Causal Inference: IJE Special Issue

Papers from the December 2016 special issue of IJE are now all available online. Several are open access, and I attach these.

Philosophers who want to engage with real life science, on topics relating to causation, epidemiology, and medicine, will find these papers a great resource. So will epidemiologists and other scientists who want or need to reflect on causal inference. Most of the papers are not written by philosophers, and most do not start from standard philosophical starting points. Yet the topics are clearly philosophical. This collection would also form a great starting point for a doctoral research projects in various science-studies disciplines.

Papers 1 and 2 were first available in January. Two letters were written in response (being made available online around April) along with a response and I have included these in the list for completeness. The remaining papers were written during the course of 2016 and are now available. Many of the authors met at a Radcliffe Workshop in Harvard in December 2016. An account of that workshop may be forthcoming at some stage, but equally it may not, since not all of the participants felt that it was necessary to prolong the discussion or to share the outcomes of the workshop more widely. At some point I might simply write up my own account, by way of part-philosophical, part-sociological story.

  1. Causality and causal inference in epidemiology: the need for  a pluralistic approach‘ Jan P Vandenbroucke, Alex Broadbent and Neil Pearce. doi: 10.1093/ije/dyv341
  2. ‘The tale wagged by the DAG: broadening the scope of causal inference and explanation for epidemiology.’ Nancy Krieger and George Davey-Smith. doi: 10.1093/ije/dyw114
    1. Letter: Tyler J. VanderWeele, Miguel A. Hernán, Eric J. Tchetgen Tchetgen, and James M. Robins. Letter to the Editor. Re: Causality and causal inference in epidemiology: the need for a pluralistic approach.
    2. Letter: Arnaud Chiolero. Letter to the Editor. Counterfactual and interventionist approach to cure risk factor epidemiology.
    3. Letter: Broadbent, A., Pearce, N., and Vandenbroucke, J. Authors’ Reply to: VanderWeele et al., Chiolero, and Schooling et al.
  3. ‘Causal inference in epidemiology: potential outcomes, pluralism and peer review.’ Douglas L Weed. doi: 10.1093/ije/dyw229
  4. ‘On Causes, Causal Inference, and Potential Outcomes.’ Tyler VanderWeele. doi: 10.1093/ije/dyw230
  5. ‘Counterfactual causation and streetlamps: what is to be done?’ James M Robins and Michael B Weissman. doi: 10.1093/ije/dyw231
  6. ‘DAGs and the restricted potential outcomes approach are tools, not theories of causation.’ Tony Blakely, John Lynch and Rebecca Bentley. doi: 10.1093/ije/dyw228
  7. ‘The formal approach to quantitative causal inference in epidemiology: misguided or misrepresented?’ Rhian M Daniel, Bianca L De Stavola and Stijn Vansteelandt. doi: 10.1093/ije/dyw227
  8. Formalism or pluralism? A reply to commentaries on ‘Causality and causal inference in epidemiology.’ Alex Broadbent, Jan P Vandenbroucke and Neil Pearce. doi: 10.1093/ije/dyw298
  9. ‘FACEing reality: productive tensions between our epidemiological questions, methods and mission.’ Nancy Krieger and George Davey-Smith. doi: 10.1093/ije/dyw330

Epidemiology and Law: two publications

Recently published:

Forensic Epidemiology, Principles and Practice. 2016. Freeman M and Zeegers M (eds). Eslevier.

(I have a paper on causation and epidemiology.)

Also, previously online but now in print:

‘Tobacco and Epidemiology in Korea: old tricks, new answers?’ Broadbent A and Hwang Ss. Journal of Epidemiology and Community Health 2016;70:527-528. doi:10.1136/jech-2015-206567 [open access]

Paper: Causality and Causal Inference in Epidemiology: the Need for a Pluralistic Approach

Delighted to announce the online publication of this paper in International Journal of Epidemiology, with Jan Vandenbroucke and Neil Pearce: ‘Causality and Causal Inference in Epidemiology: the Need for a Pluralistic Approach

This paper has already generated some controversy and I’m really looking forward to talking about it with my co-authors at the London School of Hygiene and Tropical Medicine on 7 March. (I’ll also be giving some solo talks while in the UK, at Cambridge, UCL, and Oxford, as well as one in Bergen, Norway.)

The paper is on the same topic as a single-authored paper of mine published late 2015, ‘Causation and Prediction in Epidemiology: a Guide to the Methodological Revolution.‘ But it is much shorter, and nonetheless manages to add a lot that was not present in my sole-authored paper – notably a methodological dimension that, as a philosopher by training, I was ignorant. The co-authoring process was thus really rich and interesting for me.

It also makes me think that philosophy papers should be shorter… Do we really need the first 2500 words summarising the current debate etc? I wonder if a more compressed style might actually stimulate more thinking, even if the resulting papers are less argumentatively airtight. One might wonder how often the airtight ideal is achieved even with traditional length paper… Who was it who said that in philosophy, it’s all over by the end of the first page?

Paper – Tobacco in Korea

Alex Broadbent and Seung-sik Hwang, 2016. ‘Tobacco and epidemiology in Korea: old tricks, new answers?’ Journal of Epidemiology and Community Health doi:10.1136/jech-2015-206567.

Now available online first, open access.

For those at the recent CauseHealth workshop N=1, this relates to the same key topic (viz. the application of population evidence to an individual), but in the legal rather than clinical context.


Book: B Smart, “Concepts and Causes in the Philosophy of Disease”

Recently published with Palgrave Macmillan: Concepts and Causes in the Philosophy of Disease, by Benjamin Smart. A very interesting short book that aims to summarise and progress some of the central recent work in the philosophy of medicine, concerning the nature of health and disease, causality in medicine, the classification of diseases and the relation between medicine and public health.

On Amazon:

On the Palgrave site:

Tobacco and epidemiology in Korea: old tricks, new answers?

Today I participated in a seminar hosted by the National Health Insurance Service (NHIS) of Korea, which is roughly the equivalent of the NHS in the UK, although the health systems differ. The seminar concerned a recent lawsuit in which tobacco companies were sued by the NHIS for the costs of treating lung cancer patients. The suit is part of a larger drive to get a grip on smoking in Korea, where over 40% of males smoke, and a packet of 20 cigarettes costs 4500 Korean Won (about USD 4.10 or UKP 2.80). The NHIS recently suffered a blow at the Supreme Court, where the ruling was somewhat luke-warm about a causal link between smoking and lung cancer in general, and moreover argued that such a link would anyway fail to prove anything about the two specific plaintiffs in the case at hand.

I was struck by the familiarity of some of the arguments that are apparently being used by the tobacco companies. For example, the Supreme Court has been convinced that diseases come in two kinds, specific and non-specific, and that since lung-cancer is a non-specific disease, it is wrong to seek to apply measures of attributability (excess/attributable fraction, population excess/attributable fraction) at all.

This is reminiscent of the use of non-specificity in the 1950s, when it was seen as a problem for the causal hypothesis that smoking causes lung cancer. It also gives rise to a strategy which is legally sound but dubious from a public health perspective, namely, first going for lung cancer, and leaving other health-risks of smoking for later. This is legally sound because lung cancer exhibits the highest relative risk of the smoking-related diseases, and perhaps it is good PR too because cancer of any kind catches the imagination. But the health burden of lung cancer is low, even in a population where smoking is relatively prevalent, since lung cancer is a rare disease even among smokers.

The health burden of heart disease, at the other end of the spectrum, is very large, and even though smoking less than doubles this risk (RR about 1.7), the base rate of heart disease is so high that this amounts to a very significant public health problem. I do not know what the right response to this complex of problems is: clearly, high-profile court cases are have an impact that extends far beyond their outcome, and also the reason that people stop smoking, or accept legislation, need not be an accurate reflection of the true risks in order for those risks to be mitigated. (If you stop smoking to avoid lung cancer, you also avoid heart disease, which is a much better reason to stop smoking from the perspective of a rational individual motivated to avoid fatal disease.) Nonetheless I am struck by the way that legal and health policy objectives interact here.

I was also interested to hear that the case of McTear was a significant blow to the Korean case because of its findings about causality, which indeed are exactly those of the Korean case. That case is not well regarded in the UK, and not authoritative (being first instance), so it is interesting – and unfortunate – that it has had an effect here.

The event was an extremely good-spirited affair, and the other speakers had some interesting things to say. My book, in Korean, received a significant plug, not least, I suspect, because the audience not understanding much of my talk, were repeatedly referred to it for more detail. The most shocking thing about the event was to hear the same obfuscatory strategies that are now history in Europe and America being used, to good effect, by the very same companies in this part of the world. It is one thing to defend a case on grounds that one believes, but there is not anyone who still reasonably believes that smoking does not cause lung cancer, which seems to be the initial burden that plaintiffs in this sort of case need to prove. It is a bit like being asked to begin your case against a scaffolder who dropped a metal bar on your head with a proof of the law of gravity, and then being asked to prove that the general evidence concerning gravity proves that gravity was the cause in this particular case, given that not all downward motions are caused by gravity. – Not exactly like that, of course, but not exactly unlike, either.

On the positive side, I am hoping that a clear explanation of the reasoning behind the PC Inequality that I favour might help with the next stage of the case, although I am unclear what that stage might be.

Is consistency trivial in randomized controlled trials?

Here are some more thoughts on Hernan and Taubman’s famous 2008 paper, from a chapter I am finalising for the epidemiology entry in a collection on the philosophy of medicine. I realise I have made a similar point in an earlier post on this blog, but I think I am getting closer to a crisp expression. The point concerns the claimed advantage of RCTs for ensuring consistency. Thoughts welcome!

Hernan and Taubman are surely right to warn against too-easy claims about “the effect of obesity on mortality”, when there are multiple ways to reduce obesity, each with different effects on mortality, and perhaps no ethically acceptable way to bring about a sudden change in body mass index from say 30 to 22 (Hernán and Taubman 2008, 22). To this extent, their insistence on assessing causal claims as contrasts to well-defined interventions is useful.

On the other hand, they imply some conclusions that are harder to accept. They suggest, for example, that observational studies are inherently more likely to suffer from this sort of difficulty, and that experimental studies (randomized controlled trials) will ensure that interventions are well-specified. They express their point using the technical term “consistency”:

consistency… can be thought of as the condition that the causal contrast involves two or more well-defined interventions. (Hernán and Taubman 2008, S10)

They go on:

…consistency is a trivial condition in randomized experiments. For example, consider a subject who was assigned to the intervention group … in your randomized trial. By definition, it is true that, had he been assigned to the intervention, his counterfactual out- come would have been equal to his observed outcome. But the condition is not so obvious in observational studies. (Hernán and Taubman 2008, s11)

This is a non-sequitur, however, unless we appeal to a background assumption that an intervention—something that an actual human investigator actually does—is necessarily well-defined. Without this assumption, there is nothing to underwrite the claim that “by definition”, if a subject actually assigned to the intervention had been assigned to the intervention, he would have had the outcome that he actually did have.

Consider the intervention in their paper, one hour of strenuous exercise per day. “Strenuous exercise” is not a well-defined intervention. Weightlifting? Karate? Swimming? The assumption behind their paper seems to be that if an investigator “does” an intervention, it is necessarily well-defined; but on reflection this is obviously not true. An investigator needs to have some knowledge of which features of the intervention might affect the outcome (such as what kind of exercise one performs), and thus need to be controlled, and which don’t (such as how far west of Beijing one lives). Even randomization will not protect against confounding arising from preference for a certain type of exercise (perhaps because people with healthy hearts are predisposed both to choose running and to live longer, for example), unless one knows to randomize the assignment of exercise-types and not to leave it to the subjects’ choice.

This is exactly the same kind of difficulty that Hernan and Taubman press against observational studies. So the contrast they wish to draw, between “trivial” consistency in randomized trials and a much more problematic situation in observational studies, is a mirage. Both can suffer from failure to define interventions.