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Similarly, contemporary biology has rejected the notion that the evolution of organism populations just is the evolution of individual genes in the organisms of the population. This move away from “selfish gene” type approaches to evolutionary theory might be thought of as mirroring the move away from strict eliminative computationalism in cognitive neuroscience; the appreciation of epigenetic influences on evolution[1] exemplifies this trend in biology, as does the proliferation of the “-omics” biological sciences (e.g. genomics, proteomics, biomics).

In rejecting the decompositionist approach to cognition (or evolution), though, neuroscientists (or biologists) have not returned to the vitalist or emergentist positions of the 19th and early 20th centuries—it is certainly not the case that the only alternative to the Pinker/Churchland position about the mind is a return to Cartesian dualism, or the sort of spooky emergentism of Morgan (1921). Rejecting the notion that interesting facts about cognition are exhausted by interesting facts about neuronal firings need not entail embracing the notion that cognitive facts float free of physics and chemistry; rather, it just entails a recognition that neural networks (and the organisms that have them) are embedded in active environments that contribute to their states just as much as the behavior of the network’s (proper) parts do, and that the decompositionist assumption that an understanding of the parts entails an understanding of the whole need not hold in all cases. In studying organisms as complex systems, we need not reject the vast and important insights of traditional decompositionist science (including biology, neuroscience, and


  1. Epigenetics is the study of how factors other than changes in the underlying molecular structure of DNA can influence the expression and heritability of phenotypic traits, and encompasses everything from the study of how environmental changes can affect the expression of different genes to the exploration of how sets of genes can function as regulatory networks within an organism, affecting each others’ behavior and expression in heritable ways without actually modifying genotypic code. As a simple example, consider the way in which restricted calorie diets have been shown to modulate the activity of the SIR2/SIRT1 genes in laboratory rats, resulting in longer life-spans without change to the actual structure of the genes in question. See Oberdoerffer et. al. (2008). The most important point here is that these changes can be heritable, meaning that any account of evolution that treats evolution as a process that works strictly on genes can’t be the whole story.

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