Horizontal persistence and the complexity hypothesis Abstract This paper investigates the complexity hypothesis in microbial evolutionary genetics from a philosophical vantage. This hypothesis, in its current version, states that genes with high connectivity (more functional connections to other genes) are likely to be resistant to being horizontally transferred. We defend four claims. (1) There is an important distinction between two different ways in which a gene family can persist: vertically and horizontally. There is a trade-off between these two modes of persistence, such that a gene better at achieving one will be worse at achieving the other. (2) At least some genes are likely to experience selection favoring increased transferability. One consequence of this can be encapsulated as the “simplicity hypothesis”: horizontally persisting genes will experience selection favoring reduced connectivity. (3) In order to make sense of the simplicity hypothesis, we need to consider evolutionary populations that transcend species boundaries. Vertical and horizontal persistence are therefore not two competing ways of succeeding at the same game, but involve playing two different games altogether. (4) The complexity hypothesis can be understood in terms of two related notions: entrenchment and Cuvierian functionalism. This framing reveals previously unrecognized and philosophically interesting connections between reasoning about deep conservation and horizontal transfer.

A dual decomposition strategy of both microbial and phenotypic components for a better understanding of causal claims Abstract In our commentary on Lynch et al.’s target paper (Biol Philos, 2019. https://doi.org/10.1007/s10539-019-9702-2), we focus on decomposition as a research strategy. We argue that not only the presumptive microbial causes but also their supposed phenotypic effects need to be decomposed relative to each other. Such a dual decomposition strategy ought to improve the way in which causal claims in microbiome research can be made and understood.

Mental machines Abstract Cognitive neuroscientists are turning to an increasingly rich array of neurodynamical systems to explain mental phenomena. In these explanations, cognitive capacities are decomposed into a set of functions, each of which is described mathematically, and then these descriptions are mapped on to corresponding mathematical descriptions of the dynamics of neural systems. In this paper, I outline a novel explanatory schema based on these explanations. I then argue that these explanations present a novel type of dynamicism for the philosophy of mind and neuroscience, componential dynamicism, that focuses on the parts of cognitive systems that fill certain functional roles in producing cognitive phenomena.

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

Why expect causation at all? A pessimistic parallel with neuroscience Abstract In their target article, Lynch, Parke, and O’Malley argue against the quick application of causal, interventionist explanatory frameworks to microbiomes and their purported role in many disparate states, from obesity to anxiety. I think the authors have undersold the force of their argument. A careful consideration of the scope of their claims, made easier by a parallel drawn from the history of explanation in neuroscience, yields a productive pessimism: that causal explanations likely operate at the wrong level of analysis for dynamic, distributed, Quineian entities like the microbiome. That is, we shouldn’t expect causal explanations for microbiomes at all—and this includes the authors’ own “microbiome success story” of C. difficile. Neuroscience, with its own computationally challenging, dynamic entity—the brain—may provide lessons for how to approach something like predictive control over the microbiome.

The problem of mooted models for analyses of microbiome causality Abstract Lynch, Parke, and O’Malley highlight the need for better evaluative criteria for causal explanations in microbiome research. They propose new interventionist criteria, show that paradigmatic examples of microbiome explanations are flawed using those criteria, and suggest numerous ways microbiome explanations can be improved. While we endorse their primary criticisms and suggestions for improvements in microbiome research, we make several observations regarding the use of mooted causal models in microbiome research that have significant implications for their overall argument. In sum, we contend that their critique is too modest and that even flawed causal inferences like those they criticize can be valuable for generating better causal models and evaluating explanatory outcomes in individual cases.

Can communities cause? Abstract Lynch et al. (Biol Philos, 2019) propose an extremely useful framework to assess microbiome research. By utilising advances in the causation literature, they argue that many of the claims in microbiome research are ‘weak or misleading’ as these claims lack stability, specificity, or proportionality. In the final paragraph before the conclusion they entertain and rapidly dismiss the ‘ecological version’ of microbiomes, in which microbiome properties are emergent from their constituent populations and can fulfil Koch’s postulates. I assess the possibility of microbiomes having emergent causal efficacy on host health and suggest they can.

Commentary on ‘How causal are microbiomes?’

Commentary on Kate E. Lynch, Emily C. Parke, and Maureen A. O’Malley: ‘How Causal are Microbiomes? A Comparison with the Helicobacter pylori Explanation of Ulcers’ Abstract This commentary focuses on the authors’ treatment of Koch’s postulates. It argues in favour of a modification of Koch’s postulates and their analysis in terms of necessary and sufficient conditions. This leads to a criticism of the authors’ treatment of the C. difficile case, and to query the need for the criteria of specificity and proportionality.

Trojan Horses and Black Queens: ‘causal core’ explanations in microbiome research Abstract Lynch et al., in an article in this issue, argue that an entire microbiome is rarely, if ever, the right target of analysis for causal explanations in microbiome research. They argue, using interventionist criteria of proportionality, specificity and stability, for restricting causal claims to the smallest subset of microbes—a causal core—that generate the effect of interest. A further question remains: what kind of interactions generate a consortium of microbes that can operate as causal agents in this manner? Here I introduce two possible kinds of such consortia: ‘trojan horses’ and ‘syntrophic’ individuals.