Justin Garson

This book is a critical survey of and guidebook to the literature on biological functions. It ties in with current debates and developments, and at the same time, it looks back on the state of discourse in naturalized teleology prior to the 1970s. It also presents three significant new proposals. First, it describes the generalized selected effects theory, which is one version of the selected effects theory, maintaining that the function of a trait consists in the activity that led to its differential persistence or reproduction in a population, and not merely its differential reproduction. Secondly, it advances “within-discipline pluralism” (as opposed to between-discipline pluralism) a new form of function pluralism, which emphasizes the coexistence of function concepts within diverse biological sub-disciplines. Lastly, it provides a critical assessment of recent alternatives to the selected effects theory of function, namely, the weak etiological theory and the systems-theoretic theory. The book argues that, to the extent that functions purport to offer causal explanations for the existence of a trait, there are no viable alternatives to the selected effects view. The debate about biological functions is still as relevant and important to biology and philosophy as it ever was. Recent controversies surrounding the ENCODE Project Consortium in genetics, the nature of psychiatric classification, and the value of ecological restoration, all point to the continuing relevance to biology of philosophical discussion about the nature of functions. In philosophy, ongoing debates about the nature of biological information, intentionality, health and disease, mechanism, and even biological trait classification, are closely related to debates about biological functions.

Scientists, philosophers, and even the lay public commonly accept that schizophrenia stems from a biological or internal ‘dysfunction.’ However, this assessment is typically accompanied neither by well-defined criteria for determining that something is dysfunctional nor empirical evidence that schizophrenia satisfies those criteria. In the following, a concept of biological function is developed and applied to a neurobiological model of schizophrenia. It concludes that current evidence does not warrant the claim that schizophrenia stems from a biological dysfunction, and, in fact, that unusual neural structures associated with schizophrenia may have functional or adaptive significance. The fact that current evidence is ambivalent between these two possibilities (dysfunction versus adaptive function) implies that schizophrenia researchers should be much more cautious in using the ‘dysfunction’ label than they currently are. This has implications for both psychiatric treatment as well as public perception of mental disorders.

As historian Henning Schmidgen notes, the scientific study of the nervous system would have been “unthinkable” without the industrialization of communication in the 1830s. Historians have investigated extensively the way nerve physiologists have borrowed concepts and tools from the field of communications, particularly regarding the nineteenth-century work of figures like Helmholtz and in the American Cold War Era. The following focuses specifically on the interwar research of the Cambridge physiologist Edgar Douglas Adrian, and on the technology that led to his Nobel-Prize-winning research, the thermionic vacuum tube. Many countries used the vacuum tube during the war for the purpose of amplifying and intercepting coded messages. These events provided a context for Adrian's evolving understanding of the nerve fiber in the 1920s. In particular, they provide the background for Adrian's transition around 1926 to describing the nerve impulse in terms of “information,” “messages,” “signals,” or even “codes,” and for translating the basic principles of the nerve, such as the all-or-none principle and adaptation, into such an “informational” context. The following also places Adrian's research in the broader context of the changing relationship between science and technology, and between physics and physiology, in the first few decades of the twentieth century.

The following describes one distinct sense of ‘mechanism’ which is prevalent in biology and biomedicine and which has important epistemic benefits. According to this sense, mechanisms are defined by the functions they facilitate. This construal has two important implications. Firstly, mechanisms that facilitate functions are capable of breaking. Secondly, on this construal, there are rigid constraints on the sorts of phenomena ‘for which’ there can be a mechanism. In this sense, there are no ‘mechanisms for’ pathology, and natural selection is not a ‘mechanism of’ evolution, because it does not serve a function.

I develop a distinction between two types of psychological hedonism. Inferential hedonism (or “I-hedonism”) holds that each person only has ultimate desires regarding his or her own hedonic states (pleasure and pain). Reinforcement hedonism (or “R–hedonism”) holds that each person's ultimate desires, whatever their contents are, are differentially reinforced in that person’s cognitive system only by virtue of their association with hedonic states. I’ll argue that accepting R-hedonism and rejecting I-hedonism provides a conciliatory position on the traditional altruism debate, and that it coheres well with the neuroscientist Anthony Dickinson’s theory about the evolutionary function of hedonic states, the “hedonic interface theory.” Finally, I’ll defend R-hedonism from potential objections.

I develop a distinction between two types of psychological hedonism. Inferential hedonism (or “I-hedonism”) holds that each person only has ultimate desires regarding his or her own hedonic states (pleasure and pain). Reinforcement hedonism (or “R–hedonism”) holds that each person's ultimate desires, whatever their contents are, are differentially reinforced in that person’s cognitive system only by virtue of their association with hedonic states. I’ll argue that accepting R-hedonism and rejecting I-hedonism provides a conciliatory position on the traditional altruism debate, and that it coheres well with the neuroscientist Anthony Dickinson’s theory about the evolutionary function of hedonic states, the “hedonic interface theory.” Finally, I’ll defend R-hedonism from potential objections.

The Harvard physiologists Alexander Forbes (1882-1965) and Walter Bradford Cannon (1871-1945) had an enormous impact on the physiology and neuroscience of the twentieth century. In addition to their voluminous scientific output, they also used literature to reflect on the nature of science itself and its social significance. Forbes wrote a novel, The Radio Gunner, a literary memoir, Quest for a Northern Air Route, and several short stories. Cannon, in addition to several books of popular science, wrote a literary memoir in the last year of his life, The Way of an Investigator. The following will provide a brief overview of the life and work of Forbes and Cannon. It will then discuss the way that Forbes used literature to express his views about the changing role of communications technology in the military, and his evolving view of the nervous system itself as a kind of information-processing device. It will go on to discuss the way that Cannon used literature to articulate the horrors he witnessed on the battlefield, as well as to contribute to the philosophy of science, and in particular, to the logic of scientific discovery. Finally, it will consider the historical and philosophical value of deeper investigation of the literary productions of scientists.

This article presents a distinct sense of ‘mechanism’, which I call the functional sense of mechanism. According to this sense, mechanisms serve functions, and this fact places substantive restrictions on the kinds of system activities ‘for which’ there can be a mechanism. On this view, there are no mechanisms for pathology; pathologies result from disrupting mechanisms for functions. Second, on this sense, natural selection is probably not a mechanism for evolution because it does not serve a function. After distinguishing this sense fromsimilar explications of ‘mechanism’, I argue that it is ubiquitous in biology and has valuable epistemic benefits.

Carl F. Craver and Lindley Darden’s new book, In Search of Mechanisms: Discoveries across the Life Sciences, is a fantastic and lucid introduction to the “new mechanism” tradition in the philosophy of science. Over the last 2 decades, but particularly since the turn of the century, this has become an influential framework for thinking about core problems in the history and philosophy of science, with a strong emphasis on biology. There are at least four major aims. First, the new mechanism tradition purports to resolve conventional problems in the philosophy of science, such as the nature of explanation, theory evaluation, reduction, the unity of science, and the levels of the scientific hierarchy. Second, it constitutes what Karl Popper called a Logik der Forschung: a set of maxims and precepts to propel the process of scientific discovery itself. This emphasis on the process of discovery distinguishes the tradition from much of twentieth-century philosophy of science, with its emphasis on the logic of justification. Third, the new mechanism tradition, at least in Craver and Darden’s view, recommends a certain historiographical framework for organizing the history of biology, a framework that depicts the history of biology primarily as a search for mechanisms. Fourth, it constitutes a fundamental metaphysics—a picture of what the physical world is like, in which entities possess various properties, which allow them to have various powers and which are organized in such a way as to give rise to observable phenomena. As the authors provocatively conclude, “nothing in biology makes any sense without the idea that biologists are searching for mechanisms” (202). I do not know whether the authors are correct in their assessment, but this book certainly demonstrates the scope of their ambitions.

During the 1990s, many philosophers wrestled with the problem of function indeterminacy. Although interest in the problem has waned, I argue that solving the problem is of value for biomedical research and practice. This is because a solution to the problem is required in order to specify rigorously the conditions under which a given item is “dysfunctional.” In the following I revisit a solution developed originally by Neander, which uses functional analysis to solve the problem. I situate her solution in the framework of mechanistic explanation and suggest two improvements.

Despite the voluminous literature on biological functions produced over the last 40 years, few philosophers have studied the concept of function as it is used in neuroscience. Recently, Craver (forthcoming; also see Craver 2001) defended the causal role theory against the selected effects theory as the most appropriate theory of function for neuroscience. The following argues that though neuroscientists do study causal role functions, the scope of that theory is not as universal as claimed. Despite the strong prima facie superiority of the causal role theory, the selected effects theory (when properly developed) can handle many cases from neuroscience with equal facility. It argues this by presenting a new theory of function that generalizes the notion of a ‘selection process’ to include processes such as neural selection, antibody selection, and some forms of learning—that is, to include structures that have been differentially retained as well as those that have been differentially reproduced. This view, called the generalized selected effects theory of function, will be defended from criticism and distinguished from similar views in the literature