Paul Edmund Griffiths

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.

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.

Emotion theory is beset by category disputes. Examining the nature and function of scientific classification can make some of these more tractable. The aim of classification is to group particulars into <<natural>> classes - classes whose members share a rich cluster of properties in addition to those used to place them in the class. Classification is inextricably linked to theories of the causal processes that explain why certain particulars resemble one another and so are usefully regarded as <<of the same kind>>. The need to base categories on underlying causal processes explains why mere careful definition (including operational definition) need not produce categories that are productive objects of scientific study. Because different causal processes produce different patterns of similarity there is unlikely to be a single classification that is optimal for addressing all scientific questions. Cultural categories should not be contrasted to natural categories, but should be treated as natural classes generated by underlying social processes. Our capacity to introduce epistemically optimal categories is often restricted because categories play a role in social and political, as well as epistemic, projects. This account of classification has many implications for emotion theory.

Throughout his career David Hull has sought to bring the philosophy of science into closer contact with science and especially with biological science (Hull 1969, 1997b). This effort has taken many forms. Sometimes it has meant ‘either explaining basic biology to philosophers or explaining basic philosophy to biologists’ (Hull 1996, p. 77). The first of these tasks, simple as it sounds, has been responsible for revolutionary changes. It is well known that traditional philosophy of science, modeled as it was on theoretical physics, proved inadequate when philosophers turned their attention to biological science. Biological examples have driven major revisions of accounts of reduction (Hull 1974; Schaffner 1993, Ch. 9), laws of nature (Beatty et al. 1997), theories (Lloyd 1988) and natural kinds (Wilson 1999, Part III). Nor is explaining basic philosophy to biologists a task to be looked down upon. It is useful, not because philosophy has all the answers, but because scientists must think about how to do science, that is doing philosophy of science and scientists frequently reinvent philosophical views with known flaws. Early in his career Hull found biological systematists in the grip of a crude operationalism about scientific concepts and said so in the pages of Systematic Zoology (Hull 1968). For the next thirty years, as biologists debated the nature of species and the correct principles of classification, Hull added a philosophical note at the same congresses and in the same journals (Hull 1970, 1976, 1980, 1997a, 1999).

Kenneth C. Schaffner's paper is an important contribution to the literature on behavioral genetics and on genetics in general. Schaffner has a long record of injecting real molecular biology into philosophical discussions of genetics. His treatments of the reduction of Mendelian to molecular genetics first drew philosophical attention to the problems of detail that have fuelled both anti-reductionism and more sophisticated models of theory reduction. An injection of molecular detail into discussions of genetics is particularly necessary at the present time, when so many philosophers seem happy to discuss the philosophical and ethical implications of molecular biology using gene concepts derived from evolutionary biology ). Schaffner has long advocated the view that the philosophy of biology should be more than the philosophy of evolution. This paper shows how radically a picture of gene action derived from molecular biology undercuts the popular picture associated with a more evolutionary view of genes as units of heredity or as ‘difference-makers’ mediated by the ‘black box’ of development.

At the beginning of the 1950s most students of animal behavior in Britain saw the instinct concept developed by Konrad Lorenz in the 1930s as the central theoretical construct of the new ethology. In the mid 1950s J.B.S. Haldane made substantial efforts to undermine Lorenz''s status as the founder of the new discipline, challenging his priority on key ethological concepts. Haldane was also critical of Lorenz''s sharp distinction between instinctive and learnt behavior. This was inconsistent with Haldane''s account of the evolution of language, and, according to Haldane, inconsistent with elementary genetics. British attitudes to the instinct concept changed dramatically in the wake of Daniel S. Lehraman''s 1953 critique of Lorenz, and by the 1960s Lorenz drew a clear distinction between his own views and those of the English-speaking ethologists. The inconsistencies between Lorenz''s ideas and the trends in contemporary evolutionary genetics that are reflected in Haldane''s critiques may help to explain why the Lorenzian instinct concept was unable to maintain itself in Britian.

Genetic determinism is the idea that many significant human characteristics are rendered inevitable by the presence of certain genes. The psychologist Susan Oyama has famously compared arguing against genetic determinism to battling the undead. Oyama suggests that genetic determinism is inherent in the way we currently represent genes and what genes do. As long as genes are represented as containing information about how the organism will develop, they will continue to be regarded as determining causes no matter how much evidence exists to the contrary. Philip Kitcher has strongly disputed Oyama’s diagnosis, arguing that the conventional ‘interactionist’ perspective on development is the correct framework for understanding the role of the genes in development. While acknowledging the legitimacy of many of Kitcher’s observations, I believe that Oyama’s view is substantially correct. In this paper I provide several lines of support for support the Oyama diagnosis.

The widely cited Nuffield Council on Bioethics ‘Intervention Ladder’ structurally embodies the assumption that personal autonomy is maximized by non-intervention. Consequently, the Intervention Ladder encourages an extreme ‘negative liberty’ view of autonomy. Yet there are several alternative accounts of autonomy that are both arguably superior as accounts of autonomy and better suited to the issues facing public health ethics. We propose to replace the one-sided ladder, which has any intervention coming at a cost to autonomy, with a two-sided ‘Balanced Intervention Ladder,’ where intervention can either enhance or diminish autonomy. We show that not only the alternative, richer accounts of autonomy but even Mill’s classic version of negative liberty puts some interventions on the positive side of the ladder

The 23rd volume in the respected series Ô Basic Bioethics’, this book contains seven original and two reprinted essays and a substantial introductory chapter by the editor. The main concern of the editor, and of several contributors, is to dispel the view that organised reli- gion has been consistently hostile to new biomedical developments. Instead, they emphasise that the practice of medicine is endorsed by the Church and by Jewish tradition. In principle, germline mod- ification might count as an extension of medicine. A consensus emerges in the volume that germline modification would be accept- able if it could be developed and applied with safety and social equity, without destroying any human embryos, and if conducted purely for therapeutic purposes rather than for any form of genetic enhancement.

Experimental philosophy of science gathers empirical data on how key scientific concepts are understood by particular scientific communities. In this paper we briefly describe two recent studies in experimental philosophy of biology, one investigating the concept of the gene, the other the concept of innateness. The use of experimental methods reveals facts about these concepts that would not be accessible using the traditional method of intuitions about possible cases. It also contributes to the study of conceptual change in science, which we understand as the result of a form of conceptual ecology, in which concepts become adapted to specific epistemic niches.

The Royal Institute of Philosophy’s London lecture series for 2004–2005 offers a useful snapshot of the current state of philosophy of biology in Britain. With one or two exceptions the papers are not simply current research articles. The authors map out questions they feel need more research, analyse ongoing debates, or outline the program of their own previously published work. This presumably reflects the fact that the papers are based closely on public lectures. It also makes for surprisingly easy and enjoyable reading in the context of such a volume.