With the advent of the Human Genome Project there have been many claims for the genetic origins of complex human behavior including insanity, criminality, and intelligence. But what does it really mean to call something 'genetic'? This is the fundamental question that Sahotra Sarkar's book addresses. The author analyses the nature of reductionism in classical and molecular genetics. He shows that there are two radically different kinds of reductionist explanation: genetic reduction (as found in classical genetics) and physical reduction (found (...) in molecular genetics). This important book clarifies the meaning of the term 'genetic', shows how molecular studies have affected genetics, and provides the philosophical background necessary to understand the debates over the Human Genome Project. It will be of particular interest to professionals and students in the philosophy of science, the history of science, and the social studies of science, medicine, and technology. (shrink)

In this book, Neven Sesardic defends the view that it is both possible and useful to measure the separate contributions of heredity and environment to the explanation of human psychological differences. He critically examines the view - very widely accepted by scientists, social scientists and philosophers of science - that heritability estimates have no causal implications and are devoid of any interest. In a series of clearly written chapters he introduces the reader to the problems and subjects the arguments to (...) close philosophical scrutiny. His conclusion is that anti-heritability arguments are based on conceptual confusions and misunderstandings of behavioural genetics. His book is a fresh and compelling intervention in a very contentious debate. (shrink)

Can a heritability value tell us something about the weight of genetic versus environmental causes that have acted in the development of a particular individual? Two possible questions arise. Q1: what portion of the phenotype of X is due to its genes and what portion to its environment? Q2: what portion of X’s phenotypic deviation from the mean is a result of its genetic deviation and what portion a result of its environmental deviation? An answer to Q1 provides the full (...) information about X’s development, while an answer to Q2 leaves out a large portion unexplained—that portion which corresponds to the phenotypic mean. Q1 is unanswerable, but I show it is nevertheless legitimate under certain quantitative genetics models. With regard to Q2, opinions in the philosophical and biological literature differ as to its legitimacy. I argue that not only is it legitimate, but in particular, under a few simplifying assumptions, it allows for a quantitative probabilistic answer: for normally distributed quantitative traits with no G-E correlation or statistical G × E interaction, we can assess the probability that X’s genes had a greater effect than its environment on its deviation from the mean population value. This probability is expressed as a function the heritability and the individual’s phenotypic value; we can also provide a quantitative probabilistic answer to Q2 for an arbitrary individual where the probability is a function only of heritability. (shrink)

Philosophers of science have developed an account of causal-mechanical explanation that captures regularity, but this account neglects variation. In this article I amend the philosophy of mechanisms to capture variation. The task is to explicate the relationship between regular causal mechanisms responsible for individual development and causes of variation responsible for variation in populations. As it turns out, disputes over this relationship have rested at the heart of the nature–nurture debate. Thus, an explication of the relationship between regular causal mechanisms (...) and causes of variation and between individual development and variation offers both the necessary amendment to the philosophy of mechanisms and the resources to mediate the dispute. (shrink)

The method in human genetics of ascribing causal responsibility to genotype by the use of heritability estimates has been heavily criticized over the years. It has been argued that these estimates are rarely valid and do not serve the purpose of tracing genetic causes. Recent contributions strike back at this criticism. I present and discuss two opposing views on these matters represented by Richard Lewontin and Neven Sesardic, and I suggest that some of the disagreement is based on differing concepts (...) of genetic causation. I use the distinction of structuring and triggering causes to help clarifying the basis for the opposing views. (shrink)