The canonical version of the history of twentieth century philosophy of science tells us that Lakatos was Popper’s disciple, but it is rarely mentioned that Popper would have learned anything from Lakatos. The aim of this paper is to examine Lakatos’ influence on Popper’s philosophical system and to argue that Lakatos did have an important, yet somewhat unexpected, impact on Popper’s thinking: he influenced Popper’s evolutionary model for ‘progress’ in science. And Lakatos’ influence sheds new light on why and how (...) Popper continually revised one of the central claims of his philosophy of science: the evolutionary account of scientific theory change. (shrink)

The aim of this paper is to outline a typologyof selection processes, and show that differentsub-categories have different explanatorypower. The basis of this typology of selectionprocesses is argued to be the difference ofreplication processes involved in them. Inorder to show this, I argue that: 1.Replication is necessary for selection and 2.Different types of replication lead todifferent types of selection. Finally, it isargued that this typology is philosophicallysignificant, since it contrasts cases ofselection (on the basis of the replicationprocesses involved in them) (...) whereby selectioncauses adaptation – and, therefore, can beused in explanations of the (real or apparent)teleology of Nature – and cases in whichselection lacks such explanatory power. (shrink)

One of the most influential arguments against the claim that computers can think is that while our intentionality is intrinsic, that of computers is derived: it is parasitic on the intentionality of the programmer who designed the computer-program. Daniel Dennett chose a surprising strategy for arguing against this asymmetry: instead of denying that the intentionality of computers is derived, he endeavours to argue that human intentionality is derived too. I intend to examine that biological plausibility of Dennett’s suggestion and show (...) that Dennett’s argument for the claim that human intentionality is derived because it was designed by natural selection is based on the misunderstanding of how natural selection works. (shrink)

Causalism is the thesis that natural selection can cause evolution. A standard argument for causalism involves showing that a hypothetical intervention on some population-level property that is identified with natural selection will result in evolution. In a pair of articles, one of which recently appeared in the pages of this journal, Jun Otsuka has put forward a quite different argument for causalism. Otsuka attempts to show that natural selection can cause evolution by considering a hypothetical intervention on an individual-level property. (...) Specifically, Otsuka identifies natural selection with the causal relationship between a trait and fitness, claims an intervention on the strength of this relationship can cause evolution, then concludes that natural selection can cause evolution. Below I describe why Otsuka’s argument for causalism is unconvincing. Central to my criticism is that Otsuka’s argument works only if one adopts an indefensible account of natural selection, according to which natural selection can occur in the absence of trait or fitness variation. I go on to explain why any attempt to demonstrate the truth of causalism via a hypothetical intervention on an individual-level property would appear to require one to adopt an account of natural selection that is inadequate for the same reason. This in turn means the plausibility of causalism does indeed depend on the plausibility of the claim that population-level properties, which supervene on the properties of the individuals in the population, can be causally efficacious. (shrink)

Recent papers by a number of philosophers have been concerned with the question of whether natural selection is a causal process, and if it is, whether the causes of selection are properties of individuals or properties of populations. I shall argue that much confusion in this debate arises because of a failure to distinguish between causal productivity and causal relevance. Causal productivity is a relation that holds between events connected via continuous causal processes, while causal relevance is a relationship that (...) can hold between a variety of different kinds of facts and the events that counterfactually depend upon them. I shall argue that the productive character of natural selection derives from the aggregation of individual processes in which organisms live, reproduce and die. At the same time, a causal explanation of the distribution of traits will necessarily appeal both to causally relevant properties of individuals and to causally relevant properties that exist only at the level of the population. (shrink)

It is an ongoing controversy whether natural selection is a cause of population change, or a mere statistical description of how individual births and deaths accumulate. In this paper I restate the problem in terms of the reference class problem, and propose how the structure of stable equilibrium can provide a solution in continuity with biological practice. Insofar natural selection can be understood as a tendency towards equilibrium, key statisticalist criticisms are avoided. Further, in a modification of the Newtonian-force analogy, (...) it can be suggested that a better metaphor for natural selection is that of an emergent force, similar in nature to entropic forces: with magnitude and direction, but lacking a spatiotemporal origin or point of application. (shrink)

The probability that the fitter of two alleles will increase in frequency in a population goes up as the product of N (the effective population size) and s (the selection coefficient) increases. Discovering the distribution of values for this product across different alleles in different populations is a very important biological task. However, biologists often use the product Ns to define a different concept; they say that drift “dominates” selection or that drift is “stronger than” selection when Ns is much (...) smaller than some threshold quantity (e.g., ½) and that the reverse is true when Ns is much larger than that threshold. We argue that the question of whether drift dominates selection for a single allele in a single population makes no sense. Selection and drift are causes of evolution, but there is no fact of the matter as to which cause is stronger in the evolution of any given allele. (shrink)

The target of this article is the claim that natural selection accounts for the multiple realisation of biological and psychological kinds. I argue that the explanation actually offered does not provide any insight about the phenomenon since it presupposes multiple realisation as an unexplained premise, and this is what does all the work. The purported explanation mistakenly invokes the ?indifference? of selection to structure as an additional explanatorily relevant factor. While such indifference can be explanatory in intentional contexts, it is (...) not a causal factor at all in non-intentional nature. The upshot is that, once the necessary initial assumption about heterogeneity is accepted, there is no further explanation to do. (shrink)

In this paper I critically evaluate Reisman and Forber’s :1113–1123, 2005) arguments that drift and natural selection are population-level causes of evolution based on what they call the manipulation condition. Although I agree that this condition is an important step for identifying causes for evolutionary change, it is insufficient. Following Woodward, I argue that the invariance of a relationship is another crucial parameter to take into consideration for causal explanations. Starting from Reisman and Forber’s example on drift and after having (...) briefly presented the criterion of invariance, I show that once both the manipulation condition and the criterion of invariance are taken into account, drift, in this example, should better be understood as an individual-level rather than a population-level cause. Later, I concede that it is legitimate to interpret natural selection and drift as population-level causes when they rely on genuinely indeterministic events and some cases of frequency-dependent selection. (shrink)

Shapiro and Sober claim that Walsh, Ariew, Lewens, and Matthen give a mistaken, a priori defense of natural selection and drift as epiphenomenal. Contrary to Shapiro and Sober’s claims, we first argue that WALM’s explanatory doctrine does not require a defense of epiphenomenalism. We then defend WALM’s explanatory doctrine by arguing that the explanations provided by the modern genetical theory of natural selection are ‘autonomous-statistical explanations’ analogous to Galton’s explanation of reversion to mediocrity and an explanation of the diffusion ofgases. (...) We then argue that whereas Sober’s theory of forces is an adequate description of Darwin’s theory, WALM’s explanatory doctrine is required to understand how themodern genetical theory of natural selection explains large-scale statistical regularities. 1 Introduction2 Shapiro and Sober’s ‘Epiphenomenalism Do’s and Don’ts’3 WALM’s Explanatory Doctrine4 Galton’s Autonomous-Statistical Explanation5 A Second Example: The Statistical Explanation of the Diffusion of Gases6 Distinguishing Two Theories of Evolution by Natural Selection7 A Possible Objection: Are Statistical Laws Sufficient for Explanation?8 Conclusion. (shrink)

There are several different ways in which chance affects evolutionary change. That all of these processes are called “random genetic drift” is in part a due to common elements across these different processes, but is also a product of historical borrowing of models and language across different levels of organization in the biological hierarchy. A history of the concept of drift will reveal the variety of contexts in which drift has played an explanatory role in biology, and will shed light (...) on some of the philosophical controversy surrounding whether drift is a cause of evolutionary change. (shrink)

One controversy about the existence of so called evolutionary forces such as natural selection and random genetic drift concerns the sense in which such “forces” can be said to interact. In this paper I explain how natural selection and random drift can interact. In particular, I show how population-level probabilities can be derived from individual-level probabilities, and explain the sense in which natural selection and drift are embodied in these population-level probabilities. I argue that whatever causal character the individual-level probabilities (...) have is then shared by the population-level probabilities, and that natural selection and random drift then have that same causal character. Moreover, natural selection and drift can then be viewed as two aspects of probability distributions over frequencies in populations of organisms. My characterization of population-level probabilities is largely neutral about what interpretation of probability is required, allowing my approach to support various positions on biological probabilities, including those which give biological probabilities one or another sort of causal character. ‡This paper has benefited from feedback on and discussions of this and earlier work. I want to thank André Ariew, Matt Barker, Lindley Darden, Patrick Forber, Nancy Hall, Mohan Matthen, Samir Okasha, Jeremy Pober, Robert Richardson, Alex Rosenberg, Eric Seidel, Denis Walsh, and Bill Wimsatt. †To contact the author, please write to: Department of Philosophy, University of Alabama at Birmingham, HB 414A, 900 13th Street South, Birmingham, AL 35294-1260; e-mail: [email protected]. (shrink)