Federica Russo

The experimental revolution in the social sciences is one of the most significant methodological shifts undergone by the field since the ‘quantitative revolution’ in the nineteenth century. One of the often valued features of social science experimentation is precisely the fact that there are clear methodological rules regarding hypothesis testing that come from the methods of the natural sciences and from the methodology of RCTs in the biomedical sciences, and that allow for the adjudication among contentious causal claims. We examine critically this claim and argue that some current understandings of the practices that surround social science experimentation overestimate the degree to which experiments can actually fulfil this role as “objective” adjudicators, by neglecting the importance of shared background knowledge or assumptions and of consensus regarding the validity of the constructs involved in an experiment. We take issue with the way the distinction between internal and external validity is often used to comment on the inferential import of experiments, used both among practitioners and among philosophers of science. We describe the ways in which the more common use of the internal/external distinction differs from Cook and Campbell’s original methodological project, in which construct validity and the four-fold validity typology were all important in assessing the inferential import of experiments. We argue that the current uses of the labels internal and external, as applied to experimental validity, help to encroach a simplistic view on the inferential import of experiments that, in turn, misrepresents their capacity to provide objective knowledge about the causal relations between variables.

COVID-19 has revealed that science needs to learn how to better deal with the irreducible uncertainty that comes with global systemic risks as well as with the social responsibility of science towards the public good. Further developing the epistemological principles of new theories and experimental practices, alternative investigative pathways and communication, and diverse voices can be an important contribution of history and philosophy of science and of science studies to ongoing transformations of the scientific enterprise.

Critical Data Studies explore the unique cultural, ethical, and critical challenges posed by Big Data. Rather than treat Big Data as only scientifically empirical and therefore largely neutral phenomena, CDS advocates the view that Big Data should be seen as always-already constituted within wider data assemblages. Assemblages is a concept that helps capture the multitude of ways that already-composed data structures inflect and interact with society, its organization and functioning, and the resulting impact on individuals’ daily lives. CDS questions the many assumptions about Big Data that permeate contemporary literature on information and society by locating instances where Big Data may be naively taken to denote objective and transparent informational entities. In this introduction to the Big Data & Society CDS special theme, we briefly describe CDS work, its orientations, and principles.

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.

According to Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007, Hist Philos Life Sci 33:389–396, 2011a, Philos Sci 1(1):47–69, 2011b ), in order to establish a causal claim of the form, ‘_C_ is a cause of _E_’, one typically needs evidence that there is an underlying mechanism between _C_ and _E_ as well as evidence that _C_ makes a difference to _E_. This thesis has been used to argue that hierarchies of evidence, as championed by evidence-based movements, tend to give primacy to evidence of difference making over evidence of mechanisms and are flawed because the two sorts of evidence are required and they should be treated on a par. An alternative approach gives primacy to evidence of mechanism over evidence of difference making. In this paper, we argue that this alternative approach is equally flawed, again because both sorts of evidence need to be treated on a par. As an illustration of this parity, we explain how scientists working in the ‘EnviroGenomarkers’ project constantly make use of the two evidential components in a dynamic and intertwined way. We argue that such an interplay is needed not only for causal assessment but also for policy purposes.

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.

Causal claims in biomedical contexts are ubiquitous albeit they are not always made explicit. This paper addresses the question of what causal claims mean in the context of disease. It is argued that in medical contexts causality ought to be interpreted according to the epistemic theory. The epistemic theory offers an alternative to traditional accounts that cash out causation either in terms of “difference-making” relations or in terms of mechanisms. According to the epistemic approach, causal claims tell us about which inferences (e.g., diagnoses and prognoses) are appropriate, rather than about the presence of some physical causal relation analogous to distance or gravitational attraction. It is shown that the epistemic theory has important consequences for medical practice, in particular with regard to evidence-based causal assessment

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.