According to The Bell Curve, Black Americans are genetically inferior to Whites. That's not the only point in Richard Herrnstein and Charles Murray's book. They also argue that there is something called "general intelligence" which is measured by IQ tests, socially important, and 60 percent "heritable" within whites. (I'll explain heritability below.) But the claim about genetic inferiority is my target here. It has been subject to wide-ranging criticism since the book was first published last year. Those criticisms, however, have (...) missed its deepest flaws. Indeed, the Herrnstein/Murray argument depends on conceptual confusions that have been tacitly accepted to some degree by many of the book's sharpest critics. (shrink)

According to The Bell Curve , Black Americans are genetically inferior to Whites. That's not the only point in Richard Herrnstein and Charles Murray's book. They also argue that there is something called "general intelligence" which is measured by IQ tests, socially important, and 60 percent "heritable" within whites. (I'll explain heritability below.) But the claim about genetic inferiority is my target here. It has been subject to wide-ranging criticism since the book was first published last year. Those criticisms, however, (...) have missed its deepest flaws. Indeed, the Herrnstein/Murray argument depends on conceptual confusions that have been tacitly accepted to some degree by many of the book's sharpest critics. (shrink)

Anxious temperament (AT) in human and non-human primates is a trait-like phenotype evident early in life that is characterized by increased behavioural and physiological reactivity to mildly threatening stimuli1–4. Studies in children demonstrate that AT is an important risk factor for the later development of anxiety disorders, depression and comorbid substance abuse5. Despite its importance as an early predictor of psychopathology, little is known about the factors that predispose vulnerable children to develop AT and the brain systems that underlie its (...) expression. To characterize the neural circuitry associated with AT and the extent to which the function of this circuit is heritable, we studied a large sample of rhesus monkeys phenotyped for AT. Using 238 young monkeys from a multigenerational single-family pedigree, we simultaneously assessed brain metabolic activity and AT while monkeys were exposed to the relevant ethological condition that elicits the phenotype. High-resolution 18F-labelled deoxyglucose positron-emission tomography (FDG–PET) was selected as the imaging modality because it provides semi-quantitative indices of absolute glucose metabolic rate, allows for simultaneous measurement of behaviour and brain activity, and has a time course suited for assessing temperament-associated sustained brain responses. Here we demonstrate that the central nucleus region of the amygdala and the anterior hippocampus are key components of the neural circuit predictive of AT. We also show significant heritability of the AT phenotype by using quantitative genetic analysis. Additionally, using voxelwise analyses, we reveal significant heritability of metabolic activity in AT-associated hippocampal regions. However, activity in the amygdala region predictive of AT is not significantly heritable. Furthermore, the heritabilities of the hippocampal and amygdala regions significantly differ from each other. Even though these structures are closely linked, the results suggest differential influences of genes and environment on how these brain regions mediate AT and the ongoing risk of developing anxiety and depression. Anxiety disorders are among the most common forms of psychopathology6, and frequently begin during childhood and adolescence. Although all children experience acute anxiety, children with AT display extreme behavioural and physiological reactivity to novel stimuli, and in the presence of strangers inhibit their locomotor activity and vocalizations3.. (shrink)

In "The pitfalls of heritability," a review of Edward O. Wilson’s Consilience Times Literary Supplement, Feb 12, 1999, p33], Jerry Hirsch claims to have convicted Wilson of a "confusion about genetic similarity and difference." In his book, Wilson claims that if we assume that "a mere one thousand genes out of the fifty to a hundred thousand genes in the human genome were to exist in two forms in the population," the probability of any two humans--excluding identical siblings--having the same (...) genotype is vanishingly small. Hirsch points out that a single genotype can be produced in more than one way, thus increasing the likelihood of a single genotype recurring in the human population. Hirsch’s point is fair enough as far it goes, but it does not go nearly far enough. Hirsch has failed to carry out all the relevant calculations needed to determine the probability of two humans having the same genotype. In the realm of Vast numbers ("Very much greater than ASTronomical"--Dennett, 1995, p109), increased likelihood in and of itself tells us nothing. Here, then, are some of the relevant calculations. (shrink)

This paper examines some criticisms that have been made of two standard genetic methodologies: heritability and path analysis. I conclude that the criticisms should be taken seriously, concerning both the accuracy of heritability measures and their significance. In light of the fact that such studies remain prominent in the literature, I consider what possible rationale they can retain consistent with these criticisms. In particular, I consider (1) a role in the identification of high-risk individuals and (2) a heuristic role in (...) the planning of research strategy. (shrink)

In a previous study, using experimental metapopulations of the flour beetle, Tribolium castaneum, we investigated phase III of Wright's shifting balance process (Wade and Griesemer 1998). We experimentally modeled migration of varying amounts from demes of high mean fitness into demes of lower mean fitness (as in Wright's characterization of phase III) as well as the reciprocal (the opposite of phase III). We estimated the meta-populational heritability for this level of selection by regression of offspring deme means on the weighted (...) parental deme means.Here we develop a Punnett Square representation of the inheritance of the group mean to place our empirical findings in a conceptual context similar to Mendelian inheritance of individual traits. The comparison of Punnett Squares for individual and group inheritance shows how the latter concept can be rigorously defined and extended despite the lack of explicitly formulated, simple Mendelian laws of inheritance at the group level. Whereas Wright's phase III combines both interdemic selection and meta-populational inheritance, our formulation separates the issue of meta-populational heritability from that of interdemic selection. We use this conceptual context to discuss the controversies over the levels of selection and the units of inheritance. (shrink)

Many natural and biological phenomena can be depicted as networks. Theoretical and empirical analyses of networks have become prevalent. I discuss theoretical biases involved in the delineation of biological networks. The network perspective is shown to dissolve the distinction between regulatory architecture and regulatory state, consistent with the theoretical impossibility of distinguishing a priori between “program” and “data”. The evolutionary significance of the dynamics of trans-generational and inter-organism regulatory networks is explored and implications are presented for understanding the evolution of (...) the biological categories development-heredity; plasticity-evolvability; and epigenetic-genetic. (shrink)

The dichotomy between Nature and Nurture, which has been dismantled within the framework of development, remains embodied in the notions of plasticity and evolvability. We argue that plasticity and evolvability, like development and heredity, are neither dichotomous nor distinct: the very same mechanisms may be involved in both, and the research perspective chosen depends to a large extent on the type of problem being explored and the kinds of questions being asked. Epigenetic inheritance leads to transgenerationally extended plasticity, and developmentally-induced (...) heritable epigenetic variations provide additional foci for selection that can lead to evolutionary change. Moreover, hereditary innovations may result from developmentally induced large-scale genomic repatterning events, which are akin to Goldschmidtian “systemic mutations”. The epigenetic mechanisms involved in repatterning can be activated by both environmental and genomic stress, and lead to phylogenetic as well as ontogenetic changes. Hence, the effects and the mechanisms of plasticity directly contribute to evolvability. (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)

This paper investigates the role of the concept of group heritability in group selection theory, in relation to the well-known distinction between type 1 and type 2 group selection (GS1 and GS2). I argue that group heritability is required for the operation of GS1 but not GS2, despite what a number of authors have claimed. I offer a numerical example of the evolution of altruism in a multi-group population which demonstrates that a group heritability coefficient of zero is perfectly compatible (...) with the successful operation of group selection in the GS2 sense. A diagnosis of why group heritability has wrongly been regarded as necessary for GS2 is suggested. (shrink)

In recent years, biologists have increasingly been asking whether the ability to evolve — the evolvability — of biological systems, itself evolves, and whether this phenomenon is the result of natural selection or a by-product of other evolutionary processes. The concept of evolvability, and the increasing theoretical and empirical literature that refers to it, may constitute one of several pillars on which an extended evolutionary synthesis will take shape during the next few years, although much work remains to be done (...) on how evolvability comes about. (shrink)

The derivation of heritability from human twin studies involves serious methodological flaws. Heritability is consistently overestimated because of biological confounds of twinning, consistent and often gross underestimation of the environmental variance, and nonadditive genetic influences that can hugely exaggerate heritability values. Despite this bad research design, behaviour geneticists continue to publish results implying that their heritability results are valid.

Genetic differences can lead to phenotypic differences either directly or indirectly (via causing differences in external environments, which then affect phenotype). This possibility of genetic effects being mediated by environmental influences is often used by scientists and philosophers to argue that heritability is not a very helpful causal or explanatory notion. In this paper it is shown that these criticisms are based on serious misconceptions about methods of behavior genetics.

Philosophers of science widely believe that the hereditarian theory about racial differences in IQ is based on methodological mistakes and confusions involving the concept of heritability. I argue that this "received view" is wrong: methodological criticisms popular among philosophers are seriously misconceived, and the discussion in philosophy of science about these matters is largely disconnected from the real, empirically complex issues debated in science.

The critics of "hereditarianism" often claim that any attempt to explain human behavior by invoking genes is confronted with insurmountable methodological difficulties. They reject the idea that heritability estimates could lead to genetic explanations by pointing out that these estimates are strictly valid only for a given population and that they are exposed to the irremovable confounding effects of genotype-environment interaction and genotype-environment correlation. I argue that these difficulties are greatly exaggerated, and that we would be wrong to regard them (...) as presenting a fundamental obstacle to the search for genetic explanations. I also show that, to the extent they are cogent, these objections may prove to be even more damaging to the "environmentalist" standpoint. (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)

This article examines eight “gaps” in order to clarify why the quantitative genetics methods of partitioning variation of a trait into heritability and other components has very limited power to show anything clear and useful about genetic and environmental influences, especially for human behaviors and other traits. The first two gaps should be kept open; the others should be bridged or the difficulty of doing so should be acknowledged: 1. Key terms have multiple meanings that are distinct; 2. Statistical patterns (...) are distinct from measurable underlying factors; 3. Translation from statistical analyses to hypotheses about measurable factors is difficult; 4. Predictions based on extrapolations from existing patterns of variation may not match outcomes; 5. The partitioning of variation in human studies does not reliably estimate the intended quantities; 6. Translation from statistical analyses to hypotheses about the measurable factors is even more difficult in light of the possible heterogeneity of underlying genetic or environmental factors; 7. Many steps lie between the analysis of observed traits and interventions based on well-founded claims about the causal influence of genetic or environmental factors; 8. Explanation of variation within groups does not translate to explanation of differences among groups. At the start, I engage readers’ attention with three puzzles that have not been resolved by past debates. The puzzles concern generational increases in IQ test scores, the possibility of underlying heterogeneity, and the translation of methods from selective breeding into human genetics. After discussing the gaps, I present each puzzle in a new light and point to several new puzzles that invite attention from analysts of variation in quantitative genetics and in social science more generally. The article’s critical perspectives on agricultural, laboratory, and human heritability studies are intended to elicit further contributions from readers across the fields of history, philosophy, sociology, and politics of biology and in the sciences. (shrink)