Not all models are explanatory. Some models are data summaries. Some models sketch explanations but leave crucial details unspecified or hidden behind filler terms. Some models are used to conjecture a how-possibly explanation without regard to whether it is a how-actually explanation. I use the Hodgkin and Huxley model of the action potential to illustrate these ways that models can be useful without explaining. I then use the subsequent development of the explanation of the action potential to show what is (...) required of an adequate mechanistic model. Mechanistic models are explanatory. (shrink)

What are the relative epistemic merits of building prosthetic models versus building nonprosthetic models and simulations? I argue that prosthetic models provide a sufficient test of affordance validity, that is, of whether the target system affords mechanisms that can be commandeered by a prosthesis. In other respects, prosthetic models are epistemically on par with nonprosthetic models. I focus on prosthetics in neuroscience, but the results are general. The goal of understanding how brain mechanisms work under ecologically and physiologically relevant conditions (...) is narrow compared to the search for maker's knowledge about how the brain can be made to work for us. (shrink)

According to a growing trend in theoretical neuroscience, the human perceptual system is akin to a Bayesian machine. The aim of this article is to clearly articulate the claims that perception can be considered Bayesian inference and that the brain can be considered a Bayesian machine, some of the epistemological challenges to these claims; and some of the implications of these claims. We address two questions: (i) How are Bayesian models used in theoretical neuroscience? (ii) From the use of Bayesian (...) models in theoretical neuroscience, have we learned or can we hope to learn that perception is Bayesian inference or that the brain is a Bayesian machine? From actual practice in theoretical neuroscience, we argue for three claims. First, currently Bayesian models do not provide mechanistic explanations; instead they are useful devices for predicting and systematizing observational statements about people's performances in a variety of perceptual tasks. That is, currently we should have an instrumentalist attitude towards Bayesian models in neuroscience. Second, the inference typically drawn from Bayesian behavioural performance in a variety of perceptual tasks to underlying Bayesian mechanisms should be understood within the three-level framework laid out by David Marr ( [1982] ). Third, we can hope to learn that perception is Bayesian inference or that the brain is a Bayesian machine to the extent that Bayesian models will prove successful in yielding secure and informative predictions of both subjects' perceptual performance and features of the underlying neural mechanisms. (shrink)

Ever since Wesley Salmon’s theory, the mechanical approach to causality has found an increasing number of supporters who have developed it in different directions. Mechanical views such as those advanced by Stuart Glennan, Jim Bogen and Peter Machamer, Lindley Darden and Carl Craver have met with broad consensus in recent years. This paper analyses the main features of these mechanical positions and some of the major problems they still face, referring to the latest debate on mechanisms, causal explanation and the (...) relationship between mechanisms and counterfactuals. I shall claim that the mechanical approach can be recognised as having a fundamental explanatory power, whereas the counterfactual approach, recently developed mainly by Jim Woodward and essentially linked to the notion of intervention, has an important heuristic role. Claiming that mechanisms are by no means to be seen as parasitic on counterfactuals or less fundamental than them – as it has been recently suggested –, and that yet counterfactuals can play a part in a conceptual analysis of causation, I shall look for hints in support of the peaceful coexistence of the two. (shrink)

The paper discusses how systems biology is working toward complex accounts that integrate explanation in terms of mechanisms and explanation by mathematical models—which some philosophers have viewed as rival models of explanation. Systems biology is an integrative approach, and it strongly relies on mathematical modeling. Philosophical accounts of mechanisms capture integrative in the sense of multilevel and multifield explanations, yet accounts of mechanistic explanation have failed to address how a mathematical model could contribute to such explanations. I discuss how mathematical (...) equations can be explanatorily relevant. Several cases from systems biology are discussed to illustrate the interplay between mechanistic research and mathematical modeling, and I point to questions about qualitative phenomena, where quantitative models are still indispensable to the explanation. Systems biology shows that a broader philosophical conception of mechanisms is needed, which takes into account functional-dynamical aspects, interaction in complex networks with feedback loops, system-wide functional properties such as distributed functionality and robustness, and a mechanism’s ability to respond to perturbations. I offer general conclusions for philosophical accounts of explanation. (shrink)

We outline a framework of multilevel neurocognitive mechanisms that incorporates representation and computation. We argue that paradigmatic explanations in cognitive neuroscience fit this framework and thus that cognitive neuroscience constitutes a revolutionary break from traditional cognitive science. Whereas traditional cognitive scientific explanations were supposed to be distinct and autonomous from mechanistic explanations, neurocognitive explanations aim to be mechanistic through and through. Neurocognitive explanations aim to integrate computational and representational functions and structures across multiple levels of organization in order to explain (...) cognition. To a large extent, practicing cognitive neuroscientists have already accepted this shift, but philosophical theory has not fully acknowledged and appreciated its significance. As a result, the explanatory framework underlying cognitive neuroscience has remained largely implicit. We explicate this framework and demonstrate its contrast with previous approaches. (shrink)

Not only has the philosophical debate on causation been gaining ground in the last few decades, but it has also increasingly addressed the sciences. The biomedical sciences are among the most prominent fields that have been considered, with a number of works tackling the understanding of the notion of cause, the assessment of genuinely causal relations and the use of causal knowledge in applied contexts. Far from denying the merits of the debate on causation and the major theories it comprises, (...) this paper is meant as a stimulus for theorists of causation in the philosophy of biomedicine, with a focus on clinical matters. Without aiming at putting forward an original theory of causation and starting from the narration of two actual but paradigmatic cases at the joints between biomedical research and clinical practice, we want to point out that some pathological situations addressed by molecular medicine actually prove resistant to some of our major epistemological accounts of causal explanation. Given this scenario, which is very frequent in our hospitals, our analysis aims to provide a stimulus for the debate among theorists of causation in biomedicine interested in real cases in science in practice. We believe that this might in turn encourage some more general rethinking of the complex intertwinement of science, philosophy of science and ethics, as well as of the role of philosophy of science for clinical medicine itself. (shrink)

This article introduces comparative process tracing as a two-step methodological approach that combines theory, chronology, and comparison. For each studied case, the processes leading “from A to B” are reconstructed and analyzed in terms of ideal-type social mechanisms and then compared by making use of the identified mechanisms and ideal-type periodization. Central elements of CPT are path dependence, critical junctures and focal points, social mechanisms, context, periodization, and counterfactual analysis. The CPT approach is described, discussed, and compared with more formal (...) and deterministic forms of process tracing, which are found to be less fruitful for systematic comparison. (shrink)

Skipper and Millstein (2005) argued that existing conceptions of mechanisms failed to "get at" natural selection, but left open the possibility that a refined conception of mechanisms could resolve the problems that they identified. I respond to Skipper and Millstein, and argue that while many of their points have merit, their objections can be overcome and that natural selection can be characterized as a mechanism. In making this argument, I discuss the role of regularity in mechanisms, and develop an account (...) of stochastic (i.e., probabilistic) mechanisms. Explaining the phenomenon of adaptation through the mechanism of natural selection illustrates the power and flexibility of using mechanistic strategies to explain natural phenomena. (shrink)

Understanding the role mechanistic constraints play in shaping evolution can relieve the tension between the generally accepted intuition that there are no strict laws in biology and empirical findings showing that evolutionary processes are biased toward preferred outcomes. Mechanistic constraints explain why some evolutionary outcomes are more probable than others and allow for predictions in specific lineages. At the same time, mechanistic constraints are neither necessary nor universal in the way laws are traditionally characterized: they remain contingent on the past (...) evolution of the biological mechanisms underpinning them and only constrain the future evolution of the organisms possessing them. (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)

How regular do mechanisms need to be, in order to count as mechanisms? This paper addresses two arguments for dropping the requirement of regularity from the definition of a mechanism, one motivated by examples from the sciences and the other motivated by metaphysical considerations regarding causation. I defend a broadened regularity requirement on mechanisms that takes the form of a taxonomy of kinds of regularity that mechanisms may exhibit. This taxonomy allows precise explication of the degree and location of regular (...) operation within a mechanism, and highlights the role that various kinds of regularity play in scientific explanation. I defend this regularity requirement in terms of regularity’s role in individuating mechanisms against a background of other causal processes, and by prioritizing mechanisms’ ability to serve as a model of scientific explanation, rather than as a metaphysical account of causation. It is because mechanisms are regular, in the expanded sense described here, that they are capable of supporting the kinds of generalizations that figure prominently in scientific explanations. (shrink)

Leuridan (2010) argued that mechanisms cannot provide a genuine alternative to laws of nature as a model of explanation in the sciences, and advocates Mitchell’s (1997) pragmatic account of laws. I first demonstrate that Leuridan gets the order of priority wrong between mechanisms, regularity, and laws, and then make some clarifying remarks about how laws and mechanisms relate to regularities. Mechanisms are not an explanatory alternative to regularities; they are an alternative to laws. The existence of stable regularities in nature (...) is necessary for either model of explanation: regularities are what laws describe and what mechanisms explain. (shrink)

In this field guide, I distinguish five separate senses with which the term ‘mechanism’ is used in contemporary philosophy of science. Many of these senses have overlapping areas of application but involve distinct philosophical claims and characterize the target mechanisms in relevantly different ways. This field guide will clarify the key features of each sense and introduce some main debates, distinguishing those that transpire within a given sense from those that are best understood as concerning two distinct senses. The ‘new (...) mechanisms’ sense is the primary sense from which other senses will be distinguished. In part II of this field guide, I consider three further senses of the term that are ontologically ‘flat’ or at least not explicitly hierarchical in character: equations in structural equation models of causation, causal-physical processes, and information-theoretic constraints on states available to systems. After characterizing each sense, I clarify its ontological commitments, its methodological implications, how it figures in explanations, its implications for reduction, and the key manners in which it differs from other senses of mechanism. I conclude that there is no substantive core meaning shared by all senses, and that debates in contemporary philosophy of science can benefit from clarification regarding precisely which sense of mechanism is at stake. (shrink)

In the recent literature on causal and non-causal scientific explanations, there is an intuitive assumption according to which an explanation is non-causal by virtue of being abstract. In this context, to be ‘abstract’ means that the explanans in question leaves out many or almost all causal microphysical details of the target system. After motivating this assumption, we argue that the abstractness assumption, in placing the abstract and the causal character of an explanation in tension, is misguided in ways that are (...) independent of which view of causation or causal explanation one takes to be most accurate. On major accounts of causation, as well as on major accounts of causal explanation, the abstractness of an explanation is not sufficient for it being non-causal. That is, explanations are not non-causal by dint of being abstract. (shrink)

Accounts of ontic explanation have often been devised so as to provide an understanding of mechanism and of causation. Ontic accounts differ quite radically in their ontologies, and one of the latest additions to this tradition proposed by Peter Machamer, Lindley Darden and Carl Craver reintroduces the concept of activity. In this paper I ask whether this influential and activity-based account of mechanisms is viable as an ontic account. I focus on polygenic scenarios—scenarios in which the causal truths depend on (...) more than one cause. The importance of polygenic causation was noticed early on by Mill (1893). It has since been shown to be a problem for both causal-law approaches to causation (Cartwright 1983) and accounts of causation cast in terms of capacities (Dupré 1993; Glennan 1997, pp. 605-626). However, whereas mechanistic accounts seem to be attractive precisely because they promise to handle complicated causal scenarios, polygenic causation needs to be examined more thoroughly in the emerging literature on activity-based mechanisms. The activity-based account proposed in Machamer et al. (2000, pp. 1-25) is problematic as an ontic account, I will argue. It seems necessary to ask, of any ontic account, how well it performs in causal situations where—at the explanandum level of mechanism—no activity occurs. In addition, it should be asked how well the activity-based account performs in situations where there are too few activities around to match the polygenic causal origin of the explanandum. The first situation presents an explanandum-problem and the second situation presents an explanans-problem—I will argue—both of which threaten activity-based frameworks. (shrink)

In this paper, I propose two theses, and then examine what the consequences of those theses are for discussions of reduction and emergence. The first thesis is that what have traditionally been seen as robust, reductions of one theory or one branch of science by another more fundamental one are a largely a myth. Although there are such reductions in the physical sciences, they are quite rare, and depend on special requirements. In the biological sciences, these prima facie sweeping reductions (...) fade away, like the body of the famous Cheshire cat, leaving only a smile.... The second thesis is that the "smiles" are fragmentary patchy explanations, and though patchy and fragmentary, they are very important, potentially Nobel-prize winning advances. To get the best grasp of these "smiles," I want to argue that, we need to return to the roots of discussions and analyses of scientific explanation more generally, and not focus mainly on reduction models, though three conditions based on earlier reduction models are retained in the present analysis. I briefly review the scientific explanation literature as it relates to reduction, and then offer my account of explanation. The account of scientific explanation I present is one I have discussed before, but in this paper I try to simplify it, and characterize it as involving field elements and a preferred causal model system abbreviated as FE and PCMS. In an important sense, this FE and PCMS analysis locates an "explanation" in a typical scientific research article. This FE and PCMS account is illustrated using a recent set of neurogenetic papers on two kinds of worm foraging behaviors: solitary and social feeding. One of the preferred model systems from a 2002 Nature article in this set is used to exemplify the FE and PCMS analysis, which is shown to have both reductive and nonreductive aspects. The paper closes with a brief discussion of how this FE and PCMS approach differs from and is congruent with Bickle's "ruthless reductionism" and the recently revived mechanistic philosophy of science of Machamer, Darden, and Craver. (shrink)

A shared problem across the sciences is to make sense of correlational data coming from observations and/or from experiments. Arguably, this means establishing when correlations are causal and when they are not. This is an old problem in philosophy. This paper, narrowing down the scope to quantitative causal analysis in social science, reformulates the problem in terms of the validity of statistical models. Two strategies to make sense of correlational data are presented: first, a 'structural strategy', the goal of which (...) is to model and test causal structures that explain correlational data; second, a 'manipulationist or interventionist strategy', that hinges upon the notion of invariance under intervention. It is argued that while the former can offer a solution the latter cannot. (shrink)

How are scientific explanations possible in ecology, given that there do not appear to be many—if any—ecological laws? To answer this question, I present and defend an account of scientific causal explanation in which ecological generalizations are explanatory if they are invariant rather than lawlike. An invariant generalization continues to hold or be valid under a special change—called an intervention—that changes the value of its variables. According to this account, causes are difference-makers that can be intervened upon to manipulate or (...) control their effects. I apply the account to ecological generalizations to show that invariance under interventions as a criterion of explanatory relevance provides interesting interpretations for the explanatory status of many ecological generalizations. Thus, I argue that there could be causal explanations in ecology by generalizations that are not, in a strict sense, laws. I also address the issue of mechanistic explanations in ecology by arguing that invariance and modularity constitute such explanations. (shrink)

Mechanistic explanations satisfy widely held norms of explanation: the ability to manipulate and answer counterfactual questions about the explanandum phenomenon. A currently debated issue is whether any nonmechanistic explanations can satisfy these explanatory norms. Weiskopf argues that the models of object recognition and categorization, JIM, SUSTAIN, and ALCOVE, are not mechanistic yet satisfy these norms of explanation. In this article I argue that these models are mechanism sketches. My argument applies recent research using model-based functional magnetic resonance imaging, a novel (...) neuroimaging method whose significance for current debates on psychological models and mechanistic explanation has yet to be explored. (shrink)

Defending or attacking either functionalism or computationalism requires clarity on what they amount to and what evidence counts for or against them. My goal here is not to evaluate their plausibility. My goal is to formulate them and their relationship clearly enough that we can determine which type of evidence is relevant to them. I aim to dispel some sources of confusion that surround functionalism and computationalism, recruit recent philosophical work on mechanisms and computation to shed light on them, and (...) clarify how functionalism and computationalism may or may not legitimately come together. (shrink)

Machamer, Darden, and Craver's account of the nature and role of mechanisms in the special sciences has been very influential. Unfortunately, a confusing array of ontic, epistemic, and pragmatic distinctions is required to individuate their mechanisms, mechanism schemata, and mechanism sketches. I diagnose this as a conflation of token-level causal relations with type-level relations. I propose instead that a mechanism is an abstraction that relates entity types and activity types on the model of a directed graph. Mechanisms have an ontic (...) status distinct from the causal chains of token entities and token activities that instantiate them. (shrink)

Reductionists in biology claim that all biological events can be explained in terms of genes and macromolecules alone, while antireductionists argue that some biological events must be explained at a higher level. The literature, however, does not distinguish between different kinds of molecular explanation. The goal of this article is to identify and analyze three such kinds. The analysis of molecular explanations herein carries an important philosophical implication; in shunning crude reductionism and extreme versions of holism, we can combine the (...) insights of thoughtful reductionists with sophisticated antireductionism. When this is done, the question of explanatory reductionism becomes less substantial than often supposed. (shrink)

There is a long tradition in philosophy and the social sciences that emphasizes the meaningfulness of human action. This tradition doubts or even negates the possibility of causal explanations of human action precisely on the basis that human actions have meaning. This article provides an argument in favor of methodological naturalism in the social sciences. It grants the main argument of the Interpretivists, that is, that human actions are meaningful, but it shows how a transformation of a "nexus of meaning" (...) into a "causal nexus" can take place, proposing the "successful transformation argument.". (shrink)

The Hodgkin–Huxley (HH) model of the action potential is a theoretical pillar of modern neurobiology. In a number of recent publications, Carl Craver ([2006], [2007], [2008]) has argued that the model is explanatorily deficient because it does not reveal enough about underlying molecular mechanisms. I offer an alternative picture of the HH model, according to which it deliberately abstracts from molecular specifics. By doing so, the model explains whole-cell behaviour as the product of a mass of underlying low-level events. The (...) issue goes beyond cellular neurobiology, for the strategy of abstraction exhibited in the HH case is found in a range of biological contexts. I discuss why it has been largely neglected by advocates of the mechanist approach to explanation. 1 Introduction2 A Primer on the HH Model2.1 The basic qualitative picture2.2 The quantitative model3 Interlude: What Did Hodgkin and Huxley Think?4 Craver’s View4.1 Mechanistic explanation4.2 Sketches4.3 Craver's view: The HH model as a mechanism sketch5 An Alternative View of the HH Model5.1 Another look at the equations5.2 The discrete-gating picture5.3 The road paved by Hodgkin and Huxley5.4 Summary and comparison to Craver6 Conclusion: The HH Model and Mechanistic Explanation6.1 Sketches and abstractions6.2 Why has aggregative abstraction been overlooked? (shrink)

Most defenders of the new mechanistic approach accept ontic constraints for successful scientific explanation (Illari 2013; Craver 2014). The minimal claim is that scientific explanations have objective truthmakers, namely mechanisms that exist in the physical world independently of any observer and that cause or constitute the phenomena-to- be-explained. How can this idea be applied to type-level explanations? Many authors at least implicitly assume that in order for mechanisms to be the truthmakers of type-level explanation they need to be regular (Andersen (...) 2012; Sheredos 2015). One problem of this assumption is that most mechanisms are (highly) stochastic in the sense that they “fail more often than they succeed” (Bogen 2005; Andersen 2012). How can a mechanism type whose instances are more likely not to produce an instance of a particular phenomenon type be the truthmaker of the explanation of that particular phenomenon type? In this paper, I will give an answer to this question. I will analyze the notion of regularity and I will discuss Andersen's suggestion for how to cope with stochastic mechanisms. I will argue that her suggestion cannot account for all kinds of stochastic mechanisms and does not provide an answer as to why regularity grounds type-level explanation. According to my analysis, a mechanistic type- level explanation is true if and only if at least one of the following two conditions is satisfied: the mechanism brings about the phenomenon more often than any other phenomenon (comparative regularity) or the phenomenon is more often brought about by the mechanism than by any other mechanism/causal sequence (comparative reverse regularity). (shrink)

Recently, several authors have argued that scientific understanding should be a new topic of philosophical research. In this article, I argue that the three most developed accounts of understanding--Grimm's, de Regt's, and de Regt and Dieks's--can be replaced by earlier accounts of scientific explanation without loss. Indeed, in some cases, such replacements have clear benefits.

I examine the warrants we have in light of the empirical successes of a kind of model I call ‘ hybrid models ’, a kind that includes climate models among its members. I argue that these warrants ’ strengths depend on inferential virtues that are not just explanatory virtues, contrary to what would be the case if inference to the best explanation provided the warrants. I also argue that the warrants in question, unlike those IBE provides, guide inferences only to (...) model implications about which there is real uncertainty. My conclusion provides criteria of adequacy for epistemologies of climate and other hybrid models. (shrink)

We argue that dynamical and mathematical models in systems and cognitive neuro- science explain (rather than redescribe) a phenomenon only if there is a plausible mapping between elements in the model and elements in the mechanism for the phe- nomenon. We demonstrate how this model-to-mechanism-mapping constraint, when satisfied, endows a model with explanatory force with respect to the phenomenon to be explained. Several paradigmatic models including the Haken-Kelso-Bunz model of bimanual coordination and the difference-of-Gaussians model of visual receptive fields are (...) explored. (shrink)

Recently, it has been provocatively claimed that dynamical modeling approaches signal the emergence of a new explanatory framework distinct from that of mechanistic explanation. This paper rejects this proposal and argues that dynamical explanations are fully compatible with, even naturally construed as, instances of mechanistic explanations. Specifically, it is argued that the mathematical framework of dynamics provides a powerful descriptive scheme for revealing temporal features of activities in mechanisms and plays an explanatory role to the extent it is deployed for (...) this purpose. It is also suggested that more attention should be paid to the distinctive methodological contributions of the dynamical framework including its usefulness as a heuristic for mechanism discovery and hypothesis generation in contemporary neuroscience and biology. (shrink)

In Search Of Mechanisms is a book about the methodology of biology. It is a work by Carl Craver and Lindley Darden, both of whom are well-known individually for their advocacy of mechanistic explanation—in the neurosciences and in the fields of genetics, cytology and molecular biology . Here, the two join forces to give a unified model of biological explanation, not limited to a particular area of biological enquiry, as rooted in the search for mechanisms.The objectives of the book are (...) threefold. First, it sets out to describe what biologists do. This first objective can be described as the goal of making biology more comprehensible. If biology involves the search for mechanisms, then one cannot understand the history of biology and its current practice without understanding mechanisms. Secondly, the book seeks to give a proscriptive account of explanation and the process of explaining some phenomena. This second objective relates to an interest in contributing to the .. (shrink)

Proponents of evidence-based medicine and some philosophers of science seem to agree that knowledge of mechanisms can help solve the problem of applying results of controlled studies to target populations (‘the problem of extrapolation’). We describe the problem of extrapolation, characterize mechanisms, and outline how mechanistic knowledge might be used to solve the problem. Our main thesis is that there are four often overlooked problems with using mechanistic knowledge to solve the problem of extrapolation. First, our understanding of mechanisms is (...) often (and arguably, likely to remain) incomplete. Secondly, knowledge of mechanisms is not always applicable outside the tightly controlled laboratory conditions in which it is gained. Thirdly, mechanisms can behave paradoxically. Fourthly, as Daniel Steel points out, using mechanistic knowledge faces the problem of the ‘extrapolator’s circle’. At the same time, when the problems with mechanistic knowledge have been addressed, such knowledge can and should be used to mitigate (nothing can entirely solve) the problem of extrapolation. (shrink)

Traditionally, a scientific model is thought to provide a good scientific explanation to the extent that it satisfies certain scientific goals that are thought to be constitutive of explanation. Problems arise when we realize that individual scientific models cannot simultaneously satisfy all the scientific goals typically associated with explanation. A given model’s ability to satisfy some goals must always come at the expense of satisfying others. This has resulted in philosophical disputes regarding which of these goals are in fact necessary (...) for explanation, and as such which types of models can and cannot provide explanations. Explanatory monists argue that one goal will be explanatory in all contexts, while explanatory pluralists argue that the goal will vary based on pragmatic considerations. In this paper, I argue that such debates are misguided, and that both monists and pluralists are incorrect. Instead of any goal being given explanatory priority over others in a given context, the different goals are all deeply dependent on one another for their explanatory power. Any model that sacrifices some explanatory goals to attain others will always necessarily undermine its own explanatory power in the process. And so when forced to choose between individual scientific models, there can be no explanatory victors. Given that no model can satisfy all the goals typically associated with explanation, no one model in isolation can provide a good scientific explanation. Instead we must appeal to collections of models. Collections of models provide an explanation when they satisfy the web of interconnected goals that justify the explanatory power of one another. (shrink)

In this article, I argue that the use of scientific models that attribute intentional content to complex systems bears a striking similarity to the way in which statistical descriptions are used. To demonstrate this, I compare and contrast an intentional model with a statistical model, and argue that key similarities between the two give us compelling reasons to consider both as a type of phenomenological model. I then demonstrate how intentional descriptions play an important role in scientific methodology as a (...) type of phenomenal model, and argue that this makes them as essential as any other model of this type. (shrink)

In 1747, James Lind carried out an experiment which proved the usefulness of citrus fruit as a cure for scurvy. Nonetheless, he rejected the earlier hypothesis of Bachstrom that the absence of fresh fruit and vegetables was the only cause of the disease. I explain why it was rational for James Lind not to accept Bachstrom’s explanation. I argue that it was the urge for scientific understanding that guided Lind in his rejection and in the development of his alternative theory (...) that humidity was the primary cause of the disease. Central in this process was the search for causal mechanisms which could provide understanding of how the disease developed and which fitted in with the knowledge of the time. Given that the relevant background knowledge and statistical methods were not yet available to Lind, he was right to prefer his own explanation to that of Bachstrom. Although his explanation turned out to be wrong, and Bachstrom’s right, from a historical point of view it offered deeper causal understanding of both the development of the disease and the preventive and curative effects of fresh vegetable food. This case study illustrates how the search for causal mechanisms can not only be enlightening, but also very misleading. (shrink)

In what follows, I suggest that it makes good sense to think of the truth of the probabilistic generalizations made in the life sciences as metaphysically grounded in stochastic mechanisms in the world. To further understand these stochastic mechanisms, I take the general characterization of mechanism offered by MDC :1–25, 2000) and explore how it fits with several of the going philosophical accounts of chance: subjectivism, frequentism, Lewisian best-systems, and propensity. I argue that neither subjectivism, frequentism, nor a best-system-style interpretation (...) of chance will give us what we need from an account of stochastic mechanism, but some version of propensity theory can. I then draw a few important lessons from recent propensity interpretations of fitness in order to present a novel propensity interpretation of stochastic mechanism according to which stochastic mechanisms are thought to have probabilistic propensities to produce certain outcomes over others. This understanding of stochastic mechanism, once fully fleshed-out, provides the benefits of allowing the stochasticity of a particular mechanism to be an objective property in the world, a property investigable by science, a way of quantifying the stochasticity of a particular mechanism, and a way to avoid a problematic commitment to the causal efficacy of propensities. (shrink)