Taking the ‘Error’ Out of Ruse‘s Error Theory

Michael Ruses Darwinian metaethics has come under just criticism from Peter Woolcock (1993). But with modification it remains defensible. Ruse (1986) holds that people ordinarily have a false belief that there are objective moral obligations. He argues that the evolutionary story should be taken as an error theory, i.e., as a theory which explains the belief that there are obligations as arising from non-rational causes, rather than from inference or evidential reasons. Woolcock quite rightly objects that this position entails moral nihilism. However, I argue here that people generally have justified true beliefs about which acts promote their most coherent set of moral values, and hence, by definition, about which acts are right. What the evolutionary story explains is the existence of these values, but it is not an error theory for moral beliefs. Ordinary beliefs correspond to real moral properties, though these are not objective or absolute properties independent of anyones subjective states. On its best footing, therefore, a Darwinian metaethics of the type Ruse offers is not an error theory and does not entail moral nihilism.     

Why there are no objective values: A critique of ethical intuitionism from an evolutionary point of view

Using concepts of evolutionary game theory, this paper presents a critique of ethical intuitionism, or non-naturalism, in its cognitivist and objectivist interpretation. While epistemological considerations suggest that human rational learning through experience provides no basis for objective moral knowledge, it is argued below that modern evolutionary theory explains why this is so, i.e., why biological organisms do not evolve so as to experience objective preferences and obligations. The difference between the modes of the cognition of objective and of valuative environmental attributes is explained with reference to different modes of natural selection acting on the cognitive apparatus of the organism. The negative implications are pointed out which the observable diversity of intraspecific behavioural adaptations and of cultural values has for the cognitivist, objectivist foundation of ethics. Eventually a non-cognitivist alternative to ethical intuitionism is outlined in terms of empirical authority relations, with the ritualisation of dominance-submission patterns as the evolutionary origin of human charismatic authority.     

Some Nonhuman Animals Can Have Pains in a Morally Relevant Sense

In a series of works, Peter Carruthers has argued for the denial of the title proposition. Here, I defend that proposition by offering direct support drawn from relevant sciences and by undercutting Carruthers argument. In doing the latter, I distinguish an intrinsic theory of consciousness from Carruthers relational theory of consciousness. This relational theory has two readings, one of which makes essential appeal to evolutionary theory. I argue that neither reading offers a successful view.     

Evolutionary epidemiology

Epidemiology is a science of disease which specifies rates (illness prevalences, incidences, distributions, etc.). Evolution is a science of life which specifies changes (gene frequencies, generations, forms, function, etc.). Evolutionary Epidemiology is a synthesis of these two sciences which combines the empirical power of classical methods in genetical epidemiology with the interpretive capacities of neo-darwinian evolutionary genetics. In particular, prevalence rates of genetical diseases are important data points when reformulated for the purpose of analysis in terms of their evolutionary frequencies. Traits which exceedprevalences beyond the rates of mutation (in Hardy-Weinberg calculations) or evidence unusualrange of phenotypic reaction are of special interest. This is because traits which did not confer advantages in the environment of evolutionary adaptation cannot accede, through natural selection, to anything but low rates of genomic prevalence.Evolutionary epidemiology is, in all of medicine, of particular promise in ongoing efforts to better understand psychopathology. Many complexities of phenotypic adjustment arise when new developmental demands are placed on an old genome. The new and complex biosocial ecology of human mass society now evokes different phenotypes than those in the prehistorical ecology to which the genome is structurally and functionally better adapted. Some of these new phenotypes are darwinian failures. In this paper, the theoretical implications of evolutionary epidemiology are extended and some tentative points of clinical application (particularly to psychiatry) are offered.     

Cultural evolution and the variable phenotype

It is common in attempts to extend the theory of evolution to culture to generalize from the causal basis of biological evolution, so that evolutionary theory becomes the theory of copying processes. Generalizing from the formal dynamics of evolution allows greater leeway in what kinds of things cultural entities can be, if they are to evolve. By understanding the phenomenon of cultural transmission in terms of coordinated phenotypic variability, we can have a theory of cultural evolution which allows us to avoid the various difficulties with the elaboration of informational entities such as the cultural replicator, or meme. Such an account is a boon to the project of evolutionary epistemology since it confirms the presumption in favor of the general adaptiveness of culture, illuminating rather than obscuring the inherent intimacy of our relationship to (e.g.) our ideas.     

Genetic analysis of life-history constraint and evolution in a wild ungulate population

Trade-offs among life-history traits are central to evolutionary theory. In quantitative genetic terms, trade-offs may be manifested as negative genetic covariances relative to the direction of selection on phenotypic traits. Although the expression and selection of ecologically important phenotypic variation are fundamentally multivariate phenomena, the in situ quantification of genetic covariances is challenging. Even for life-history traits, where well-developed theory exists with which to relate phenotypic variation to fitness variation, little evidence exists from in situ studies that negative genetic covariances are an important aspect of the genetic architecture of life-history traits. In fact, the majority of reported estimates of genetic covariances among life-history traits are positive. Here we apply theory of the genetics and selection of life histories in organisms with complex life cycles to provide a framework for quantifying the contribution of multivariate genetically based relationships among traits to evolutionary constraint. We use a Bayesian framework to link pedigree-based inference of the genetic basis of variation in life-history traits to evolutionary demography theory regarding how life histories are selected. Our results suggest that genetic covariances may be acting to constrain the evolution of female life-history traits in a wild population of red deer Cervus elaphus: genetic covariances are estimated to reduce the rate of adaptation by about 40%, relative to predicted evolutionary change in the absence of genetic covariances. Furthermore, multivariate phenotypic (rather than genetic) relationships among female life-history traits do not reveal this constraint.     

Really taking Darwin seriously: An alternative to Michael Ruse's Darwinian metaethics

Michael Ruse has proposed in his recent book Taking Darwin Seriously and elsewhere a new Darwinian ethics distinct from traditional evolutionary ethics, one that avoids the latter's inadequate accounts of the nature of morality and its failed attempts to provide a naturalistic justification of morality. Ruse argues for a sociobiologically based account of moral sentiments, and an evolutionary based casual explanation of their function, rejecting the possibility of ultimate ethical justification. We find that Ruse's proposal distorts, overextends and weakens both Darwinism and naturalism. So we propose an alternative Darwinian metaethics that both remedies the problems in Ruse's proposal and shows how a Darwinian naturalistic account of the moral good in terms of human fitness avoids the naturalistic fallacy and can provide genuine, even if limited, justifications for substantive ethical claims. Thus, we propose to really take Darwin seriously.The authors are equally responsible for the writing of this paper.     

Evolutionary consequences of simulated global change: genetic adaptation or adaptive phenotypic plasticity

During the next century, natural and agricultural systems might need to adjust to a rapid increase in atmospheric CO₂ concentration and global temperature. Evolution of genotypes adapted to this global change could play a central role in plants' response. The main purpose of this study was to determine the relative importance of phenotypic and genotypic responses of plants to global change. To do so, we selected two populations of the short-lived Brassica juncea, one under ambient conditions and another one under conditions simulating global change. After seven generations of selection, differences between the two populations were examined using a reciprocal transplant garden. We monitored 14 different traits and found evidence for genetic adaptation only once, for vegetative biomass early in the growth cycle. Of the 14 traits, 11 responded plastically to the environment, but only one of these plastic changes had a possible adaptive value. Overall, the long-term evolutionary consequences of global change will depend on the response of fitness-related traits. None of the five reproductive traits measured showed any evolutionary responses. The main conclusion of our study is that Brassica juncea was apparently unable to respond evolutionarily to simulated global change either by genetic adaptation or by adaptive phenotypic plasticity. The limit to selection was apparently due to inbreeding depression induced by the harsh conditions of the predicted environment.     

Evolutionary perspectives on the links between mitochondrial genotype and disease phenotype

Background

Disorders of the mitochondrial respiratory chain are heterogeneous in their symptoms and underlying genetics. Simple links between candidate mutations and expression of disease phenotype typically do not exist. It thus remains unclear how the genetic variation in the mitochondrial genome contributes to the phenotypic expression of complex traits and disease phenotypes.

Scope of review

I summarize the basic genetic processes known to underpin mitochondrial disease. I highlight other plausible processes, drawn from the evolutionary biological literature, whose contribution to mitochondrial disease expression remains largely empirically unexplored. I highlight recent advances to the field, and discuss common-ground and -goals shared by researchers across medical and evolutionary domains.

Major conclusions

Mitochondrial genetic variance is linked to phenotypic variance across a variety of traits (e.g. reproductive function, life expectancy) fundamental to the upkeep of good health. Evolutionary theory predicts that mitochondrial genomes are destined to accumulate male-harming (but female-friendly) mutations, and this prediction has received proof-of-principle support. Furthermore, mitochondrial effects on the phenotype are typically manifested via interactions between mitochondrial and nuclear genes. Thus, whether a mitochondrial mutation is pathogenic in effect can depend on the nuclear genotype in which is it expressed.

General significance

Many disease phenotypes associated with OXPHOS malfunction might be determined by the outcomes of mitochondrial–nuclear interactions, and by the evolutionary forces that historically shaped mitochondrial DNA (mtDNA) sequences. Concepts and results drawn from the evolutionary sciences can have broad, but currently under-utilized, applicability to the medical sciences and provide new insights into understanding the complex genetics of mitochondrial disease. This article is part of a Special Issue entitled Frontiers of Mitochondrial Research.     

Cross entropy minimization in uninvadable states of complex populations

Selection is often. viewed as a process that maximizes the average fitness of a population. However, there are often constraints even on the phenotypic level which may prevent fitness optimization. Consequently, in evolutionary game theory, models of frequency dependent selection are investigated, which focus on equilibrium states that are characterized by stability (or uninvadability) rather than by optimality. The aim of this article is to show that nevertheless there is a biologically meaningful quantity, namely cross (fitness) entropy, which is optimized during the course of evolution: a dynamical model adapted to evolutionary games is presented which has the property that relative entropy decreases monotonically, if the state of a (complex) population is close to an uninvadable state. This result may be interpreted as if evolution has an order stabilizing effect.     

Genome size reduction can trigger rapid phenotypic evolution in invasive plants

Background and Aims

The study of rapid evolution in invasive species has highlighted the fundamental role played by founder events, emergence of genetic novelties through recombination and rapid response to new selective pressures. However, whether rapid adaptation of introduced species can be driven by punctual changes in genome organization has received little attention. In plants, variation in genome size, i.e. variation in the amount of DNA per monoploid set of chromosomes through loss or gain of repeated DNA sequences, is known to influence a number of physiological, phenological and life-history features. The present study investigated whether change in genome size has contributed to the evolution of greater potential of vegetative growth in invasive populations of an introduced grass.

Methods

The study was based on the recent demonstration that invasive genotypes of reed canarygrass (Phalaris arundinacea) occurring in North America have emerged from recombination between introduced European strains. The genome sizes of more than 200 invasive and native genotypes were measured and their genome size was related to their phenotypic traits measured in a common glasshouse environment. Population genetics data were used to infer phylogeographical relationships between study populations, and the evolutionary history of genome size within the study species was inferred.

Key Results

Invasive genotypes had a smaller genome than European native genotypes from which they are derived. This smaller genome size had phenotypic effects that increased the species'' invasive potential, including a higher early growth rate, due to a negative relationship between genome size and rate of stem elongation. Based on inferred phylogeographical relationships of invasive and native populations, evolutionary models were consistent with a scenario of genome reduction by natural selection during the invasion process, rather than a scenario of stochastic change.

Conclusions

Punctual reduction in genome size could cause rapid changes in key phenotypic traits that enhance invasive ability. Although the generality of genome size variation leading to phenotypic evolution and the specific genomic mechanisms involved are not known, change in genome size may constitute an important but previously under-appreciated mechanism of rapid evolutionary change that may promote evolutionary novelties over short time scales.Key words: Biological invasion, evolutionary models, genome size, Phalaris arundinacea, quantile regression, relative growth rate, rapid evolution     

Contrasting Levels of Variation in Neutral and Quantitative Genetic Loci on Island Populations of Moor Frogs (<Emphasis Type="Italic">Rana arvalis</Emphasis>)

Reduced levels of genetic variability and a prominent differentiation in both neutral marker genes and phenotypic traits are typical for many island populations as compared to their mainland conspecifics. However, whether genetic diversity in neutral marker genes reflects genetic variability in quantitative traits, and thus, their evolutionary potential, remains typically unclear. Moreover, the phenotypic differentiation on islands could be attributable to phenotypic plasticity, selection or drift; something which seldom has been tested. Using eight polymorphic microsatellite loci and quantitative genetic breeding experiments we conducted a detailed comparison on genetic variability and differentiation between Nordic islands (viz. Gotland, Öland and Læsø) and neighbouring mainland populations of moor frogs (Rana arvalis). As expected, the neutral variation was generally lower in island than in mainland populations. But as opposed to this, higher levels of additive genetic variation (V _A) in body size and tibia length were found on the island of Gotland as compared to the mainland population. When comparing the differentiation seen in neutral marker genes (F _ST) with the differentiation in genes coding quantitative traits (Q _ST) two different evolutionary scenarios were found: while selection might explain a smaller size of moor frogs on Gotland, the differentiation seen in tibia length could be explained by genetic drift. These results highlight the limited utility of microsatellite loci alone in inferring the causes behind an observed phenotypic differentiation, or in predicting the amount of genetic variation in ecologically important quantitative traits.     

A general multivariate extension of Fisher's geometrical model and the distribution of mutation fitness effects across species

The evolution of complex organisms is a puzzle for evolutionary theory because beneficial mutations should be less frequent in complex organisms, an effect termed "cost of complexity." However, little is known about how the distribution of mutation fitness effects (f(s)) varies across genomes. The main theoretical framework to address this issue is Fisher's geometric model and related phenotypic landscape models. However, it suffers from several restrictive assumptions. In this paper, we intend to show how several of these limitations may be overcome. We then propose a model of f(s) that extends Fisher's model to account for arbitrary mutational and selective interactions among n traits. We show that these interactions result in f(s) that would be predicted by a much smaller number of independent traits. We test our predictions by comparing empirical f(s) across species of various gene numbers as a surrogate to complexity. This survey reveals, as predicted, that mutations tend to be more deleterious, less variable, and less skewed in higher organisms. However, only limited difference in the shape of f(s) is observed from Escherichia coli to nematodes or fruit flies, a pattern consistent with a model of random phenotypic interactions across many traits. Overall, these results suggest that there may be a cost to phenotypic complexity although much weaker than previously suggested by earlier theoretical works. More generally, the model seems to qualitatively capture and possibly explain the variation of f(s) from lower to higher organisms, which opens a large array of potential applications in evolutionary genetics.     

Molecular marker-assisted selection for malting quality traits in barley

Selection for malting quality in breeding programs by micromalting and micromashing is time-consuming, and resource-intensive. More efficient and feasible approaches for identifying genotypes with good malting quality would be highly desirable. With the advent of molecular markers, it is possible to map and tag the loci affecting malting quality. The objective of this study was to assess the effectiveness of molecular marker assisted selection for malting quality traits. Two major quantitative trait loci (QTL) regions in six-row barley for malt extract percentage, -amylase activity, diastatic power, and malt -glucan content on chromosomes 1 (QTL1) and 4 (QTL2) have been previously identified. The flanking markers, Brz and Amy2, and WG622 and BCD402B, for these two major QTL regions were used in marker-assisted selection. Four alternative selection strategies; phenotypic selection, genotypic selection, tandem genotypic and phenotypic selection, and combined phenotypic and genotypic selection, were compared for both single and multiple trait selection in a population consisting of 92 doubled haploid lines derived from Steptoe × Morex crosses. Marker assisted selection for QTL1 (tandem genotypic and phenotypic selection, and combined phenotypic and genotypic selection) was more effective than phenotypic selection, but for QTL2 was not as effective as phenotypic selection due to a lack of QTL2 effects in the selection population. The effectiveness of tandem genotypic and phenotypic selection makes marker assisted selection practical for traits which are extremely difficult or expensive to measure such as most malting quality traits. It can substantially eliminate undesirable genotypes by early genotyping and keeping only desirable genotypes for later phenotypic selection.     

Darwinian adaptation,population genetics and the streetcar theory of evolution

 This paper investigates the problem of how to conceive a robust theory of phenotypic adaptation in non-trivial models of evolutionary biology. A particular effort is made to develop a foundation of this theory in the context of n-locus population genetics. Therefore, the evolution of phenotypic traits is considered that are coded for by more than one gene. The potential for epistatic gene interactions is not a priori excluded. Furthermore, emphasis is laid on the intricacies of frequency-dependent selection. It is first discussed how strongly the scope for phenotypic adaptation is restricted by the complex nature of ‘reproduction mechanics’ in sexually reproducing diploid populations. This discussion shows that one can easily lose the traces of Darwinism in n-locus models of population genetics. In order to retrieve these traces, the outline of a new theory is given that I call ‘streetcar theory of evolution’. This theory is based on the same models that geneticists have used in order to demonstrate substantial problems with the ‘adaptationist programme’. However, these models are now analyzed differently by including thoughts about the evolutionary removal of genetic constraints. This requires consideration of a sufficiently wide range of potential mutant alleles and careful examination of what to consider as a stable state of the evolutionary process. A particular notion of stability is introduced in order to describe population states that are phenotypically stable against the effects of all mutant alleles that are to be expected in the long-run. Surprisingly, a long-term stable state can be characterized at the phenotypic level as a fitness maximum, a Nash equilibrium or an ESS. The paper presents these mathematical results and discusses – at unusual length for a mathematical journal – their fundamental role in our current understanding of evolution. Received 22 April 1994; received in revised form 10 July 1995     

Moral commitment without objectivity or illusion: Comments on Ruse and Woolcock

Peter Woolcock, in Ruse's Darwinian Meta-Ethics: A Critique, argues that the subjectivist (nonobjectivist) Darwinian metaethics proposed by Michael Ruse (in Taking Darwin Seriously) cannot work, because the illusion of objectivity that Ruse claims is essential to morality breaks down when it is recognized as illusion, and there then remain no good reasons for acknowledging or following moral obligations. Woolcock, however, is mistaken in supposing that moral behaviour requires rational motivation. Ruse's Darwinian metaethical analysis shows why such objective support for morality is neither plausible nor necessary; and when that is recognized, it can also be seen that Ruse's proposed illusion of moral objectivity is superfluous.     

Possible consequences of genes of major effect: transient changes in the G-matrix

Understanding the process of evolutionary divergence requires knowledge of the strength, form, and targets of selection, as well as the genetic architecture of the divergent traits. Quantitative genetic approaches to understanding multivariate selection and genetic response to selection have proven to be powerful tools in this endeavor, particularly with respect to short-term evolution. However, the application of quantitative genetic theory over periods of substantial phenotypic change is controversial because it requires that the requisite genetic parameters remain constant over the period of time in question. We show herein how attempts to determine the stability of key genetic parameters may be misled by the many genes of small effect type of genetic architecture generally assumed in quantitative genetics. The presence of genes of major effect (GOMEs) can alter the genetic variance-covariance matrix dramatically for brief periods of time, significantly alter the rate and trajectory of multivariate evolution, and thereby mislead attempts to reconstruct or predict long term evolution.     

Biological invasions and phenotypic evolution: a quantitative genetic perspective

Among the many different components of global environmental change, biological invasions represent the one with the most long-term ecological and evolutionary consequences, as effects are irreversible. Although the ecological impact of invasive species has been under great scrutiny, its evolutionary aspects and consequences have remained less explored. Once established, an important part of the success of an invasive species will depend on the presence of genetic variation in populations at the geographic boundaries upon which natural selection can act. This information is integrated in G, the matrix of additive genetic variances and covariances for a suite of traits. The G-matrix shows the restrictions and potentialities of adaptive evolution and, together with natural selection determine the direction and rate of phenotypic evolution. Here I propose that a geographic analysis of G in populations of the introduced and native range becomes essential to understand critical evolutionary issues associated with invasion success.     

Darwinian Ethics and Error

Suppose that the human tendency to think of certain actions andomissions as morally required – a notion that surely lies at the heart of moral discourse – is a trait that has been naturallyselected for. Many have thought that from this premise we canjustify or vindicate moral concepts. I argue that this is mistaken, and defend Michael Ruse's view that the moreplausible implication is an error theory – the idea thatmorality is an illusion foisted upon us by evolution. Thenaturalistic fallacy is a red herring in this debate,since there is really nothing that counts as a fallacy at all. If morality is an illusion, it appears to followthat we should, upon discovering this, abolish moraldiscourse on pain of irrationality. I argue that thisconclusion is too hasty, and that we may be able usefullyto employ a moral discourse, warts and all, withoutbelieving in it.