Abstract
There are some philosophical questions that can be answered without attention to the social context in which evidence is produced and distributed. Abstracting away from social context is an excellent way to ignore messy details and lay bare the underlying structure of the limits of inference. Idealization is entirely appropriate when one is essentially asking: In the best of all possible worlds, what am I entitled to infer? Yet, philosophers’ concerns often go beyond this domain. As an example I examine the debate on mechanistic evidence and then reevaluate a canonical case study in this debate. I show that for the assessment of actual evidence, produced in a world that is far from ideal, omission of the social aspects of medical epistemology (e.g. commercial drivers of medical research) leads philosophers to draw the wrong lessons from cases they take as paradigmatic cases for their views. I close by arguing that social epistemology provides an avenue to incorporate these complications and provides the necessary framework to understand medical evidence.
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Notes
Similar arguments for the necessity of causal accounts for extrapolating from an RCT have been put forward by others (e.g. Clarke et al. 2014), though there remain fundamental philosophical differences between the views (Dragulinescu 2012). In this section and the next, I focus on Cartwright and Howick; however, the argument applies to any account that ignores industry funding and seeks to have practical application.
Studies had shown that 25% of patients that died suddenly had no symptoms of heart disease. The treatment population at issue below, on the other hand, were patients thought to be at risk for sudden cardiac death because they had both asymptomatic arrhythmias and had suffered from a myocardial infarction.
The various terms used in the medical literature for this phenomenon were “premature ventricular complexes,” “ventricular premature complexes,” and “extrasystoles.” I have chosen to stick with Howick’s acronym for the sake of simplicity.
Figure 1 (and the death toll estimates) does not include a large number of patients who died in the first 2 weeks of the trial, when all patients were on an antiarrhythmic drugs to establish the effectiveness of VEB suppression in that patient. Of the first 91 deaths in CAST I, 41 occurred during the 2-week titration phase of the trial (during which there was no placebo group for comparison). These deaths were not included in the analysis. In CAST II, with another class I antiarrhythmic drug, a placebo group was added to the initial phase of the trial. Before this trial was stopped, researchers recorded 17 deaths during titration compared to 3 on placebo. Antecedently, the drug studied in CAST II was thought to be the “most benign” member of the class. Since the initial dose given was low and high doses increase risk, the results “may be considered a minimal estimate of the risk of the initiation of drug therapy” (CAST II, 1992, p. 230).
My thanks to the anonymous reviewer for their suggestion to add such citations and for bringing the Jureidini et al. (2016) study to my attention.
This account draws heavily on the book Deadly Medicine (Moore 1995) referenced by the EBM advocates as their source for information on arrhythmias. I will indicate where my account differs from Moore’s rendition in footnotes.
Moore suggests that the cardiac suppression hypothesis was only based on simple correlation and that it was equally plausible that heart arrhythmias and subsequent cardiac arrests had a common cause, but were not themselves causally related: “Every doctor has been taught that an association between two events does not prove a causal link. In this case it was equally plausible that premature beats were nothing more than a telltale indicator of underlying permanent damage” (p. 49). Howick repeats this claim: “The available evidence suggested an epidemiologic link between VEBs and mortality, but association is not causation. Moreover, even at the time there were good reasons [he does not specify what these were] to believe that after myocardial infarction, the heart is damaged in a way that both causes VEBs and raises the risk of sudden death” (p. 138). The supposition that the arrhythmia suppression hypothesis confused correlation with causation is simply untrue. For example, in the very speech in which Lown described his theory, he addressed the topic: “It may be argued cogently that prognostic implications are not determined by the ventricular premature complex [VEBs] but by the extent of cardiac disease because the grade of ectopic activity is largely an expression of the severity of the disease. A corollary inference is that the attempt to control ventricular arrhythmia is futile because the ultimate outcome is determined by the extent of heart disease. A recent study of Schulze et al. contradicts such a conclusion” (Lown 1979, p. 316).
A familiar, though controversial example is the use of t-cell counts—rather than death—to evaluate AIDS treatments (Epstein 1996).
To be fair, Morganroth’s position was that we must first establish that drugs suppress VEBs, then “once antiarrhythmic agents are available which are effective, safe and well-tolerated for long periods of time, we will have the ability to test [the arrhythmia] hypothesis (Morganroth 1983, p. 64). While a reasonable plan for research, it confuses the mandate of the FDA. Drugs are not made available so they can be shown to be effective, they are shown to be effective so they can be made available. As Moore (1995) details, Morganroth was personally brought in by 3M to meetings with FDA director Robert Temple and was successful in convincing him to approve the drug for the wider indication solely on the basis of surrogate endpoint data—a stance Temple had initially regarded as unwarranted and potentially dangerous without further trials (i.e. a trial like CAST).
It is difficult to determine the exact causes for rejection and whether bias (conscious or unconscious) plays a role in any individual case. Nevertheless, some of the referee comments that Winkle received were difficult to understand. For example, his article was rejected from Circulation “because the literature does not at present contain an overall description of the antiarrhythmic efficacy of Enkaid, it seems somewhat inappropriate to include a separate article about this specific adverse side-effect” (quoted in Moore 1995, p. 66). This explanation is odd given the existence of four separate studies describing the antiarrhythmic efficacy of Enkaid, all cited in Winkle’s manuscript (1981).
The loss of advertising is a real possibility. In 1992 when the Annals of Internal Medicine ran an article that identified false claims made in contemporary medical advertisements, the journal lost $1.5 million from cancelled ad contracts (Altman 1999). Marcia Angell (former editor in chief of NEJM) explains that pharmaceutical companies don’t even have to be involved explicitly; simply the threat of legal action and potential loss of advertising revenue can lead journal editors to self-censor (Abramson 2004, p. 113).
Precise numbers are not available, but this figure is consistent with industry averages for such arrangements.
Woosley wrote this in the sobering year after the CAST-I trial was published in 1989. It should be noted that pre- approval seeding trials were specifically prohibited by the Kefauver–Harris amendments in 1962. Though Woosley was employed by pharmaceutical manufacturers, he was also on the FDA advisory panel and thus—assuming he knew of the seeding trials at the time—had reason to vote against approving antiarrhythmic drugs or in some way censuring the manufacturers when the advisory panel addressed antiarrhythmic drugs in 1984.
The Holter heart monitor had become a popular way to diagnose VEBs and could be used to ensure the drugs suppressed VEBs as well.
It does no good to object that the CAST study happened nearly 40 years ago. The continued use of statins after the ALLHAT study in 2001 is a modern day examples of irrational prescription due to heavy promotion (Lenzer 2003).
Longino (2002) adds “tempered” to her earlier (1990) criterion of equality to ensure that authority is not doled out irrespective of training or track record. A member of the community can lose authority if, for example, they dogmatically adhere to their position in light of cogent criticism. It is also worth noting that in the ideal community, not only must opposing views be given a venue, but the community has a positive duty to “take active steps to ensure that alternative points of view are developed enough to be a source of criticism and new perspectives” (2002, p. 132).
For a full defense of veritistic value see pp. 87–99; for Goldman’s development of infospheres see Chapt. 6, esp. pp. 161–165.
For a full treatment of decision vectors, see chapter 4 of Solomon (2001).
Solomon classes an egocentric bias towards one’s own data as an empirical vector because it is preference for a theory on an empirical basis. In this case, recall that Winkle was one of the first to publish on arrhythmogenic effects and Morganroth was conducting research on using VEBs as a proxy for establishing the efficacy of antiarrhythmic drugs. Accordingly, the salience of their own data would be an empirical decision vector for each of their respective views. Incidentally, contrary to his portrayal by Moore (1995), my reading is that Morganroth was largely operating in good faith.
Which is not to say that this is what the analysis would in fact show, I mean to highlight here that Solomon’s view has the virtue of neither being naïve to the presence of industry funding nor too cynical to think that industry-funded research is never dispositive. Goldman’s (1999) view has this virtue as well, whereas the power imbalances created by industry seem to make it impossible to satisfy Longino’s (2002) account within the current system (see especially p. 131).
I would like to thank Manuela Fernández Pinto, Phyllis Illari, and an anonymous reviewer for pushing me on this point. While, the general trend within social epistemology has been a movement to examine particular cases which produce narrowly tailored normative suggestions, I believe that there is also philosophical work to be done that will apply to medical epistemology writ large (indeed, even industry-funded science generally). In part, this is because companies are using the same tactics across industrial sectors (White and Bero 2010).
For critiques of Longino with specific reference to commercial pressures in science see Biddle (2007), Jukola (2015), Fernández Pinto (2014). For Solomon’s emendation on her own view see Solomon (2015a). Solomon (2015b) has recently written extensively on medicine, but while a work in social epistemology, it does not draw heavily on social empiricism.
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Acknowledgements
Drafts of this paper have been circulating for four years now, which has left me with a long list of people who have each made it incrementally better. I am particularly grateful for the feedback and comments of Jeff Barrett, Nancy Cartwright, Sir Iain Chalmers, Christopher ChoGlueck, Joseph Gabriel, Manuela Fernández Pinto, Jonathan Fuller, Timothy Fuller, Phillip Holman, Mark Robinson, Kyle Stanford, Jacob Stegenga, and David Teira. I also benefitted from the audiences at SRPoiSE 2015, Medical Knowledge in a Social World, the Cologne Medical Epistemology Workshop, and the EBM+ consortium at the University of College London, especially from the helpful comments of Heather Douglas, Joyce Havstad, Miriam Solomon, Sven Bernecker, Brendan Clarke, Phyllis Illari, and Jon Williamson. I am also thankful for the opportunity afforded to me by Richard Price to hold a trial run of a “mega session” with a final draft of this paper on academia.edu and for the many thoughtful comments and corrections to embarrassing mistakes it received as a result. Though I reached out to her as a stranger, Dawn Altman was tremendously kind with her time, looking through her vast collection of images to locate the strip used in Fig. 3. Finally, I wish to thank the two anonymous reviewers for their extremely helpful referee reports and especially for their encouragement to elaborate a positive view, which now appears as Sect. 6. All remaining errors remain my own.
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Holman, B. Philosophers on drugs. Synthese 196, 4363–4390 (2019). https://doi.org/10.1007/s11229-017-1642-2
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DOI: https://doi.org/10.1007/s11229-017-1642-2