Glymour (Philos Sci 73:369–389, 2006) claims that classical population genetic models can reliably predict short and medium run population dynamics only given information about future fitnesses those models cannot themselves predict, and that in consequence the causal, ecological models which can predict future fitnesses afford a more foundational description of natural selection than do population genetic models. This paper defends the first claim from objections offered by Gildenhuys (Biol Philos, 2011).
We argue that current discussions of criteria for actual causation are ill-posed in several respects. (1) The methodology of current discussions is by induction from intuitions about an infinitesimal fraction of the possible examples and counterexamples; (2) cases with larger numbers of causes generate novel puzzles; (3) "neuron" and causal Bayes net diagrams are, as deployed in discussions of actual causation, almost always ambiguous; (4) actual causation is (intuitively) relative to an initial system state since state changes are relevant, but (...) most current accounts ignore state changes through time; (5) more generally, there is no reason to think that philosophical judgements about these sorts of cases are normative; but (6) there is a dearth of relevant psychological research that bears on whether various philosophical accounts are descriptive. Our skepticism is not directed towards the possibility of a correct account of actual causation; rather, we argue that standard methods will not lead to such an account. A different approach is required. (shrink)
argues that correlated interactions are necessary for group selection. His argument turns on a particular procedure for measuring the strength of selection, and employs a restricted conception of correlated interaction. It is here shown that the procedure in question is unreliable, and that while related procedures are reliable in special contexts, they do not require correlated interactions for group selection to occur. It is also shown that none of these procedures, all of which employ partial regression methods, are reliable when (...) correlated interactions of a specific kind arise, and it is argued that such correlated interactions will likely be ubiquitous in natural populations. Introduction Process and Product Fitness, Mean Fitness, and Phenotypic Change Correlated Interactions Causation Implications CiteULike Connotea Del.icio.us What's this? (shrink)
Models that fail to satisfy the Markov condition are unstable because changes in state variable values may cause changes in the values of background variables, and these changes in background lead to predictive error. Such error arises because non‐Markovian models fail to track the causal relations generating the values of response variables. This has implications for discussions of the level of selection: under certain plausible conditoins most standard models of group selection will not satisfy the Markov condition when fit to (...) data from real populations. These models neither correctly represent the causal structure generating nor correctly explain the phenomena of interest. †To contact the author, please write to: Bruce Glymour, Department of Philosophy, 201 Dickens Hall, Kansas State University, Manhattan KS, 66506; e‐mail: email@example.com. (shrink)
Since the introduction of mathematical population genetics, its machinery has shaped our fundamental understanding of natural selection. Selection is taken to occur when differential fitnesses produce differential rates of reproductive success, where fitnesses are understood as parameters in a population genetics model. To understand selection is to understand what these parameter values measure and how differences in them lead to frequency changes. I argue that this traditional view is mistaken. The descriptions of natural selection rendered by population genetics models are (...) in general neither predictive nor explanatory and introduce avoidable conceptual confusions. I conclude that a correct understanding of natural selection requires explicitly causal models of reproductive success. *Received May 2006; revised December 2006. †To contact the author, please write to: Department of Philosophy, Kansas State University, 201 Dickens Hall, Manhattan, KS 66506; e‐mail: firstname.lastname@example.org . (shrink)
I argue that the orthodox account of probabilistic causation, on which probabilistic causes determine the probability of their effects, is inconsistent with certain ontological assumptions implicit in scientific practice. In particular, scientists recognize the possibility that properties of populations can cause the behavior of members of the populations. Such emergent population‐level causation is metaphysically impossible on the orthodoxy.
I argue that results from foraging theory give us good reason to think some evolutionary phenomena are indeterministic and hence that evolutionary theory must be probabilistic. Foraging theory implies that random search is sometimes selectively advantageous, and experimental work suggests that it is employed by a variety of organisms. There are reasons to think such search will sometimes be genuinely indeterministic. If it is, then individual reproductive success will also be indeterministic, and so too will frequency change in populations of (...) organisms employing such search. (shrink)
Bogen and Woodward (1988) advance adistinction between data and phenomena. Roughly, theformer are the observations reported by experimentalscientists, the latter are objective, stable featuresof the world to which scientists infer based onpatterns in reliable data. While phenomena areexplained by theories, data are not, and so theempirical basis for an inference to a theory consistsin claims about phenomena. McAllister (1997) hasrecently offered a critique of their version of thisdistinction, offering in its place a version on whichphenomena are theory laden, and hence (...) on which theempirical support for inferences to theories is also,unavoidably, theory laden. In this commentary I arguethat McAllister and Bogen and Woodward are mistaken inthinking that the distinction is necessary, and thatthe empirical support for inferences to theories isnot necessarily theory laden in the way McAllister'saccount entails they are. (shrink)
Lennox and Wilson (1994) critique dispositional accounts of selection on the grounds that such accounts will class evolutionary events as cases of selection whether or not the environment constrains population growth. Lennox and Wilson claim that pure r-selection involves no environmental checks on growth, and that accounts of natural selection ought to distinguish between the two sorts of cases. I argue that Lennox and Wilson are mistaken in claiming that pure r-selection involves no environmental checks, but suggest that two related (...) cases support their substantive complaint, namely that dispositional accounts of selection have resources insufficient for making important distinctions in causal structure. (shrink)
Sober (1984) presents an account of selection motivated by the view that one property can causally explain the occurrence of another only if the first plays a unique role in the causal production of the second. Sober holds that a causal property will play such a unique role if it is a population level cause of its effect, and on this basis argues that there is selection for a trait T only if T is a population level cause of survival (...) and reproductive success. Sterelny and Kitcher (1988) claim against Sober that some traits directly subject to selection will not satisfy the probabilistic condition on population level causation. In this paper I show that Sober has the resources to resist the Sterelny-Kitcher complaint, but I argue that not all traits that satisfy the probabilistic condition play the required unique role in the production of their effects. (shrink)
Standard models of statistical explanation face two intractable difficulties. In his 1984 Salmon argues that because statistical explanations are essentially probabilistic we can make sense of statistical explanation only by rejecting the intuition that scientific explanations are contrastive. Further, frequently the point of a statistical explanation is to identify the etiology of its explanandum, but on standard models probabilistic explanations often fail to do so. This paper offers an alternative conception of statistical explanations on which explanations of the frequency of (...) a property consist in the derivation of that frequency from a statistical specification of the mechanism by which instances of the relevant property are produced. Such explanations are contrastive precisely because they identify the determinate causal etiologies of their explananda. (shrink)