valve may (still) be unaffected. Of course, there are variants of AoI in which the displacement is smaller and thus the evolution of the disease takes longer. In such cases, by the time AoI reaches the stage of cardiac insufficiency (in which the role of the RAAS takes central stage) the volume of blood as such ejected through the aortic valve is also diminished. But in these variants as well, no matter the stage of the disease, the stimulation of the RAAS worsens the condition by bringing about hypertension, for instance. That is why medicines such as ACIs (angiotensin convertase inhibitors) (drugs that block a crucial pathway of the RAAS) are administered in aortic insufficiency; see Sharpe and Swedberg (1996).

  64. Angiotensin II induces, among others, the secretion of growth factors from the cardiac fibroblasts and endothelial cells. See Willenheimer et al. (1999).

  65. As I have noted in the previous section, Canguilhem has actually provided a metaphysics of medicine which, even if not discussing explicitly the causation aspects I am concerned with in the present chapter, is grounded on the idea that the pathological emerges from an exacerbation or diminishing of the physiological; see Canguilhem (1991), Horton (1995). As for the case of cancers mentioned above, it does appear that that they could not be readily assimilated to my scheme, simply because the morphological transformations they presuppose are often so dramatic that the link to the physiological background is lost (see for instance the case of Burkitt's lymphoma). Notably though, there are some cancers in which metaplasia simply presupposes that a type of tissue, in its pathological behaviour, assumes the physiological background of another type of tissue. For example, the small cell lung cancer induces high levels of cortisol in the blood by way of secreting a hormone called ACTH, which is physiologically secreted by the pituitary gland; see Chabner and Chabner-Thompson (2008) and their discussion of paraneoplastic syndromes.

  66. That this anti-Humean reading can be viewed as delineating a sum of ‘causal laws’ for diseases is due to the fact that the ‘context of diseases, even if situated ‘outside’ vis-à-vis the nomological machines of physiology, exhibit nevertheless a degree of regularity. When the nomological machines of physiology are disrupted and interferences, abnormal stimuli, etc. show up, the biological capacities do not manifest completely waywardly. In a sense, organisms with chronic illnesses themselves can be viewed as a sort of nomological machines that enable us to know about stimuli and interferences, and their influence on the manifesting of capacities. The full-blown nomological machines should, however, be taken to be the physiological ones, at least for reasons related to the principle of parsimony; see also the discussion of the worry concerning the multiplication of capacities, in Section 3.

  67. Of course, what I try to frame above is what could count, for this imaginary patient, as a variation in the causal context that would mark the difference between the ‘internal validity’ and the ‘external validity’ of our causal claims discussed by Cartwright; see Cartwright (2007a, 61) and also Section 3.

  68. Examples here could be the microbiological studies simpliciter that isolate systems, organs, tissues, cells down to the level of cellular components. Animal experimentation could also be adduced; see Cartwright’s discussion of laboratory conditions and Galilean idealisation in her (1989, 185-188, 227, 228). Randomisation in medical trials is discussed in Cartwright (2007a, 58-68) (2010).

  69. This is a variant described in Fernet et al. (1987).

  70. The third being the so called Riedel’s lobe, an inferior projection of the right lobe on the right of the gallbladder; Cf. Gillard et al. (1998).

  71. On this Humean reading, knowing physiology is knowing about the physiological capacities and what stimulates (or interferes) with their manifestations. This knowledge is translated into the medical research and practice. Arguably, physicians possess a knowledge of stimuli and interferences that is not limited to the textbook information but is also accumulated in practice and can be used to differentiate between particular cases and particular patients. The latter experience is important because it cannot be codified in general rules of thumb. It is not a ‘catcher’, to use one of Cartwright’s suggestive expressions (Cartwright 2007a, 62-64), which could provide us deductively the causes at work in individual cases.

  72. See for instance Papineau (1991, 409), Russo and Williamson (2007, 13) Schrenk (2006).

  73. This epistemological point is important, in as much as the main critique raised by Humeans to “powers” and “capacities” schemes is how can we know about such powers and capacities (Psillos, 2008). But when looking at the actual practice of science it turn out to be even harder to see how we could know about the requisite regularities, adorned as they must be with monstrous ceteris paribus clauses, which would be ideally grasped by consulting Laplacian demons or systematizing the entire history; in this respect, see Carwright’s reply to Lipton’s comments on ‘The Dappled World’ in Cartwright (2002c, 271-279).

  74. For instance Lowe (1989) and Armstrong (1997) have drawn such a conclusion with regard to the crucial (non-repeatable) experiments in physics. Cartwright has made a similar point when discussing the Stanford gravitational experiment in her (1989) and (1999).

  75. Recall that, according to Cartwright, not even physics and chemistry exhibit the sort of regularities that would fit the Humean stance on causation; see Section 2.2 and Cartwright (1999).

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Acknowledgements

Work for the present paper was undertaken during my doctoral studies at Lancaster University, for which I gratefully acknowledge financial support from the UK Arts and Humanities Research Council (fees doctoral bursary, awarded July 2007, Ref. No. 2007/135148/Lancaster University) and the British Society for the Philosophy of Science (doctoral scholarship, awarded July 2007). A version of this paper was presented at the Probabilistic Causality Summer School organized by CEU Budapest in August 2008, and I thank the participants for very useful comments. As always, I am very grateful to Rachel Cooper for her constant encouragement. I also thank one referee of this journal for excellent suggestions and criticism. Last but not least, I thank Iuliana Sandu for invaluable help with the muddled figures of this paper.

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Correspondence to Stefan Dragulinescu.

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Dragulinescu, S. On Anti Humeanism and Medical Singular Causation. Acta Anal 27, 265–292 (2012). https://doi.org/10.1007/s12136-011-0141-1

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