Paul Edmund Griffiths

The aim of appraisal theory in the psychology of emotion is to identify the features of the emotion-eliciting situation that lead to the production of one emotion rather than another². A model of emotional appraisal takes the form of a set of dimensions against which potentially emotion-eliciting situations are assessed. The dimensions of the emotion hyperspace might include, for example, whether the eliciting situation fulfills or frustrates the subject’s goals or whether an actor in the eliciting situation has violated a norm. Richard Lazarus’s well-known model of emotional appraisal has six dimensions, and the regions of the resulting hyperspace that correspond to particular emotions are summarized by Lazarus as the ‘core relational themes’ of those emotions. Anger, for examples, is elicited by the core relational theme ‘a demeaning offence against me and mine’, sadness by ‘having experienced an irrevocable loss’ and guilt by ‘having transgressed a moral imperative’ (Lazarus, 1991)

Mismatch is a prominent concept in evolutionary medicine, and a number of philosophers have published analyses of this concept. The word ‘mismatch’ has been used in a diversity of ways across a range of sciences, leading these authors to regard it as a vague concept in need of philosophical clarification. Here, in contrast, we concentrate on the use of mismatch in modelling and experimentation in evolutionary medicine. This reveals a rigorous theory of mismatch within which the term ‘mismatch’ is indeed used in several ways, not because it is ill defined but because different forms of mismatch are distinguished within the theory. Contemporary evolutionary medicine has unified the idea of ‘evolutionary mismatch’, derived from the older idea of ‘adaptive lag’ in evolution, with ideas about mismatch in development and physiology derived from the developmental origins of health and disease (DOHaD) paradigm. A number of publications in evolutionary medicine have tried to make this theoretical framework explicit. We build on these to present the theory in as simple and general a form as possible. We introduce terminology, largely drawn from the existing literature, to distinguish the different forms of mismatch. This integrative theory of mismatch captures how organisms track environments across space and time on multiple scales in order to maintain an adaptive match to the environment, and how failures of adaptive tracking lead to disease. Mismatch is a productive organizing concept within this theory that helps researchers articulate how physiology, development, and evolution interact with one another and with environmental change to explain health outcomes.

Several authors have argued that causes differ in the degree to which they are ‘specific’ to their effects. Woodward has used this idea to enrich his influential interventionist theory of causal explanation. Here we propose a way to measure causal specificity using tools from information theory. We show that the specificity of a causal variable is not well-defined without a probability distribution over the states of that variable. We demonstrate the tractability and interest of our proposed measure by measuring the specificity of coding DNA and other factors in a simple model of the production of mRNA.

We assess the arguments for recognising functionally integrated multispecies consortia as genuine biological individuals, including cases of so-called ‘holobionts’. We provide two examples in which the same core biochemical processes that sustain life are distributed across a consortium of individuals of different species. Although the same chemistry features in both examples, proponents of the holobiont as unit of evolution would recognize one of the two cases as a multispecies individual whilst they would consider the other as a compelling case of ecological dependence between separate individuals. Some widely used arguments in support of the ‘holobiont’ concept apply equally to both cases, suggesting that those arguments have misidentified what is at stake when seeking to identify a new level of biological individuality. One important aspect of biological individuality is evolutionary individuality. In line with other work on the evolution of individuality, we show that our cases can be distinguished by focusing on the fitness alignment between the partners of the consortia. We conclude that much of the evidence currently presented for the ubiquity and importance of multi-species individuals is simply not to the point, at least unless the issue of biological individuality is firmly divorced from the question of evolutionary individuality.

The interventionist account of causation offers a criterion to distinguish causes from non-causes. It also aims at defining various desirable properties of causal relationships, such as specificity, proportionality and stability. Here we apply an information-theoretic approach to these properties. We show that the interventionist criterion of causation is formally equivalent to non-zero specificity, and that there are natural, information-theoretic ways to explicate the distinction between potential and actual causal influence. We explicate the idea that the description of causes should be proportional to that of their effects. Then we draw a distinction between two ideas in the existing literature, the range of invariance of a causal relationship and its stability. The range of invariance is related to specificity and range of causal values. Stability concerns the effect of additional variables on the relationship between some focal pair of cause and effect variables. We show how to distinguish and measure the direct influence of background variables on the effect variable, and their influence on the relationship between the focal cause and the effect variable. Finally, we discuss the limitations of the information-theoretic approach, and offer prospects for complementary approaches.

John Maynard Smith has defended against philosophical criticism the view that developmental biology is the study of the expression of information encoded in the genes by natural selection. However, like other naturalistic concepts of information, this ‘teleosemantic’ information applies to many non-genetic factors in development. Maynard Smith also fails to show that developmental biology is concerned with teleosemantic information. Some other ways to support Maynard Smith’s conclusion are considered. It is argued that on any definition of information the view that development is the expression of genetic information is misleading. Some reasons for the popularity of that view are suggested.

Recent work by Brian Skyrms offers a very general way to think about how information flows and evolves in biological networks—from the way monkeys in a troop communicate to the way cells in a body coordinate their actions. A central feature of his account is a way to formally measure the quantity of information contained in the signals in these networks. In this article, we argue there is a tension between how Skyrms talks of signalling networks and his formal measure of information. Although Skyrms refers to both how information flows through networks and that signals carry information, we show that his formal measure only captures the latter. We then suggest that to capture the notion of flow in signalling networks, we need to treat them as causal networks. This provides the formal tools to define a measure that does capture flow, and we do so by drawing on recent work defining causal specificity. Finally, we suggest that this new measure is crucial if we wish to explain how evolution creates information. For signals to play a role in explaining their own origins and stability, they can’t just carry information about acts; they must be difference-makers for acts. _1_ Signalling, Evolution, and Information _2_ Skyrms’s Measure of Information _3_ Carrying Information versus Information Flow _3.1_ Example 1 _3.2_ Example 2 _3.3_ Example 3 _4_ Signalling Networks Are Causal Networks _4.1_ Causal specificity _4.2_ Formalizing causal specificity _5_ Information Flow as Causal Control _5.1_ Example 1 _5.2_ Examples 2 and 3 _5.3_ Average control implicitly ‘holds fixed’ other pathways _6_ How Does Evolution Create Information? _7_ Conclusion Appendix >

We defend a view of the distinction between the normal and the pathological according to which that distinction has an objective, biological component. We accept that there is a normative component to the concept of disease, especially as applied to human beings. Nevertheless, an organism cannot be in a pathological state unless something has gone wrong for that organism from a purely biological point of view. Biology, we argue, recognises two sources of biological normativity, which jointly generate four “ways of going wrong” from a biological perspective. These findings show why previous attempts to provide objective criteria for pathology have fallen short: Biological science recognizes a broader range of ways in which living things can do better or worse than has previously been recognized in the philosophy of medicine.

We argue that there are three coherent, nontrivial notions of basic-ness: conceptual basic-ness, biological basic-ness, and psychological basic-ness. There is considerable evidence for conceptually basic emotion categories (e.g., “anger,” “fear”). These categories do not designate biologically basic emotions, but some forms of anger, fear, and so on that are biologically basic in a sense we will specify. Finally, two notions of psychological basic-ness are distinguished, and the evidence for them is evaluated. The framework we offer acknowledges the force of some of the objections to basic emotion theory whilst demonstrating that the notion of a basic emotion, once properly reformulated, is still of scientific value.

When explaining the causes of human behavior, genes are often given a special status. They are thought to relate to an intrinsic human 'essence', and essentialist biases have been shown to skew the way in which causation is assessed. Causal reasoning in general is subject to other pre-existing biases, including beliefs about normativity and morality. In this synthesis we show how factors which influence causal reasoning can be mapped to a framework of genetic essentialism, which reveals both the shared and unique factors underpinning biases in causal reasoning and genetic essentialism. This comparison identifies overlooked areas of research which could provide fruitful investigation, such as whether normative assessments of behaviors influence the way that genetic causes are ascribed or endorsed. We also outline the importance of distinguishing reasoning processes regarding genetic causal influences on one's self versus others, as different cognitive processes and biases are likely to be at play.

Developmental systems theory is a general theoretical perspective on development, heredity and evolution. It is intended to facilitate the study of interactions between the many factors that influence development without reviving `dichotomous' debates over nature or nurture, gene or environment, biology or culture. Several recent papers have addressed the relationship between DST and the thriving new discipline of evolutionary developmental biology. The contributions to this literature by evolutionary developmental biologists contain three important misunderstandings of DST.

Developmental systems theory (DST) is a wholeheartedly epigenetic approach to development, inheritance and evolution. The developmental system of an organism is the entire matrix of resources that are needed to reproduce the life cycle. The range of developmental resources that are properly described as being inherited, and which are subject to natural selection, is far wider than has traditionally been allowed. Evolution acts on this extended set of developmental resources. From a developmental systems perspective, development does not proceed according to a preformed plan; what is inherited is much more than DNA; and evolution is change not only in gene frequencies, but in entire developmental systems.

Integrating the study of human diversity into the human evolutionary sciences requires substantial revision of traditional conceptions of a shared human nature. This process may be made more difficult by entrenched, 'folkbiological' modes of thought. Earlier work by the authors suggests that biologically naive subjects hold an implicit theory according to which some traits are expressions of an animal's inner nature while others are imposed by its environment. In this paper, we report further studies that extend and refine our account of this aspect of folkbiology. We examine biologically naive subjects' judgments about whether traits of an animal are 'innate', 'in its DNA' or 'part of its nature'. Subjects do not understand these three descriptions to be equivalent. Both innate and in its DNA have the connotation that the trait is species-typical. This poses an obstacle to the assimilation of the biology of polymorphic and plastic traits by biologically naive audiences. Researchers themselves may not be immune to the continuing pull of folkbiological modes of thought.

I defend the view that many biological categories are defined by homology against a series of arguments designed to show that all biological categories are defined, at least in part, by selected function. I show that categories of homology are `abnormality inclusive'—something often alleged to be unique to selected function categories. I show that classifications by selected function are logically dependent on classifications by homology, but not vice-versa. Finally, I reject the view that biologists must use considerations of selected function to abstract away from variation and pathology to form a canonical description of a class of biological systems.

We describe an approach to measuring biological information where ‘information’ is understood in the sense found in Francis Crick’s foundational contributions to molecular biology. Genes contain information in this sense, but so do epigenetic factors, as many biologists have recognized. The term ‘epigenetic’ is ambiguous, and we introduce a distinction between epigenetic and exogenetic inheritance to clarify one aspect of this ambiguity. These three heredity systems play complementary roles in supplying information for development. We then consider the evolutionary significance of the three inheritance systems. Whilst the genetic inheritance system was the key innovation in the evolution of heredity, in modern organisms the three systems each play important and complementary roles in heredity and evolution. Our focus in the earlier part of the paper is on ‘proximate biology’, where information is a substantial causal factor that causes organisms to develop and causes offspring to resemble their parents. But much philosophical work has focused on information in ‘ultimate biology’. Ultimate information is a way of talking about the evolutionary design of the mechanisms of development and inheritance. We conclude by clarifying the relationship between the two. Ultimate information is not a causal factor that acts in development or heredity, but it can help to explain the evolution of proximate information, which is.

The idea that development is the expression of information accumulated during evolution and that heredity is the transmission of this information is surprisingly hard to cash out in strict, scientific terms. This paper seeks to do so using the sense of information introduced by Francis Crick in his sequence hypothesis and central dogma of molecular biology. It focuses on Crick's idea of precise determination. This is analysed using an information-theoretic measure of causal specificity. This allows us to reconstruct some of Crick's claims about information in transcription and translation. Crick's approach to information has natural extensions to non-coding regions of DNA, to epigenetic marks, and to the genetic or environmental upstream causes of those epigenetic marks. Epigenetic information cannot be reduced to genetic information. The existence of biological information in epigenetic and exogenetic factors is relevant to evolution as well as to development.

Paul E. Griffiths defends an account of biological information that can be used to buttress Kitcher’s causal democracy principle. He argues that we can combine the insights of interventionist accounts of causation with Shannon’s information theory to develop an account of proximate information in terms of causal specificity. Moreover Griffiths defends an ahistorical notion of biological teleology that can figure in proximate explanations of development. Both notions of information are consistent with Kitcher’s principle, since both leave open which causal factors—genetic or environmental—might be carriers of information. Hence Griffiths argues that rather than being a barrier to understanding gene-environment interaction, such notions of biological information might prove useful in vindicating Kitcher’s principle.

It is now widely accepted that a scientifically credible conception of human nature must reject the folkbiological idea of a fixed, inner essence that makes us human. We argue here that to understand human nature is to understand the plastic process of human development and the diversity it produces. Drawing on the framework of developmental systems theory and the idea of developmental niche construction we argue that human nature is not embodied in only one input to development, such as the genome, and that it should not be confined to universal or typical human characteristics. Both similarities and certain classes of differences are explained by a human developmental system that reaches well out into the 'environment'. We point to a significant overlap between our account and the ‘Life History Trait Cluster’ account of Grant Ramsey, and defend the developmental systems account against the accusation that trying to encompass developmental plasticity and human diversity leads to an unmanageably complex account of human nature.

Griffiths and Russell D. Gray (1994, 1997, 2001) have argued that the fundamental unit of analysis in developmental systems theory should be a process – the life cycle – and not a set of developmental resources and interactions between those resources. The key concepts of developmental systems theory, epigenesis and developmental dynamics, both also suggest a process view of the units of development. This chapter explores in more depth the features of developmental systems theory that favour treating processes as fundamental in biology and examines the continuity between developmental systems theory and ideas about process in the work of several major figures in early 20th century biology, most notable C.H Waddington.

I adopt a cladistic view of species, and explore the possibility that there exists an equally valuable cladistic view of organismic traits. This suggestion seems to run counter to the stress on functional views of biological traits in recent work in philosophy and psychology. I show how the tension between these two views can be defused with a multilevel view of biological explanation. Despite the attractions of this compromise, I conclude that we must reject it, and adopt an essentially cladistic conception of biological traits

The air of consensus in these reviews is, as McNaughton notes, methodological. The future of philosophical emotion theory is in synthesising what a wide range of science has to tell us and using this to reflect on the nature of mind in general. In this respect the philosophy of emotion has been seriously out of step with the rest of a very exciting contemporary scene in the philosophy of mind. Whatever the shortcomings of my own attempt to bring the philosophy of emotion into contact with the rest of the discipline, I predict that this ‘reclaimed land’ will prove fertile