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How causal are microbiomes? A comparison with the Helicobacter pylori explanation of ulcers

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Abstract

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made.

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Notes

  1. E.g., https://www.viome.com/services/; https://www.the-scientist.com/notebook/athletes-microbiomes-differ-from-nonathletes-31428; https://kellybroganmd.com/depression-starts-in-your-gut/; https://www.marsvenus.com/blog/john-gray/staying-happy-with-a-healthy-microbiome (accessed October 2018).

  2. We are grateful to John Matthewson for suggesting this comparison.

  3. Although some animals—especially gerbils—now model gastric symptoms concomitant with H. pylori infections, they are argued to be ‘inadequate’ models because H. pylori alone cannot produce human-like symptoms (e.g., Chen et al. 2007).

  4. Typically, more distal causes will have less specificity than more proximate ones, simply because the longer a causal chain, the more associated causes would need to be mapped to unique values of the effect.

  5. These issues point to a possible interpretation of Koch’s postulates as being about necessary and sufficient conditions. While they are sometimes interpreted this way (e.g., Susser 1991), this is not what is claimed under an interventionist account of the postulates (Ross and Woodward 2016).

  6. Stability is also related to proximity. The more proximal a pair of cause and effect variables, the fewer causal links or steps between them. The fewer causal links there are, the fewer background conditions (per causal link) can perturb the total causal relationship. Generally, therefore, distal causal relationships are considered less stable than proximal ones (Woodward 2010: 294).

  7. Note that this sense of proportionality can apply to both the selection of causes and effects. Whether or not proportionality is used to select causes or effects depends upon the explanatory project: whether it is focused on explaining what causes an outcome, or on explaining what kinds of outcomes are produced by a particular factor. When selecting the most appropriate effect, proximity is also a good indicator of proportionality. This is because proximate effects often encompass the entire causal output, whereas more distal effects are parsed into different variables, some of which have other contributing causes influencing them.

  8. This sense of proportionality can also be applied to both causes and effects, again depending on the explanatory project. When trying to understand the effects of a particular factor, effects may be invoked that are inappropriately broad or narrow, such as claiming that H. pylori causes illness, rather than more exactly ulcers.

  9. Philosopher Paul Thagard (1998) has long argued that the interacting causal factors in the H. pylori-ulcer explanation make a ‘causal network’ explanation more effective than a single-cause explanation.

  10. This is generally due to pragmatic factors such as ease of intervention. While diet may be a distal cause, it is often easier to manipulate compared to more proximate physiological factors.

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Acknowledgements

We thank Brett Calcott, Austen Ganley, David Kelley, John Matthewson, Sam Woolley, and the audience at PBDB 12 who provided crucial feedback on earlier versions of this manuscript, and acknowledge Pierrick Bourrat for earlier discussion of some of these ideas.

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Authors and Affiliations

  1. Department of Philosophy and Charles Perkins Centre, University of Sydney, Sydney, Australia

    Kate E. Lynch

  2. Department of Biological Sciences, Macquarie University, Sydney, Australia

    Kate E. Lynch

  3. Philosophy, School of Humanities, University of Auckland, Auckland, New Zealand

    Emily C. Parke

  4. School of History and Philosophy of Science, University of Sydney, Sydney, Australia

    Maureen A. O’Malley

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  1. Kate E. Lynch
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Correspondence to Kate E. Lynch.

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Lynch, K.E., Parke, E.C. & O’Malley, M.A. How causal are microbiomes? A comparison with the Helicobacter pylori explanation of ulcers. Biol Philos 34, 62 (2019). https://doi.org/10.1007/s10539-019-9702-2

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