Check the entry on Pearl’s blog which includes a write-up provided by the organisers
Video of the event is available too
Check the entry on Pearl’s blog which includes a write-up provided by the organisers
Video of the event is available too
Freddie Sayers of Unherd interviews Michael Levitt (a Nobel-prize-winning non-epidemiologist) on a purely statistical observations of the pattern of the epidemic. Given that the only way we have of measuring effectiveness of government interventions is statistical, that’s interesting. The fun stuff (epidemiological and statistical) comes in deciding whether the correlation is causal. But there’s been no progress with that, in my opinion; in fact for me it is here that the epidemiological profession has disappointed me – it is at if epidemiology has forgotten everything it ever taught itself about causal inference. Against that background, this is ought to give pause for thought.
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.
Forensic Epidemiology, Principles and Practice. 2016. Freeman M and Zeegers M (eds). Eslevier. http://store.elsevier.com/Forensic-Epidemiology/isbn-9780124046443/
(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. http://jech.bmj.com/content/70/6/527.full doi:10.1136/jech-2015-206567 [open access]
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?
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.
Next week I’ll be visiting America to talk in Pittsburgh, Richmond, and twice at Tufts. I do not expect audience overlap so I’ll give the same talk in all venues, with adjustments for audience depending on whether it’s primarily philosophers or epidemiologists I’m talking to. The abstract is below. I haven’t got a written version of the paper that I can share yet but would of course welcome comments at this stage.
Attribution, prediction, and the causal interpretation problem in epidemiology
In contemporary epidemiology, there is a movement, part theoretical and part pedagogical, attempting to discipline and clarify causal thinking. I refer to this movement as the Potential Outcomes Aproach (POA). It draws inspiration from the work of Donald Ruben and, more recently, Judea Pearl, among others. It is most easily recognized by its use of Directed Acycylic Graphs (DAGs) to describe causal situations, but DAGs are not the conceptual basis of the POA in epidemiology. The conceptual basis (as I have argued elsewhere) is a commitment to the view that the hallmark of a meaningful causal claim is that they can be used to make predictions about hypothetical scenarios. Elsewhere I have argued that this commitment is problematic (notwithstanding the clear connections with counterfactual, contrastive and interventionist views in philosophy). In this paper I take a more constructive approach, seeking to address the problem that troubles advocates of the POA. This is the causal interpretation problem (CIP). We can calculate various quantities that are supposed to be measures of causal strength, but it is not always clear how to interpret these quantities. Measures of attributability are most troublesome here, and these are the measures on which POA advocates focus. What does it mean, they ask, to say that a certain fraction of population risk of mortality is attributable to obesity? The pre-POA textbook answer is that, if obesity were reduced, mortality would be correspondingly lower. But this is not obviously true, because there are methods for reducing obesity (smoking, cholera infection) which will not reduce mortality. In general, say the POA advocates, a measure of attributability tells us next to nothing about the likely effect of any proposed public health intervention, rendering these measures useless, and so, for epidemiological purposes, meaningless. In this paper I ask whether there is a way to address and resolve the causal interpretation problem without resorting to the extreme view that a meaningful causal claim must always support predictions in hypothetical scenarios. I also seek connections with the notorious debates about heritability.
AID Forum: “Epidemiology: an approach with multidisciplinary applicability”
(Unfamiliar with AID forum? For the very idea and the programme of Agora for Interdisciplinary Debate, see www.helsinki.fi/tint/aid.htm)
Mervi Toivanen (economics, Bank of Finland)
Jaakko Kaprio (genetic epidemiology, U of Helsinki)
Alex Broadbent (philosophy of science, U of Johannesburg)
Moderated by Academy professor Uskali Mäki
TIME AND PLACE:
Monday 9 February, 16:15-18
University Main Building, 3rd Floor, Room 5
TOPIC: What do diseases and financial crises have in common?
Epidemiology has traditionally been used to model the spreading of diseases in populations at risk. By applying parameters related to agents’ responses to infection and network of contacts it helps to study how diseases occur, why they spread and how one could prevent epidemic outbreaks. For decades, epidemiology has studied also non-communicable diseases, such as cancer, cardiovascular disease, addictions and accidents. Descriptive epidemiology focuses on providing accurate information on the occurrence (incidence, prevalence and survival) of the condition. Etiological epidemiology seeks to identify the determinants be they infectious agents, environmental or social exposures, or genetic variants. A central goal is to identify determinants amenable to intervention, and hence prevention of disease.
There is thus a need to consider both reverse causation and confounding as possible alternative explanations to a causal one. Novel designs are providing new tools to address these issues. But epidemiology also provides an approach that has broad applicability to a number of domains covered by multiple disciplines. For example, it is widely and successfully used to explain the propagation of computer viruses, macroeconomic expectations and rumours in a population over time.
As a consequence, epidemiological concepts such as “super-spreader” have found their way also to economic literature that deals with financial stability issues. There is an obvious analogy between the prevention of diseases and the design of economic policies against the threat of financial crises. The purpose of this session is to discuss the applicability of epidemiology across various domains and the possibilities to mutually benefit from common concepts and methods.
1. Why is epidemiology so broadly applicable?
2. What similarities and differences prevail between these various disciplinary applications?
3. What can they learn from one another, and could the cooperation within disciplines be enhanced?
4. How could the endorsement of concepts and ideas across disciplines be improved?
5. Can epidemiology help to resolve causality?
Alex Broadent, Philosophy of Epidemiology (Palgrave Macmillan 2013)
Alex Broadbent’s blog on the philosophy of epidemiology:
Rothman KJ, Greenland S, Lash TL. Modern Epidemiology 3rd edition.
Lippincott, Philadelphia 2008
D’Onofrio BM, Lahey BB, Turkheimer E, Lichtenstein P. Critical need for family-based, quasi-experimental designs in integrating genetic and social science research. Am J Public Health. 2013 Oct;103 Suppl 1:S46-55. doi:10.2105/AJPH.2013.301252.
Taylor, AE, Davies, NM, Ware, JJ, Vanderweele, T, Smith, GD & Munafò, MR 2014, ‘Mendelian randomization in health research: Using appropriate genetic variants and avoiding biased estimates’. Economics and Human Biology, vol 13., pp. 99-106
Engholm G, Ferlay J, Christensen N, Kejs AMT, Johannesen TB, Khan S, Milter MC, Ólafsdóttir E, Petersen T, Pukkala E, Stenz F, Storm HH. NORDCAN: Cancer Incidence, Mortality, Prevalence and Survival in the Nordic Countries, Version 7.0 (17.12.2014). Association of the Nordic Cancer Registries. Danish Cancer Society. Available from http://www.ancr.nu.
Andrew G. Haldane, Rethinking of financial networks; Speech by Mr Haldane, Executive Director, Financial Stability, Bank of England, at the Financial Student Association, Amsterdam, 28 April 2009: http://www.bis.org/review/r090505e.pdf
Antonios Garas et al., Worldwide spreading of economic crisis: http://iopscience.iop.org/1367-2630/12/11/113043/pdf/1367-2630_12_11_113043.pdf
Christopher D. Carroll, The epidemiology of macroeconomic expectations: http://www.econ2.jhu.edu/people/ccarroll/epidemiologySFI.pdf
Hernan, VanderWeele, and others argue that causation (or a causal question) is well-defined when interventions are well-specified. I take this to be a sort of methodological axiom of the approach.
But what is a well-specified intervention?
Consider an example from Hernan & Taubman’s influential 2008 paper on obesity. In that paper, BMI is shown up as failing to correspond to a well-specified intervention; better-specifed interventions include one hour of strenuous physical exercise per day (among others).
But what kind of exercise? One hour of running? Powerlifting? Yoga? Boxing?
It might matter – it might turn out that, say, boxing and running for an hour a day reduce BMI by similar amounts but that one of them is associated with longer life. Or it might turn out not to matter. Either way, it would be a matter of empirical inquiry.
This has two consequences for the mantra that well-defined causal questions require well-specified interventions.
First, as I’ve pointed out before on this blog, it means that experimental studies don’t necessarily guarantee well-specified interventions. Just because you can do it doesn’t mean you know what you are doing. The differences you might think don’t matter might matter: different strains of broccoli might have totally different effects on mortality, etc.
Second, more fundamentally, it means that the whole approach is circular. You need a well-specified intervention for a good empirical inquiry into causes and you need good empirical inquiry into causes to know whether your intervention is well-specified.
To me this seems to be a potentially fatal consequence for the claim that well-defined causal questions require well-specified interventions. For if that were true, we would be trapped in a circle, and could never have any well-specified interventions, and thus no well-defined causal questions either. Therefore either we really are trapped in that circle; or we can have well-defined causal questions, in which case, it is false that these always require well-specified interventions.
This is a line of argument I’m developing at present, inspired in part by Vandebroucke and Pearce’s critique of the “methodological revolution” at the recent WCE 2014 in Anchorage. I would welcome comments.
Perhaps an odd thing to do, but I’m posting the abstracts of my two next talks, which will also become papers. Any offers to discuss/read welcome!
The talks will be at Rhodes on 1 and 3 October. I’ll probably deliver a descendant of one of them at the Cambridge Philosophy of Science Seminar on 3 December, and may also give a very short version of 1 at the World Health Summit in Berlin on 22 Oct.
1. Causation and Prediction in Epidemiology
There is an ongoing “methodological revolution” in epidemiology, according to some commentators. The revolution is prompted by the development of a conceptual framework for thinking about causation called the “potential outcomes approach”, and the mathematical apparatus of directed acyclic graphs that accompanies it. But once the mathematics are stripped away, a number of striking assumptions about causation become evident: that a cause is something that makes a difference; that a cause is something that humans can intervene on; and that epidemiologists need nothing more from a notion of causation than picking out events satisfying those two criteria. This is especially remarkable in a discipline that has variously identified factors such as race and sex as determinants of health. In this talk I seek to explain the significance of this movement in epidemiology, separate its insights from its errors, and draw a general philosophical lesson about confusing causal knowledge with predictive knowledge.
2. Causal Selection, Prediction, and Natural Kinds
Causal judgements are typically – invariably – selective. We say that striking the match caused it to light, but we do not mention the presence of oxygen, the ancestry of the striker, the chain of events that led to that particular match being in her hand at that time, and so forth. Philosophers have typically but not universally put this down to the pragmatic difficulty of listing the entire history of the universe every time one wants to make a causal judgement. The selective aspect of causal judgements is typically thought of as picking out causes that are salient for explanatory or moral purposes. A minority, including me, think that selection is more integral than that to the notion of causation. The difficulty with this view is that it seems to make causal facts non-objective, since selective judgements clearly vary with our interests. In this paper I seek to make a case for the inherently selective nature of causal judgements by appealing to two contexts where interest-relativity is clearly inadequate to fully account for selection. Those are the use of causal judgements in formulating predictions, and the relation between causation and natural kinds.