Federica Russo

The advantage of examining causality from the perspective of modelling is thus that it puts us naturally closer to the practice of the sciences. This means being able to set up an interdisciplinary dialogue that contrasts and compares modelling practices in different fields, say economics and biology, medicine and statistics, climate change and physics. It also means that it helps philosophers looking for questions that go beyond the narrow ‘what-is-causality’ or ‘what-are-relata’ and thus puts causality right at the centre of a complex crossroad: epistemology/methodology, metaphysics, politics/ethics. This special issue collects nine papers that touch upon various scientific fields, from system biology to medicine to quantum mechanics to economics, and different questions, from explanation and prediction to the role of both true and false assumptions in modelling.

The anti-causal prophecies of last century have been disproved. Causality is neither a ‘relic of a bygone’ nor ‘another fetish of modern science’; it still occupies a large part of the current debate in philosophy and the sciences. This investigation into causal modelling presents the rationale of causality, i.e. the notion that guides causal reasoning in causal modelling. It is argued that causal models are regimented by a rationale of variation, nor of regularity neither invariance, thus breaking down the dominant Human paradigm. The notion of variation is shown to be embedded in the scheme of reasoning behind various causal models: e.g. Rubin’s model, contingency tables, and multilevel analysis. It is also shown to be latent – yet fundamental – in many philosophical accounts. Moreover, it has significant consequences for methodological issues: the warranty of the causal interpretation of causal models, the levels of causation, the characterisation of mechanisms, and the interpretation of probability. This book offers a novel philosophical and methodological approach to causal reasoning in causal modelling and provides the reader with the tools to be up to date about various issues causality rises in social science.

One way social scientists explain phenomena is by building structural models. These models are explanatory insofar as they manage to perform a recursive decomposition on an initial multivariate probability distribution, which can be interpreted as a mechanism. Explanations in social sciences share important aspects that have been highlighted in the mechanisms literature. Notably, spelling out the functioning the mechanism gives it explanatory power. Thus social scientists should choose the variables to include in the model on the basis of their function in the mechanism. This paper examines the notion of ‘function’ within structural modelling. We argue that ‘functions’ ought to be understood as the theoretical underpinnings of the causes, namely as the role that causes play in the functioning of the mechanism

Epistemic diversity is the ability or possibility of producing diverse and rich epistemic apparati to make sense of the world around us. In this paper we discuss whether, and to what extent, different conceptions of knowledge—notably as ‘justified true belief’ and as ‘distributed and embodied cognition’—hinder or foster epistemic diversity. We then link this discussion to the widespread move in science and philosophy towards monolingual disciplinary environments. We argue that English, despite all appearance, is no Lingua Franca, and we give reasons why epistemic diversity is also deeply hindered is monolingual contexts. Finally, we sketch a proposal for multilingual academia where epistemic diversity is thereby fostered.

It is widely agreed that social factors are related to health outcomes: much research served to establish correlations between classes of social factors on the one hand and classes of disease on the other hand. However, why and how social factors are an active part in the aetiology of disease development is something that is gaining attention only recently in the health sciences and in the medical humanities. In this paper, we advance the view that, just as bio-markers help trace the causal continuum from exposure to disease development at the biological level, socio-markers ought to be introduced and studied in order to trace the social continuum from exposure to disease development. We explain how socio-markers differ from social indicators and how they can be used in combination with bio-markers in order to reconstruct the mixed mechanisms of health and disease, namely mechanisms in which both biological and social factors have an active causal role.

In the last decades, Systems Biology (including cancer research) has been driven by technology, statistical modelling and bioinformatics. In this paper we try to bring biological and philosophical thinking back. We thus aim at making diferent traditions of thought compatible: (a) causality in epidemiology and in philosophical theorizing—notably, the “sufcient-component-cause framework” and the “mark transmission” approach; (b) new acquisitions about disease pathogenesis, e.g. the “branched model” in cancer, and the role of biomarkers in this process; (c) the burgeoning of omics research, with a large number of “signals” and of associations that need to be interpreted. In the paper we summarize frst the current views on carcinogenesis, and then explore the relevance of current philosophical interpretations of “cancer causes”. We try to ofer a unifying framework to incorporate biomarkers and omic data into causal models, referring to a position called “evidential pluralism”. According to this view, causal reasoning is based on both “evidence of diference-making” (e.g. associations) and on “evidence of underlying biological mechanisms”. We conceptualize the way scientists detect and trace signals in terms of information transmission, which is a generalization of the mark transmission theory developed by philosopher Wesley Salmon. Our approach is capable of helping us conceptualize how heterogeneous factors such as micro and macro-biological and psycho-social—are causally linked. This is important not only to understand cancer etiology, but also to design public health policies that target the right causal factors at the macro-level.

Technologies have always been bearers of profound changes in science, society, and any other aspect of life. The latest technological revolution—the digital revolution—is no exception in this respect. This paper presents the revolution brought about by digital technologies through the lenses of a specific approach: the philosophy of information. It is argued that the adoption of an informational approach helps avoiding utopian or dystopian approaches to technology, both expressions of technological determinism. Such an approach provides a conceptual framework able to address the ethical challenges that digital technologies pose, without getting stuck in the dichotomous thinking of technological determinism, and to bring together ethics, ontology, and epistemology into a coherent account.

Inconsistencies between scientific theories have been studied, by and large, from the perspective of paraconsistent logic. This approach considered the formal properties of theories and the structure of inferences one can legitimately draw from theories. However, inconsistencies can be also analysed from the perspective of modelling practices, in particular how modelling practices may lead scientists to form opinions and attitudes that are different, but not necessarily inconsistent. In such cases, it is preferable to talk about disagreement, rather than inconsistency. Disagreement may originate in, or concern, a number of epistemic, socio-political or psychological factors. In this paper, we offer an account of the ‘loci and reasons’ for disagreement at different stages of the scientific process. We then present a controversial episode in the health sciences: the studies on hypercholesterolemia. The causes and effects of high levels of cholesterol in blood have been long and hotly debated, to the point of deserving the name of ‘cholesterol wars’; the debate, to be sure, isn’t settled yet. In this contribution, we focus on some selected loci and reasons for disagreement that occurred between 1920 and 1994 in the studies on hypercholesterolemia. We hope that our analysis of ‘loci and reasons’ for disagreement may shed light on the cholesterol wars, and possibly on other episodes of scientific disagreement.

Large part of contemporary science is in fact technoscience, in the sense that it crucially depends on several technologies for the generation, collection, and analysis of data. This prompts a re-examination of the relations between science and technologies. In this essay, I advance the view that we’d better move beyond the ‘subordination view’ and the ‘instrumental’ view. The first aims to establish the primacy of science over technology, and the second uses technology instrumentally to support a realist position about theoretical entities. I suggest that we should instead concentrate on how science and technology interact. This will reveal that technology has a poietic character, namely it actively partakes in the production of knowledge. But this poietic character can only be understood within the cognitive activity of scientific communities. Current research in molecular epidemiology, notably the projects funded within the ‘European exposome initiative’, serves as a motivation for such discussion and as an illustration of the claims made.

Causal assessment is the problem of establishing whether a relation between (variable) X and (variable) Y is causal. This problem, to be sure, is widespread across the sciences. According to accredited positions in the philosophy of causality and in social science methodology, invariance under intervention provides the most reliable test to decide whether X causes Y. This account of invariance (under intervention) has been criticised, among other reasons, because it makes manipulations on the putative causal factor fundamental for the causal methodology; consequently, the argument goes, the account is ill-suited to those contexts where manipulations are not performed, for instance, the social sciences. The article aims to extend the account of invariance (under intervention), in a way that manipulations on the putative causal factors are not methodologically fundamental, and yet invariance remains key for causal assessment both in experimental and non-experimental contexts

The paper addresses the question of how different types of evidence ought to inform public health policy. By analysing case studies on obesity, the paper draws lessons about the different roles that different types of evidence play in setting up public health policies. More specifically, it is argued that evidence of difference-making supports considerations about ‘what works for whom in what circumstances’, and that evidence of mechanisms provides information about the ‘causal pathways’ to intervene upon

The paper examines definitions of ‘cause’ in the epidemiological literature. Those definitions all describe causes as factors that make a difference to the distribution of disease or to individual health status. In the philosophical jargon, causes in epidemiology are difference-makers. Two claims are defended. First, it is argued that those definitions underpin an epistemology and a methodology that hinge upon the notion of variation, contra the dominant Humean paradigm according to which we infer causality from regularity. Second, despite the fact that causes be defined in terms of ‘difference-making’, this cannot fixes the causal metaphysics. Causality in epidemiology ought to be interpreted according to the epistemic theory. In this approach relations are deemed causal depending on the evidence and on the available methods. Indeed, evidence to establish causal claims requires difference-making considerations; furthermore, those definitions of cause reflect the ‘variational’ epistemology and methodology of epidemiology.

Current research in molecular epidemiology uses biomarkers to model the different disease phases from environmental exposure, to early clinical changes, to development of disease. The hope is to get a better understanding of the causal impact of a number of pollutants and chemicals on several diseases, including cancer and allergies. In a recent paper Russo and Williamson address the question of what evidential elements enter the conceptualisation and modelling stages of this type of biomarkers research. Recent research in causality has examined Ned Hall’s distinction between two concepts of causality: production and dependence. In another recent paper, Illari examined the relatively under-explored production approach to causality, arguing that at least one job of an account of causal production is to illuminate our inferential practices concerning causal linking. Illari argued that an informational account solves existing problems with traditional accounts. This paper follows up this previous work by investigating the nature of the causal links established in biomarkers research. We argue that traditional accounts of productive causality are unable to provide a sensible account of the nature of the causal link in biomarkers research, while an informational account is very promising

Econometrics applies statistical methods to study economic phenomena. Roughly, by means of equations, econometricians typically account for the response variable in terms of a number of explanatory variables. The question arises under what conditions econometric models can be given a causal interpretation. By drawing the distinction between associational models and causal models, the paper argues that a proper use of background knowledge, three distinct types of assumptions (statistical, extra-statistical, and causal), and the hypothetico-deductive methodology provide sufficient conditions for a causal interpretation of econometric models.

Evidence and CausalityCausality is a vibrant and thriving topic in philosophy of science. It is closely related to many other challenging scientific concepts, such as probability and mechanisms, which arise in many different scientific contexts, in different fields. For example, probability and mechanisms are relevant to both causal inference (finding out what causes what) and causal explanation (explaining how a cause produces its effect). They are also of interest to fields as diverse as astrophysics, biochemistry, biomedical and social sciences. At the same time, there has been an explosion of interest in evidence, most obviously in biomedical contexts with the rise of ‘evidence-based medicine’, but also elsewhere, such as in social science. What is evidence? How do we decide what our best sources of evidence are?This topos examines the relation between causality and evidence in different scientific areas. This involves questions about the foundations of the sciences, e.g. what is e ..

In social science, one objection to causal analysis is that the assumption of the closure of the system makes the analysis too narrow in scope, that is, it considers only 'closed' and 'hermetic' systems thus neglecting many other external influences. On the contrary, system analysis deals with complex structures where every element is interrelated with everything else in the system. The question arises as to whether the two approaches can be compatible and whether causal analysis can be integrated into the broader framework of system analysis. This article attempts a negative answer on the grounds of fundamental differences in their assumptions and suggests using system analysis as a post-hoc comparative tool

For my own work in philosophy of science, I find of utmost importance to exchange ideas with practicing scientists. The author of this book, Peter Rabins, is a medical doctor specializing in psychiatry. With much regret, I have not met Professor Rabins in person yet, but I’m hoping to do so soon, as his recent book The Why of Things: Causality in Science, Medicine, and Life has been a most enjoyable read and source of inspiration. The book constitutes a noteworthy addition to Professor Rabins’ academic production—which has been mainly in the area of medicine and psychiatry—as it goes to the heart of two deep, everlasting philosophical quarrels: causation and explanation.The Why of Things is written with expertise, the expertise of a doctor that devoted time and effort to reflecting upon the philosophical underpinnings of an important aspect of his own profession : how to establish causal relations and to provide causal explanations. This is not a ‘ ..

The Agency and the Manipulability theory of causation, in spite of significant differences, share at least three claims. First, that manipulation – roughly, that by manipulating causes we bring about effects – is a central notion for causation; second, that such a notion of manipulation allows a reductive – i.e. general and comprehensive – account of causation; third, that this view has its forefathers in the works of Collingwood, Gasking and von Wright. This paper mainly challenges the third claim and argues that the misreading of those authors leads to a more dangerous consequence: a confusion between epistemological, metaphysical and methodological issues about causation

Causal analysis in the social sciences takes advantage of a variety of methods and of a multi-fold source of information and evidence. This pluralistic methodology and source of information raises the question of whether we should accordingly have a pluralistic metaphysics and epistemology. This paper focuses on epistemology and argues that a pluralistic methodology and evidence don’t entail a pluralistic epistemology. It will be shown that causal models employ a single rationale of testing, based on the notion of variation. Further, I shall argue that this monistic epistemology is also involved in alternative philosophical theories of causation