Evidence-Based Medicine has little consideration for mechanisms and philosophers of science and medicine have recently made pleas to increase the place of mechanisms in the medical evidence hierarchy. However, in this debate the notions of mechanisms seem to be limited to 'mechanistic processes' and 'complex-systems mechanisms,' understood as 'componential causal systems'. I believe that this will not do full justice to how mechanisms are used in biological, psychological and social sciences and, consequently, in a more biopsychosocial approach to medicine. Here, (...) I propose, following (Kuorikoski, 2009), to pay more attention to 'abstract forms of interaction' mechanisms. The present work scrutinized review articles on depression and medically unexplained pain, which are considered to be of multifactorial pathogenesis, for their use of mechanisms. In review articles on these disorders there seemed to be a range of uses between more 'abstract forms of interaction' and 'componential causal system' mechanisms. I therefore propose to expand the notions of mechanisms considered in medicine to include that of more 'abstract forms of interaction' to better explain and manage biopsychosocial disorders. (shrink)

Both clinical research and basic science rely on the epistemic practice of extrapolation from surrogate models, to the point that explanatory accounts presented in review papers and biology textbooks are in fact composite pictures reconstituted from data gathered in a variety of distinct experimental setups. This raises two new challenges to previously proposed mechanistic-similarity solutions to the problem of extrapolation: one pertaining to the absence of mechanistic knowledge in the early stages of research and the second to the large number (...) of extrapolations underpinning explanatory accounts. An analysis of the strategies deployed in experimental research supports the conclusion that while results from validated surrogate models are treated as a legitimate line of evidence supporting claims about target systems, the overall structure of research projects also demonstrates that extrapolative inferences are not considered definitive or sufficient evidence, but only partially justified hypotheses subjected to further testing. 1 Introduction2 Surrogate Models2.1 What exactly is a surrogate model?2.2 Why use surrogate models?3 Prior Validation of Surrogate Models3.1 The validation and ranking of surrogate models in the early stages of basic research3.2 The validation of surrogate models in later stages of basic research and in clinical research4 ‘Big Picture’ Accounts and the Extrapolations Underpinning Them4.1 The mosaic nature of mechanistic descriptions in basic science4.2 Challenges for mechanistic-similarity-based validation protocols5 Retrospective Testing of Extrapolated Knowledge5.1 Holistic confirmation5.2 Fallback strategies6 Conclusions. (shrink)

The paper discusses methodological guidelines for evaluating mechanistic explanations. According to current accounts, a satisfactory mechanistic explanation should include all of the relevant features of the mechanism, its component entities and activities, and their properties and organization, as well as exhibit productive continuity. It is not specified, however, how this kind of mechanistic completeness can be demonstrated. I argue that parameter sufficiency inferences based on mathematical model simulations provide a way of determining whether a mechanism capable of producing the phenomenon (...) of interest can be constructed from mechanistic components organized, acting, and having the properties described in the mechanistic explanation. (shrink)

Multidisciplinary models aggregating ‘lower-level’ biological and ‘higher-level’ psychological and social determinants of a phenomenon raise a puzzle. How is the interaction between the physical, the psychological and the social conceptualized and explained? Using biopsychosocial models of pain as an illustration, I argue that these models are in fact level-neutral compilations of empirical findings about correlated and causally relevant factors, and as such they neither assume, nor entail a conceptual or ontological stratification into levels of description, explanation or reality. If inter-level (...) causation is deemed problematic or if debates about the superiority of a particular level of description or explanation arise, these issues are fueled by considerations other than empirical findings. (shrink)

The article analyses in detail the Meselson–Stahl experiment, identifying two novel difficulties for the crucial experiment account, namely, the fragility of the experimental results and the fact that the hypotheses under scrutiny were not mutually exclusive. The crucial experiment account is rejected in favour of an experimental-mechanistic account of the historical significance of the experiment, emphasizing that the experiment generated data about the biochemistry of DNA replication that is independent of the testing of the semi-conservative, conservative, and dispersive hypotheses. _1_ (...) Introduction _2_ The Meselson–Stahl Experiment _3_ Some Difficulties for the Crucial Experiment Account _3.1_ Additional experiments were required _3.2_ Simplicity considerations are unconvincing _3.3_ The fragility of the experimental results _3.4_ The problematic interpretation of falsifyng results _3.5_ Not all possible hypotheses considered or tested _3.6_ The tested hypotheses were not mutually exclusive _4_ The Historical and Scientific Significance of the Meselson–Stahl Experiment _4.1_ The challenge for the crucial experiment account _4.2_ A mechanistic perspective on the experiment _4.3_ The experimental design and its independence from theoretical speculations _4.4_ The advantages of a ‘bottom-up’ mechanistic account _5_ Conclusion. (shrink)

A survey of models in immunology is conducted and distinct kinds of models are characterized based on whether models are material or conceptual, the distinctiveness of their epistemic purpose, and the criteria for evaluating the goodness of a model relative to its intended purpose. I argue that the diversity of models in interdisciplinary fields such as immunology reflects the fact that information about the phenomena of interest is gathered from different sources using multiple methods of investigation. To each model is (...) attached a description specifying how information about a phenomenon of interest has been acquired, highlighting points of commonality and difference between the methodological and epistemic histories of the information encapsulated in different models. These points of commonality and difference allow investigators to integrate findings from different models into more comprehensive explanatory accounts, as well as to troubleshoot anomalies and faulty accounts by going back to the original building blocks. (shrink)

An important strategy in the discovery of biological mechanisms involves the piecing together of experimental results from interventions. However, if mechanisms are investigated by means of ideal interventions, as defined by James Woodward and others, then the kind of information revealed is insufficient to discriminate between modular and non-modular causal contributions. Ideal interventions suffice for constructing webs of causal dependencies that can be used to make some predictions about experimental outcomes, but tell us little about how causally relevant factors are (...) organized together and how they interact with each other in order to produce a phenomenon. I argue that lab research relies on more elaborated types of interventions targeting in a controlled fashion multiple variables at the same time in order to probe the temporal organization of causally-relevant factors along distinct causal pathways and to test for non-modular interaction effects, thus providing crucial spatial-temporal constraints guiding the formulation of more detailed mechanistic explanations. (shrink)

Examples from the sciences showing that mechanisms do not always succeed in producing the phenomena for which they are responsible have led some authors to conclude that the regularity requirement can be eliminated from characterizations of mechanisms. In this article, I challenge this conclusion and argue that a minimal form of regularity is inextricably embedded in examples of elucidated mechanisms that have been shown to be causally responsible for phenomena. Examples of mechanistic explanations from the sciences involve mechanisms that have (...) been shown to produce phenomena with a reproducible rate of success. By contrast, if phenomena are infrequent to the point that they amount to irreproducible observations and experimental results, they are indistinguishable from the background noise of accidental happenings. The inability to detect or measure the phenomenon of interest against the background noise of accidental correlations makes it impossible to elucidate a mechanism by experimental means, to demonstrate that a proposed mechanism actually produces the phenomenon, and ultimately to justify why a hypothetical scenario involving an irregular mechanism should be preferred over attributing irreproducible happenings to chance. (shrink)

Causal mediation mechanisms are well supported by available experimental evidence and provide a practicable way to reductive physicalism. According to the causal mediation account of mechanistic explanation, descriptions as diverse as ‘black-box’ phenomena, mechanistic sketches and schemas mixing physically interpreted and operationalized biological, psychological and social variables, and detailed descriptions of mechanisms refer to the same causal structure circumscribed within the spatiotemporal boundaries of a replicable experimental setup. The coreference of coarser- and finer-grained descriptions of causal structures opens new possibilities (...) for testing the reductive physicalism conjecture. I discuss experimental designs supporting the causal mediation account and show how recent studies demonstrating the biological mediation of mind-mind causal processes can provide evidence for reductive physicalism. (shrink)

This paper argues against the view that the standard explanation of phase transitions in statistical mechanics may be considered a causal explanation, a distortion that can nevertheless successfully represent causal relations.