Justin Garson

In this chapter, I consider three theories of function that are relatively new, in the sense that they have been developed over the last twenty years. The “weak etiological theory” says, roughly, that a trait token in an organism has a function so long as that kind of trait contributed to the fitness of that organism’s ancestors and it is inherited. It defines function in terms of inheritance and past contributions to fitness, but not selection. I assess some differences between this theory and the standard selected effects account and question the motivation for the account. A second group of theories is known as the “systems-theoretic” or “organizational” view. This is not a single theory but a family of theories based on the idea that a trait token can acquire a function by virtue of the way that very token contributes to a complex, organized, system, and thereby to its own continued persistence, as a token. I argue that the organizational approach faces liberality problems. Finally, the modal theory of function holds that the function of a trait token has to do with the behavior of that token in certain nearby possible worlds. I assess the theory and survey some problems. Bence Nanay developed the modal theory as an attempt to solve a certain circularity problem that he believes afflicts most other theories of function, but it is not clear whether there is a real problem here to be resolved.

This chapter begins by showing why one standard way of describing the functions debate—as a debate between the selected effects theory, fitness-contribution theory, and causal role theory—is misguided. I then summarize three main conclusions. First, I argue that, to the extent that function statements are causal explanations, there are no current, viable alternatives to the selected effects theory. Second, I argue that, to the extent that we accept pluralism, we should not accept what I call (in Chap. 5 ) “between-discipline pluralism,” which seeks to restrict the applicability of the selected effects theory to some branches of evolutionary biology. Third, I advocate a specific version of the selected effects theory, the generalized selected effects theory, which I described earlier (in Chap. 3 ). In closing, I outline three outstanding problems for most theories of function. The first is function indeterminacy. Typically, there are a number of different activities associated with the performance of a function and most theories of function do not have the resources to specify which of those activities, precisely, constitutes an item’s function. Second, in many cases, a trait not only has a function, but it has an appropriate rate of functioning. For example, the heart not only has the function of beating, but it has the function of beating at a certain rate. How should we specify the appropriate rate of function? Third, for many traits that have functions, we can distinguish between appropriate and inappropriate situations for the performance of those functions. How should we modify our theories to take this into account?

For some, biology explains all there is to know about the mind. Yet many big questions remain: is the mind shaped by genes or the environment? If mental traits are the result of adaptations built up over thousands of years, as evolutionary psychologists claim, how can such claims be tested? If the mind is a machine, as biologists argue, how does it allow for something as complex as human consciousness? Revised and updated to take account of new developments in the field, The Biological Mind: A Philosophical Introduction, Second Edition explores these questions and more, using the philosophy of biology to introduce and assess the nature of the mind. Drawing on the four key themes of evolutionary biology; molecular biology and genetics; neuroscience; and biomedicine and psychiatry, Justin Garson addresses the following key topics

Christie, Brusse, et al. argue that the selected effects theory of function (SE) doesn’t do what it’s supposed to do: namely, show how functions can be explanatory. They survey some well-known evolutionary dynamics such as arms races, frequency-dependent fitness, and environmental heterogeneity, some of which have been discussed in the functions literature for decades. They argue that SE only seems to work because SE theorists ignore these dynamics. Their argument fails because they misrepresent what functions are supposed to explain and how they’re supposed to do so. One reason for this failure is that they overlook the role of functions in the broader conversation about teleology in biology, one that has been unfolding for over 2000 years.

This paper argues that proper functions are proximal functions. In other words, it rejects the notion that there are distal biological functions – strictly speaking, distal functions are not functions at all, but simply beneficial effects normally associated with a trait performing its function. Once we rule out distal functions, two further positions become available: dysfunctions are simply failures of proper function, and pathological conditions are dysfunctions. Although elegant and seemingly intuitive, this simple view has had surprisingly little uptake in the literature. Indeed, our position departs from that of almost every theorist who has engaged with the issue at any depth. We start by presenting three arguments for the position that proper functions are proximal: one from the specificity of functions, one from their relation to intervention, and one from their relation to pathology. We then consider two case studies evidencing the trouble that accepting distal functions causes for philosophical reflection on the nature of pathological conditions. Finally, we anticipate and respond to three objections: that there can be failure of function without dysfunction; that our account is unacceptably revisionary in respect of normal function-talk; and that our thesis over-generalises from a narrow set of cases.

In lieu of an abstract, here is a brief excerpt of the content:Lack, Perversion, ShameJustin Garson, PhD (bio)I am extremely grateful to the commentators for giving me so much food for thought. Space considerations prevent me from engaging with all of the interesting points they raise, or responding at the length they warrant. For that reason, I chose to structure my response in terms of three recurring themes or distinctions: lack/perversion, madness/mental illness, and shame/pride. Hopefully, the philosophical richness of the commentaries has already indicated the fruitfulness of returning, anew, to the Late Modern distinction between madness and idiocy.Lack and PerversionSeveral commentators directly challenge my characterization of the distinction between idiocy and madness as one between a lack, and a perversion, of the ordinary powers of reason.On the one hand, commentators point to the extent to which Late Modern theorists of madness still frame madness in terms of a lack, rather than a positive being. Jeppsson points out correctly that the Late Modern theorist still insists that madness stems from a lack of some sort or another: “one lacks proper premises to draw conclusions from, lacks a proper appreciation of reality.” Madness is not merely a different mode of reasoning about the world, but one that issues from a certain absence. Kusters, similarly, points out that the projects of Locke and Heinroth “remain insufficient because they remain focused on the mad as lacking something…a lack that prevents them from being part of the communal,” although he thinks Kant’s Aberwitz comes closest to a genuinely positive account. Tsou minimizes the relevance of the distinction between madness and idiocy by pointing out that both represent deviations from (hence they both “lack”) “normal psychological reason.”On the other hand, Banicki points out that even to construe madness in terms of a “lack” or “failure” (a failure of function, of reason, of action) is to presume, at least indirectly, a positive account of madness: after all, the mad person can only properly be said to “fail” in the exercise of their reason because they are the sort of being that participates in reason. A tree or a stone cannot be said to “fail” in the exercise of its reason (as Gipps puts it, “a baobab cannot jump to conclusions”). These commentators have helped me to clarify and sharpen the distinction between lack and perversion and the way they intersect with the categories of idiocy and madness.To put my view summarily: idiocy is, in its essence, just a way of lacking reason, in the same way that being poor is, in its essence, just a way of lacking wealth. But madness is not, in its essence, [End Page 327] a way of lacking reason. It is a way of exercising reason, but via perversion, where perversion must be understood as having the resonance both of excessive and also of driving toward an unexpected end.As I indicated in the paper, the distinction between lack and perversion is easiest to think about in terms of sexuality. A person may lack sexual desire: They may find themselves for long stretches of time with little to no desire for sex, the absence of sexual fantasies, and the inability to stimulate themselves or be stimulated by others. Crucially, being devoid of sexual desire is not a way of being sexual, any more than being dead is a way of being alive, or being a fish a way of being a mammal. By contrast, having a meager sexual desire is a way of being sexual, but via a lack or diminution: It is a way of not having much of it around.In contrast, one can have what is called a “perverse” sexuality: Sexuality infused with the desire to dominate, or be dominated, or to be watched from afar, or to couple with beasts or machines. This is a way of being sexual; it is even a kind of rampant sexuality. One talks of “harnessing” their sexuality, “restraining” it, “unleashing” it. For some, perversions may be terrifying to contemplate, almost unthinkable, even revolting. For others perversion is ecstatic; it transports one to another world in which one sees everything differently; the one who exercises her perversions morphs into an...

A basic question of philosophy of psychiatry is “what is madness (mental illness, mental disorder…)?” Contemporary thinkers err by framing the problem as one of defining madness in contrast with sanity. For the Late Modern theorist of madness, the problem was not one of defining madness in contrast with sanity, but in contrast with “idiocy”—the apparent diminution or abolition of one’s reasoning power. This altered reading of the problem has an important consequence. For what distinguishes madness from idiocy is not the failure, absence, or lack of reason, but its presence—albeit in a perverse and mutated form. For the Late Modern theorist, madness was always, by its very nature, infused with reason. This “infusion” of madness by reason has two consequences for philosophy of psychiatry today: it reframes the project of defining “mental disorder,” and it provides intellectual scaffolding for the emerging movement known as Mad Pride, mad resistance, or mad activism.

I argue that despite the merits of Jefferson’s account of a brain disorder, which are many, the notion of function she deploys is unsuitable to the overall goals of that account. In particular, Jefferson accepts Cummins’ causal role theory of function and dysfunction. As the causal role view, in its standard elaborations, is wedded to human interests, goals, and values, it cannot serve as a value-neutral anchor for her hybrid “harm-dysfunction” account of disorder. I argue that the selected effects theory, or some comparably value-neutral account, would serve her purposes better.

What is it for an animal to be female, or male? An emerging consensus among philosophers of biology is that sex is grounded in some manner or another on anisogamy, that is, the ability to produce either large gametes (egg) or small gametes (sperm), though the exact nature of this grounding remains contentious. Here we argue for a new conception of this relation. In our view, one’s sex doesn’t depend on the kind of gamete one is capable of making, but on the kind of gamete one is designed to make, where design is understood in terms of an evolutionary or ontogenetic selection process. Specifically, we argue that what it is to be, say, male, is to have a part or process that has the (proximal or distal) biological function of producing sperm. We outline and defend our view, and sketch some implications for scientific and social problems related to sex.

Philosophers who study the problem of biological function often begin their deliberations by reflecting on the functions of parts of animals, or the behavior of animals. Applying theories of biological function to unconventional or borderline cases can help us to better evaluate and refine those theories. This is the case when we consider whether parts of transposable elements —bits of “selfish” DNA that move about within a host genome—have functions of their own, that is, whether the parts of TEs have the function of helping the TE move about within the genome. Here I argue that whether or not the parts of TEs have functions depends crucially on whether collections of TEs form “populations,” by which I mean, here, a group of individuals of the same type that impact one another’s chances of persistence or multiplication, by impacting one another’s access to a shared resource. I think there is suggestive, but not conclusive, evidence that some TEs have functions of their own. Considering the problem of TE functionality, then, has value both for philosophy and for biology.

There is a certain metaphor that has enjoyed tremendous longevity in the evolution of ageing literature. According to this metaphor, nature has a certain goal or purpose, the perpetuation of the species, or, alternatively, the reproductive success of the individual. In relation to this goal, the individual organism has a function, job, or task, namely, to breed and, in some species, to raise its brood to maturity. On this picture, those who cannot, or can no longer, reproduce are somehow invisible to, or even dispensable to, the evolutionary process. Here, I argue that the metaphor should be discarded, not on the grounds that it is a metaphor, but on the grounds that this particular metaphor distorts our understanding of the evolution of ageing. One reason the metaphor is problematic is that it frames senescence and death as nature’s verdict on the value of older individuals. Instead, we should explore a different metaphor: the lengthy post-reproductive period in humans and some other animals is not an accident of culture, but designed by nature for the purpose of supporting and guiding younger generations. On this alternate picture, different stages of life have their own evolutionary rationales, their distinctive design features, their special mandates.

At the beginning of the twentieth century, the French philosopher of science Edmond Goblot wrote three prescient papers on function and teleology. He advanced the remarkable thesis that functions are, as a matter of conceptual analysis, selected effects. He also argued that “selection” must be understood broadly to include both evolutionary natural selection and intelligent design. Here, I do three things. First, I give an overview of Goblot’s thought. Second, I identify his core thesis about function. Third, I argue that, despite its ingenuity, Goblot’s expansive construal of function cannot be right. Still, Goblot deserves long-overdue credit for his work.

Mechanisms, in the prominent biological sense of the term, are historical entities. That is, whether or not something is a mechanism for something depends on its history. Put differently, while your spontaneously-generated molecule-for-molecule double has a heart, and its heart pumps blood around its body, its heart does not have a mechanism for pumping, since it does not have the right history. My argument for this claim is that mechanisms have proper functions; proper functions are historical entities; so, mechanisms are historical entities, too. This thesis runs against the mainstream new mechanist way of thinking about mechanisms, where mechanisms are generally thought of in an ahistorical way. After arguing for this thesis, I draw out some consequences for philosophy of science and metaphysics.

A framework is presented in which the role ofdevelopmental rules in phenotypic evolution canbe studied for some simple situations. Usingtwo different implicit models of development,characterized by different developmental mapsfrom genotypes to phenotypes, it is shown bysimulation that developmental rules and driftcan result in directional phenotypic evolutionwithout selection. For both models thesimulations show that the critical parameterthat drives the final phenotypic distributionis the cardinality of the set of genotypes thatmap to each phenotype. Details of thedevelopmental map do not matter. If phenotypesare randomly assigned to genotypes, the lastresult can also be proved analytically.

Why do some organisms rely on mental representations for making decisions? Why don’t we rely merely on direct mappings from perception to behavior? Armin W. Schulz’ book, Efficient Cognition: The Evolution of Representational Decision Making, offers a novel and empirically-informed perspective on a problem that has not received the amount of philosophical attention it deserves. In his view, representational decision making evolved because creatures that use it have enhanced cognitive and neurological efficiency. Here I provide an overview of the book’s contents and a critical assessment of his proposal.

Mainstream teleosemantics is the view that mental representation should be understood in terms of biological functions, which, in turn, should be understood in terms of selection processes. One of the traditional criticisms of teleosemantics is the problem of novel contents: how can teleosemantics explain our ability to represent properties that are evolutionarily novel? In response, some have argued that by generalizing the notion of a selection process to include phenomena such as operant conditioning, and the neural selection that underlies it, we can resolve this problem. Here, we do four things: we develop this suggestion in a rigorous way through a simple example, we draw on recent neurobiological research to support its empirical plausibility, we defend the move from a host of objections in the literature, and we sketch how the picture can be extended to help us think about more complex “conceptual” representations and not just perceptual ones.

In this journal, Schulte develops a novel solution to the problem of distal content: by virtue of what is a mental representation about a distal object rather than a more proximal cause of that representation? Schulte maintains that in order for a representation to have a distal content, it must be produced by a constancy mechanism, along with two other conditions. I raise three objections to his solution. First, a core component of Schulte's solution is just a restrictive version of Dretske's solution, but Schulte gives no argument for his restriction. Second, his proposed solution to a disjunction problem is ad hoc. Finally, his ‘far-out’ version of the distality problem is not a version of the distality problem at all. I conclude that Dretske's solution is preferable to Schulte's.

This chapter is about the causal role theory of function. According to this view, roughly, a function of a part of a system consists in its contribution to some system-level effect, which effect has been picked out as especially interesting by a group of researchers. I will discuss Robert Cummins’ original formulation of the view, and then present a more sophisticated variation, the mechanistic causal role theory, due to Carl Craver and Paul Sheldon Davies. I then discuss the classic problem of overbreadth, namely, that it seems to attribute functions too liberally. I distinguish two different versions of this problem: the problem of non-functional traits and the problem of dysfunctional traits. I provide a critical assessment of the ways causal role theorists have tried to solve these problems. Many philosophers of biology today have accepted a pluralistic stance, according to which both the selected effects theory, and the causal role theory, capture important elements of biological usage. I distinguish two forms of pluralism. The first (and most popular), between-discipline pluralism, holds that the selected effects theory mainly captures the way evolutionary biologists use the term “function” and the causal role theory mainly captures the way “function” is used in other disciplines. I object to this division of labor and recommend a new form of pluralism, within-discipline pluralism, which emphasizes the co-existence of function concepts within any given discipline.

This chapter focuses on the fitness-contribution theory of function, which holds, roughly, that the function of a trait consists in its typical contribution to the fitness of the organisms that possess it. I begin by surveying several different theories within this family, and I show why any plausible version must include a statistical element. I then pose three questions that any proponent of the fitness-contribution theory must answer. First, is fitness a relative notion? When one says a trait “contributes to fitness,” is one saying it contributes to fitness better than some alternative? If so, when we attribute a function to a trait, how do we specify the relevant alternatives? Second, is fitness relative to specific environments? If so, then when we attribute a function to a trait, how do we specify the relevant environments? Third, what precisely must a trait contribute to in order to have a function? Is it survival, reproduction, inclusive fitness, or something else? I then critically assess a major argument in its favor, namely, that it coheres well with the way biologists actually use the term. I consider three different interpretations of this claim and I argue that it does not, in fact, provide an advantage over the selected effects theory in this regard. I close by considering how well it satisfies the adequacy conditions set out in Chap. 1. Theorists disagree about whether the fitness-contribution theory can make sense of the explanatory and normative aspects of function and I survey those disagreements.

Biological functions are central to several debates in science and philosophy. In science, they play a role in debates in genetics, neuroscience, biomedicine, and ecology. In philosophy, they play a role in debates about the nature of teleological reasoning, biological information, trait classification, normativity, meaning and mental representation, health, disease, and the nature of artifacts. Yet philosophers and scientists disagree about what biological functions are, or whether there are different kinds of functions. One problem is that they do not agree about what, precisely, a philosophical theory of biological function is supposed to be or to do. I begin this chapter by discussing why functions matter to philosophy and science. I lay out three very traditional desiderata for a theory of function: namely, that the theory account for the function/accident distinction and the explanatory and normative features of function. I review three main approaches to thinking about what a theory of function should be: a conceptual analysis, a theoretical definition, and a Carnapian-style explication. I argue that it does not matter which one we accept so long as we agree that a theory of function should be reasonably constrained by actual biological usage.

Contemporary philosophical debates about biological function started in the early 1970s, and they originated from earlier, related, debates about the nature of goal directed systems. These discussions were rooted in scientific advances in the 1920s and 1930s pertaining to cybernetic machines and homeostatic systems, which appear to be purposeful or goal-directed despite not having any conscious intentions. By the 1950s, there were two major philosophical traditions for analyzing goal directedness, the behavioristic and the mechanistic. According to the behavioristic approach, favored by theorists like Gerd Sommerhoff and Richard Braithwaite, a goal directed system is one that exhibits plasticity and persistence in its outward behavior. According to the mechanistic tradition, favored by Ernest Nagel and Norbert Wiener, a goal directed system must be governed by the right sort of mechanism (such as negative feedback). Both of those traditions faced severe philosophical criticism in the 1960s and 1970s. I begin this chapter by sketching the historical background of the earlier debates about goal directedness. I then present the behavioristic analyses of Sommerhoff and Braithwaite, and enumerate several serious criticisms. I discuss mechanistic approaches, namely those of Nagel and the cyberneticists, and their critics.

This chapter focuses on the selected effects theory of function. According to this view, a function of a trait is whatever it was selected for by natural selection or some natural process of selection. I show how the theory plausibly accounts for the explanatory and normative aspects of function. First, if a function of a trait is whatever it was selected for by natural selection, then when one attributes a function to a trait one provides a causal explanation for why the trait currently exists. Second, since the function of a trait is determined by its history rather than current performance, it is easy to see how a trait can have a function that it cannot perform (“dysfunction”). I sketch the somewhat complex historical background of this theory. The theory was actually developed by biologists throughout the twentieth century, and in the 1970s philosophers began to explore it systematically. I survey the major criticisms of the theory and show why they are not compelling. Critics say that it does not really account for the explanatory and normative features of function; that it is inconsistent with the way biologists actually use the term; that there are (real or imaginary) counterexamples; and that it is committed to adaptationism. I close by presenting a new version of the theory, the generalized selected effects theory, which shows how brain structures (such as synapses) can acquire new functions during an individual’s lifetime through a process that is analogous in some ways to natural selection itself.