A widely accepted tenet of evolutionary biology is that spontaneous mutations occur randomly with regard to their fitness effect. However, since the mutation rate varies along a genome and this variation can be subject to selection, organisms might evolve lower mutation rates at loci where mutations are most deleterious or increased rates where mutations are most needed. In fact, mechanisms of targeted hypermutation are known in organisms ranging from bacteria to humans. Here we review the main forces driving (...) the evolution of local mutation rates and identify the main limiting factors. Both targeted hyper‐ and hypomutation can evolve, although the former is restricted to loci under very frequent positive selection and the latter is severely limited by genetic drift. Nevertheless, we show how an association of repair with transcription or chromatin‐associated proteins could overcome the drift limit and lead to non‐random hypomutation along the genome in most organisms.Editor's suggested further reading in BioEssays Stress‐induced mutation via DNA breaks in Escherichia coli: A molecular mechanism with implications for evolution and medicine Abstract. (shrink)

This research note challenges the idea that Random Somatic Mutations are entirely random, highlighting their non-equiprobable nature and their influence on evolution, involution, or indeterminacy. It recalls the Neutrosophic Theory of Evolution, extending Darwin’s theory, and emphasizes the importance of distinguishing between different senses of ‘random mutation’ in evolutionary theory.

Although random mutation is central to models of evolutionary change, a lack of clarity remains regarding the conceptual possibilities for thinking about the nature and role of mutation in evolution. We distinguish several claims at the intersection of mutation, evolution, and directionality and then characterize a previously unrecognized category: complex conditioned mutation. Empirical evidence in support of this category suggests that the historically famous fluctuation test should be revisited, and new experiments should be undertaken with (...) emerging experimental techniques to facilitate detecting mutation rates within specific loci at an ultra‐high, individual base pair resolution. (shrink)

Evolutionary gradualism, the randomness of mutations, and the hypothesis that natural selection exerts a pervasive and substantial influence on evolutionary outcomes are pair-wise logically independent. Can the claims about selection and mutation be used to formulate an argument for gradualism? In his Genetical Theory of Natural Selection, R.A. Fisher made an important start at this project in his famous “geometric argument” by showing that a random mutation that has a smaller effect on two or more phenotypes will (...) have a higher average fitness than a random mutation that has a larger phenotypic effect. Motoo Kimura’s demonstration that a gene’s probability of fixation depends on both the selection coefficient and the effective population size shows that Fisher’s argument for gradualism was mistaken. Here we analyze Fisher’s argument and explain how Kimura’s theory leads to a conclusion that Fisher did not anticipate. We identify a fallacy that reasoning about fitness differences and their evolutionary consequences should avoid. We then distinguish forward-directed from backward-directed versions of gradualism. The backward-directed thesis about a single mutation may be correct, but the forward-directed thesis is not. After that we consider a sequence of random mutations that all affect the same cluster of phenotypes and Allen Orr’s idea that there is an optimal sequence of mutation sizes, moving from larger to smaller as the population approaches a fixed optimum. This provides a likelihood justification for a forward-directed version of gradualism when there is a fixed optimum, but it also provides an argument against forward-directed gradualism if the optimum shifts substantially as the population evolves. Finally, we consider whether genome-wide association studies (GWASs) can furnish empirical evidence that bears on the truth of gradualism. The version of gradualism that GWASs directly bear on concerns the phenotypic effect size of a gene after it arises by mutation and has reached an appreciable frequency, not the phenotypic size of the mutation event itself. (shrink)

One central tenet of the Modern Evolutionary Synthesis , and the consensus view among biologists until now, is that all genetic mutations occur by “chance” or at “random” with respect to adaptation. However, the discovery of some molecular mechanisms enhancing mutation rate in response to environmental conditions has given rise to discussions among biologists, historians and philosophers of biology about the “chance” vs “directed” character of mutations . In fact, some argue that mutations due to a particular kind (...) of mutator mechanisms challenge the Modern Synthesis because they are produced when and where needed by the organisms concerned. This paper provides a defense of the Modern Synthesis’ consensus view about the chance nature of all genetic mutations by reacting to Jablonka and Lamb’s analysis of genetic mutations and the explicit Lamarckian flavor of their arguments. I argue that biologists can continue to talk about chance mutations according to what I call and define as the notion of “evolutionary chance,” which I claim is the Modern Synthesis’ consensus view and a reformulation of Darwin’s most influential idea of “chance” variation. Advances in molecular genetics are therefore significant but not revolutionary with respect to the Modern Synthesis’ paradigm. (shrink)

Mutations are often described as being “random with respect to fitness.” Here we show that the experiments used to establish randomness with respect to fitness are only capable of showing that mutations are random with respect to current external selection. Current debates about whether or not mutations are directed may be at least partially resolved by making use of this distinction. Additionally, this distinction has important mathematical, experimental, and inferential implications.

A cell contains many copies of mitochondrial DNA. The distribution of a mitochondrial gene mutation in a cell culture is governed by the way in which the mtDNA molecules of a cell are replicated and partitioned between the two daughter cells during mitosis. Assuming that this partition process is random, we describe the evolution of the mitochondrial genetic state of a cell culture. The mutated mtDNA is ultimately segregated and the rate of the trend to segregation is relatively (...) slow. It is nevertheless greatly accelerated if the model takes into account the spatial mtDNA partition by the mitochondrial compartments. (shrink)

Evolutionary theory assumed that mutations occur constantly, gradually, and randomly over time. This formulation from the “modern synthesis” of the 1930s was embraced decades before molecular understanding of genes or mutations. Since then, our labs and others have elucidated mutation mechanisms activated by stress responses. Stress‐induced mutation mechanisms produce mutations, potentially accelerating evolution, specifically when cells are maladapted to their environment, that is, when they are stressed. The mechanisms of stress‐induced mutation that are being revealed experimentally in (...) laboratory settings provide compelling models for mutagenesis that propels pathogen–host adaptation, antibiotic resistance, cancer progression and resistance, and perhaps much of evolution generally. We discuss double‐strand‐break‐dependent stress‐induced mutation in Escherichia coli. Recent results illustrate how a stress response activates mutagenesis and demonstrate this mechanism's generality and importance to spontaneous mutation. New data also suggest a possible harmony between previous, apparently opposed, models for the molecular mechanism. They additionally strengthen the case for anti‐evolvability therapeutics for infectious disease and cancer. (shrink)

Historically, one of the most controversial aspects of Darwinian evolution has been the prominent role that randomness and random change play in it. Most biologists agree that mutations in DNA have random effects on fitness. However, fitness is a highly simplified scalar representation of an enormously complex phenotype. Challenges to Darwinian thinking have focused on such complex phenotypes. Whether mutations affect such complex phenotypes randomly is ill understood. Here I discuss three very different classes of well-studied molecular phenotypes (...) in which mutations cause nonrandom changes, based on our current knowledge. What is more, this nonrandomness facilitates evolutionary adaptation. Thus, living beings may translate DNA change into nonrandom phenotypic change that facilitates Darwinian evolution. (shrink)

The ongoing controversy about the possibility of directed mutations in bacteria is examined for its methodological, and thereby philosophical, implications. The method of fluctuation analysis, widely used to investigate whether mutations are random or directed, is described and subjected to a conceptual critique which shows that it cannot decide whether some mutations are directed while most are random. In this context, recent experiments that exploit this possibility to suggest that directed mutations occur in bacteria are described. Interpretive and (...) experimental responses to such claims are briefly analyzed. Finally it is argued that mere statistical analysis, such as fluctuation analysis, cannot resolve this dispute. What will probably be required is an investigation of mechanisms of mutagenesis, an investigation that is intrinsically reductive. (shrink)

The placenta arose during mammalian evolution, which is recent in evolutionary terms. Genetic changes underlying placental development remain identifiable by the new science of comparative genomics (approximately post‐2000). Randomly arising features of genomes including endogenous retroviruses and transposable elements have provided structural genes and gene‐regulatory motifs responsible for innovations in placental biology. Stochastic genetic events indeed contribute to new functionality. Theologically, random mutations are part of the strategy by which the divine purpose for humanity is attained. Placental function critically (...) underlies human brain development, and suboptimal function, associated with environmental conditions and maternal distress, contributes to mental health deficits in the offspring. Many enter life with handicaps arising from contingent events in utero, mandating understanding, compassion, and socioemotional support, imperatives native to moral including biblical values. The extended period of development afforded by placentation enables prenatal parenting, with implications for sensitive and devoted parental commitment. (shrink)

Genetic diversity of viral populations is almost unanimously attributed to the build‐up of random mutations along with accidental recombination events. This passive role of viruses in the selection of viable genotypes is widely acknowledged. According to the hypothesis presented here, populations of steady‐state error copies of a master viral sequence would have a dominant mutant rather than a random pool of heterogeneous viral genomes with changes scattered uniformly without any preferential distribution. It would let viruses face the selection (...) stage of host surveillance having a preceding set of potential survivors or “guard” genomes among an ordinary cloud of random quasispecies. (shrink)

A long-standing challenge to evolutionary theory has been whether it can explain the origin of complex organismal features. We examined this issue using digital organisms—computer programs that self-replicate, mutate, compete and evolve. Populations of digital organisms often evolved the ability to perform complex logic functions requiring the coordinated execution of many genomic instructions. Complex functions evolved by building on simpler functions that had evolved earlier, provided that these were also selectively favoured. However, no particular intermediate stage was essential for evolving (...) complex functions. The first genotypes able to perform complex functions differed from their non-performing parents by only one or two mutations, but differed from the ancestor by many mutations that were also crucial to the new functions. In some cases, mutations that were deleterious when they appeared served as stepping-stones in the evolution of complex features. These findings show how complex functions can originate by random mutation and natural selection. (shrink)

This chapter offers a critique of intelligent design arguments against evolution and a philosophical discussion of the nature of science, drawing several lessons for the teaching of evolution and for science education in general. I discuss why Behe’s irreducible complexity argument fails, and why his portrayal of organismal systems as machines is detrimental to biology education and any under-standing of how organismal evolution is possible. The idea that the evolution of complex organismal features is too unlikely to have occurred by (...) random mutation and selection (as recently promoted by Dembski) is very widespread, but it is easy to show students why such small probability arguments are fallacious. While intelligent design proponents have claimed that the exclusion of supernatural causes mandated by scientific methods is dogmatically presupposed by science, scientists have an empirical justification for using such methods. This justification is instructive for my discussion of how to demarcate science from pseudoscience. I argue that there is no universal account of the nature of science, but that the criteria used to judge an intellectual approach vary across historical periods and have to be specific to the scientific domain. Moreover, intellectual approaches have to be construed as practices based on institutional factors and values, and to be evaluated in terms of the activities of their practitioners. Science educators should not just teach scientific facts, but present science as a practice and make students reflect on the nature of science, as this gives them a better appreciation of the ways in which intelligent design falls short of actual science. (shrink)

Contingency-theorists have gestured to a series of phenomena such as random mutations or rare Armageddon-like events as that which accounts for evolutionary contingency. These phenomena constitute a class, which may be aptly called the ‘sources of contingency’. In this paper, I offer a probabilistic conception of what it is to be a source of contingency and then examine two major candidates: chance variation and genetic drift, both of which have historically been taken to be ‘chancy’ in a number of (...) different senses. However,contrathe gesturing of contingency-theorists, chance variation and genetic drift are not always strong sources of contingency, as they can be non-chancy in at least one sense that opposes evolutionary contingency. The probabilistic conception offered herein allows for sources of contingency to appropriately vary in strength. To this end, I import Shannon’sinformation entropyas a statistical measure for systematically assessing the strength of a source of contingency, which is part and parcel of identifying sources of contingency. In brief, the higher the entropy, the greater the strength. This is also empirically significant because molecular, mutational, and replicative studies often contain sufficient frequency or probability data to allow for entropies to be calculated. In this way, contingency-theorists can evaluate the strength of a source of contingency in real-world cases. Moreover, the probabilistic conception also makes conceptual room for the converse of sources of contingency: ‘sources of directionality’, which ought to be recognised, as they can interact with genuine sources of contingency in undermining evolutionary contingency. (shrink)

The article explores a change taking place today in the fields of biology and social anthropology, signaling a shared desire to transcend the heuristic effects of the opposition between nature and culture. Acceptance of the idea that random mutations are the sole driving force behind the process of natural selection overlooks the agentive capacity of non-human living beings, revealing an anthropocentric inspiration. To critique the rhetoric surrounding the principle of natural selection, I turn to the anthropology of Tim Ingold (...) and his analysis of the metaphors that illustrate the principle. I disagree with the author, however, when he argues that these metaphors do not adequately illustrate neo-Darwinian premises. Instead, I believe that they are faithful since their apparent contradiction expresses the unease of neo-Darwinian theory itself when it combines randomness and teleology. New currents in biology, such as biosemiotics, attribute evolutionary importance to epigenetic changes. From the evolutionary perspective, they also highlight the importance of recognizing that the entire lived world possesses the capacity for agency, not just human beings. Within social anthropology, the so-called ontological turn and multispecies ethnography have been working with a new conception of the person, extendible to non-human beings, including the latter to compose a single collective with humans. Thus we can observe an attempt on the part of biologists and anthropologists alike to move beyond anthropocentrism, producer and product of the opposition between nature and culture. (shrink)

In 2015, Tomasetti and Vogelstein published a paper in Science containing the following provocative statement: “… only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to “bad luck,” that is, random mutations arising during DNA replication in normal, noncancerous stem cells.” The paper—and perhaps especially this rather coy reference to “bad luck”—became a flash point for a series of letters and reviews, followed by replies and (...) yet further counterpoints. In this paper, I critically assess Tomasetti and Vogelstein's argument, discuss the meaning of “luck” (or, better: “chance”) in the context of the debate, and use this case study to address larger questions about methodological criteria for causal explanations of population level patterns in biomedicine. (shrink)

We discuss a new theory of the universe in which the vacuum energy is of classical origin and dominates the energy content of the universe. As usual, the Einstein equations determine the metric of the universe. However, the scale factor is controlled by total energy conservation in contrast to the practice in the Robertson–Walker formulation. This theory naturally leads to an explanation for the Big Bang and is not plagued by the horizon and cosmological constant problem. It naturally accommodates the (...) notion of dark energy and proposes a possible explanation for dark matter. It leads to a dual description of the universe, which is reminiscent of the dual theory proposed by Milne in 1937. On the one hand one can describe the universe in terms of the original Einstein coordinates in which the universe is expanding, on the other hand one can describe it in terms of co-moving coordinates which feature in measurements. In the latter representation the universe looks stationary and the age of the universe appears constant. The paper describes the evolution of this universe. It starts out in a classical state with perfect symmetry and zero entropy. Due to the vacuum metric the effective energy density is infinite at the beginning, but diminishes rapidly. Once it reaches the Planck energy density of elementary particles, the formation of particles can commence. Because of the quantum nature of creation and annihilation processes spatial and temporal inhomogeneities appear in the matter distributions, resulting in residual proton (neutron) and electron densities. Hence, quantum uncertainty plays an essential role in the creation of a diversified complex universe with increasing entropy. It thus seems that quantum fluctuations play a role in cosmology similar to that of random mutations in biology. Other analogies to biological principles, such as recapitulation, are also discussed. (shrink)

The aim of this paper is to explore in the light of recent scientific discoveries, coupled with a return to biblical orthodoxy, the question of the Fall, and the apparent intergenerational conditions of original sin. This is the human condition – East of Eden. Invoking Darwin's theory of evolution through natural selection from random mutation as a means of repudiating the existence of original sin can no longer be sustained, scientifically; the biology of horizontal gene transfer, transgenerational epigenetics, (...) accelerated evolution and biological plasticity has rendered Darwinism grounded in a Naturalistic methodology an inadequate explanation. If humanity is ‘born this way’ – mired in sin – have we condemned ourselves and our children to this status? How does this affect the relationship between biology and free will, between a form of predestination and decision-making? Therefore, this paper is towards an understanding of the ontology of the original, or first, sin, and is a biblical and scientific exploration of postlapsarian humanity's self-willed state, ‘East of Eden.’. (shrink)

The intelligent design movement aspires to create a new scientific paradigm which will replace the existing Darwinian paradigm of evolution by random mutation and natural selection. However, the creation of such a paradigm is hampered by the fact that the movement pursues a 'big tent' strategy that refuses to make a choice between young-earth creationism, old-earth (progressive) creationism, and divinely directed natural selection. The latter two options are discussed in some detail, and it becomes apparent that either one (...) presents difficult challenges that the movement shows no signs of overcoming. It is concluded that there are not good prospects for the creation of an alternative paradigm in the foreseeable future. (shrink)

Did God create life? Or did life arise via naturalistic processes, along the lines of random mutation and natural selection as suggested by Darwin? Intelligent design proponents attempt to use William Dembski’s design inference to argue that the existence of intelligent life is due to design. I will argue that the design inference is flawed, because it does not take into account the fact that the universe is spatially infinite.

When it comes to the notion of creativity, both R. Dawkins and D. Dennett argue that creativity is a matter of random mutation, in the same way that genes randomly mutate. Neither Dennett nor Dawkins see anything else in the mimetic theory of creativity than a process of Darwinian evolution. However, this complete reliance upon the extension of evolution for understanding creativity needs to be supplemented by combining it with other ideas such as those of "schema theory," because (...) creativity always occurs within a structured context and is not simply a matter of random mutation of ideas. Schema theory comes largely from the works of E.H Gombrich, who argued that "schemas" play a crucial role in how it is that we are able to be creative. He defines schemas as structure and traditions in society that help to convey the meaning of our creative efforts. Just as semantics needs syntax within language in order to formulate and convey meaning, so by analogy memes need schemas for the creation and expression of new ideas. Rather than being the antithesis of creativity, existing forms of expression and traditions are important for the creation of new ideas. This needs to be factored into any theory of creativity in order to account for the effect of the social context on creative endeavours in addition to a Darwinian account of memes. The unconscious processes at work within the brain that are involved in the generation of ideas and other creative products can be understood using the notion of a "generator", as originally conceived by D. Dennett. This notion goes beyond mere concrete Skinnerian behavioural trial and error. Within this generator, there appear to be at work processes such as those of bisociation and association, as discussed by A. Koestler, as well as processes such as the role of language, memory, generate-and-test and intentionality that must be acknowledged in addition to the syntactic operations of schemas and the replicating contents of memes. The operation of all of these ingredients within the generator, when understood together, can be seen as responsible for our ability to be creative. (shrink)

Here we discuss the challenge posed by self-organization to the Darwinian conception of evolution. As we point out, natural selection can only be the major creative agency in evolution if all or most of the adaptive complexity manifest in living organisms is built up over many generations by the cumulative selection of naturally occurring small, random mutations or variants, i.e., additive, incremental steps over an extended period of time. Biological self-organization—witnessed classically in the folding of a protein, or in (...) the formation of the cell membrane—is a fundamentally different means of generating complexity. We agree that self-organizing systems may be fine-tuned by selection and that self-organization may be therefore considered a complementary mechanism to natural selection as a causal agency in the evolution of life. But we argue that if self-organization proves to be a common mechanism for the generation of adaptive order from the molecular to the organismic level, then this will greatly undermine the Darwinian claim that natural selection is the major creative agency in evolution. We also point out that although complex self-organizing systems are easy to create in the electronic realm of cellular automata, to date translating in silico simulations into real material structures that self-organize into complex forms from local interactions between their constituents has not proved easy. This suggests that self-organizing systems analogous to those utilized by biological systems are at least rare and may indeed represent, as pre-Darwinists believed, a unique ascending hierarchy of natural forms. Such a unique adaptive hierarchy would pose another major challenge to the current Darwinian view of evolution, as it would mean the basic forms of life are necessary features of the order of nature and that the major pathways of evolution are determined by physical law, or more specifically by the self-organizing properties of biomatter, rather than natural selection. (shrink)

We investigate the emergence of iconicity, specifically a bouba-kiki effect in miniature artificial languages under different functional constraints: when the languages are reproduced and when they are used communicatively. We ran transmission chains of participant dyads who played an interactive communicative game and individual participants who played a matched learning game. An analysis of the languages over six generations in an iterated learning experiment revealed that in the Communication condition, but not in the Reproduction condition, words for spiky shapes tend (...) to be rated by naive judges as more spiky than the words for round shapes. This suggests that iconicity may not only be the outcome of innovations introduced by individuals, but, crucially, the result of interlocutor negotiation of new communicative conventions. We interpret our results as an illustration of cultural evolution by random mutation and selection. (shrink)

The Origin of Human Nature offers an original and fertile way to integrate spiritual and scientific views of human evolution. It offers a new and refreshing alternative to the way we think about our origins - random mutation (mechanistic neo-Darwinism), Genesis (God did it all personally), and Intelligent Design (God personally does what we can't otherwise account for). The result is an invigorating perspective on how our best qualities - our capacity for love, our appreciation of beauty, our (...) altruistic capability, our creativity and our intelligence - have come into being and evolved. By showing evolution as a creative and intelligent process with its own inherent logic, The Origin of Human Nature resolves the dilemma of how to have both truth and ethics at the same time. Instead of starting in an imagined remote and uncertain past and moving to the present, this book starts at the certain and immediate present and works back. That consciousness, creativity, and intelligence exist is certain. The question is, how can these have evolved? Dr. Albert Low has made a study of human nature throughout his life. In writing this book, he draws on his prolonged meditations on creativity and the human condition, his years of providing psychological and spiritual counseling, and a wide-ranging knowledge of Western psychology, philosophy, and science. He takes issue with Richard Dawkins' published texts, and provides a point-by-point rebuttal of the neo-Darwinist argument. (shrink)

Philosophers of science have used various formulations of the "random mutation--natural selection" scheme to explain the development of scientific knowledge. But the uncritical acceptance of this evolutionary model has led to substantive problems concerning the relation between fact and theory. The primary difficulty lies in the fact that those who adopt this model (Popper and Kuhn, for example) are led to claim that theories arise chiefly through the processes of relatively random change. Systems theory constitutes a general (...) criticism of this model insofar as it demonstrates the necessity of supplementing this mechanism with the non-random influences exercised by the internal organization of a system on its own development. (shrink)

Many Christian scholars have argued that standard versions of evolutionary theory and orthodox theological commitments can be reconciled. Some theistic evolutionists or “evolutionary creationists” have argued that evolutionary mechanisms such as random mutation and natural selection are nothing less than God’s way of creating. Though I dispute the logical coherence of these attempted reconciliations elsewhere, I argue here that there is little reason for Christians to attempt them, since an accumulating body of evidence from multiple subdisciplines of biology (...) casts doubt on the creative power of the main evolutionary mechanisms. Thus, rather than addressing the question, “Can a meaningful doctrine of divine providence or creation be reconciled with mainstream evolutionary theory?” this essay will address the question of whether Christians should, or need to, attempt such a reconciliation at all. (shrink)

Biological mimicry is regarded by many as a textbook illustration of Darwin’s idea of evolution by random mutation followed by differential selection of reproductively fit specimens, resulting in gradual phenotypic change in a population. In this paper, I argue that some cases of so-called mimicry are probably merely look-a-likes and do not gain an advantage due to their similarity in appearance to something else. In cases where a similar appearance does provide a benefit, I argue that it is (...) possible that these forms of mimicry were created in a single generation. An interpretive response to an appearance as a sign can make a new structure perform drastically differently in an environment. In such cases, Darwin’s natural selection mechanism only helps to explain gradual the spread of these new forms, not the creation of them. I argue that biosemiosis should be regarded as a much more powerful mechanism for affecting evolutionary trajectories than the gradualist view allows. I focus on two cases of butterfly mimicry: the Viceroy (Nymphalidae: Limenitis archippus) and Monarch (Nymphalidae: Danaus plexippus) butterflies, supposed Müllerian mimics, and deadleaf mimic butterflies (Kallima). (shrink)

La parution récente en français du livre de M. Denton : “Evolution. Une théorie en crise” , qui traite des theories explicatives actuelles de l'évolution, nous amine à rappeler les caracteres généraux des grandes theories biologiques et à présenter une critique sommaire du livre en question.La science West pas une simple accumulation de connaissances. Le scientifique ne doit pas se contenter de decrire et de mesurer des faits. Son but eat d'essayer de les relier et de construire des théories qui (...) tentent de nous faire comprendre le “reel”, objet de ses recherches.Cependant, la nature du matériel biologique — c'est-à-dire les espèces vivantes et les catégories qu'on y a reconnues, classe ou ordre par exemple — est si complexe qua la biologie actuelle est fort loin encore Wavoir réalisé une synthèse qui ressemble, méme très approximativement, à la classification de Mendéleiev pour les éléments chimiques.Malgré cette complexité, les biologques ont réussi à construire la th6orie du fait de l'evolution et ils proposent aujourd'hui une théorie explicative de cette évolution qui, bien qua critiquée, est incontestablement bien étayee. Nous allons essayer de définir la structure des grandes théories biologiques; ensuite nous analyserons sommairement quelques-unes des critiques qui sont adressees aux theories de l'évolution.Considering the publication in French version of Michael Denton's book, Evolution : A Theory in crisis , in which he critizes the synthetical theory of the biological evolution, we thought it useful to point out the main errors of argumentation contained in that book by first referring to the characteristics of general biological theories.In biology, there exist elementary theories - such as that dealing with the extinction of giant Reptiles - and general theories - such as the chromosomic theory of heredity and the explanatory theory of evolution. The latter generally consist of a group of elementary theories imbricated so that they form a whole like a jig-saw puzzle. An example is provided by the synthetic theory of evolution that can be defined in 20 propositions divided into two categories : the propositions relating to the naturalists' observations - which correspond to descriptive concepts - and those relating to the data of the population genetics - which correspond to explanatory concepts . The general scheme of the theory is formed by a network of relations between the descriptive concepts and the explanatory concepts. There also exist other theories in general biology supported by thousands of minor facts which only together can be of proof of validity. These theories are quite reliable and cannot be questioned by facts still to be explained. Questioning can only happen if they are confronted to well-established data in nearly equal numbers.In his work, Denton does not deny the phenomenon of biological evolution, but he criticizes the syntheticians' ideas by emphasizing that no great evolutive changes can be accounted for by the complex mechanism of random mutations and selection. He goes back to a typological concept of the zoological classification in some way similar to that of Vialleton's. However, Denton agrees with the phenomenon of the biological evolution and accepts the existence of "saltations" among the great zoological groups. The arguments used by Denton merely show that he is not conversant with the complexity of sciences particularly in comparative anatomy and zoology, the teaching of which is being somehow neglected today.By giving as an example the structure of the aortic arches in Amphibians and by a summary of the variations of those structures and the evolution of the blood-circulation in Vertebrates, we proved that the typological argument is of no value. As a matter of fact, a study of the now living beings clearly shows the gradual transition - e.g. a transition by a very large number of feasible stages - from the Lower Vertebrates to the Higher Vertebrates. In particular, there have been several attempts at double circulation and there still exist many species in which the blood of the double circulation is mixed. It seems therefore obvious that the double circulation has been achieved, stage by stage, with many intermediate schemes; we are inclined, therefore, to conclude that this succession of small transformations was produced by a huge mechanism of selected small mutations.Our present-day biological knowledge includes a number of examples large enough to consider the “argument of the impossible” used by Denton is due to inadequate fossil data and not to any mysterious mechanism such as macromutations. Let us say again that the typological structures seem to occur only when the data of comparative anatomy and zoology are over-simplified. (shrink)

This book explores important topics in Darwin’s theory of evolution and in the twentieth- and twenty-first-century theories that grew out of it. These topics include fitness, adaptation, altruism, intragenomic conflict, units of selection, genetic drift, the randomness of mutation, gradualism, common ancestry, taxonomy, race, phylogenetic inference, and optimality models. The book brings these and other biological topics into contact with numerous philosophical ideas − operationalism, reductionism, conventionalism, null hypotheses and default reasoning, instrumentalism versus realism, likelihoods versus probabilities, model selection, (...) essentialism, falsifiability, parsimony, the principle of the common cause, comparisons of causal power, interpretations of probaiblity, indeterminism, sensitivity to initial conditions, and the knowability of the past. (shrink)

Evolutionary epistemology has experienced a continuous rise over the last decades. Important new theoretical considerations and novel empirical findings have been integrated into the existing framework. In this paper, I would like to suggest three lines of research that I believe will significantly contribute to further advance EE: ontogenetic considerations, key ideas from cognitive biology, and the framework of the Extended Evolutionary Synthesis. EE, in particular the program of the evolution of epistemological mechanisms, seeks to provide a phylogenetic account of (...) the generation of cognitive processes underlying knowledge creation. Traditionally, EE and EEM have been oriented towards an account of evolutionary theory that mainly drew from the tenets of the Modern Synthesis. The Modern Synthesis largely dismisses ontogenetic processes and considers them irrelevant for evolutionary explanations. If anything, the role of development in evolution is believed to be that of a constraint. There is, however, ample evidence for a tight intertwinement of developmental and evolutionary processes. Organisms employ their cognitive apparatus to interact with the environment in order to achieve a fully functioning perceptual and cognitive nervous system. Also, ontogeny provides generative potentials to enable variations that natural selection can act upon. EEM’s agenda may, therefore, strongly benefit from bringing together ontogenetic and phylogenetic approaches. To grapple with this challenge, an alternative vision of the evolutionary theory termed Extended Evolutionary Synthesis could be used. This extended evolutionary theory explores relationships between the processes of individual development and phenotypic change during evolution and can provide a more suitable framework for EEM to draw from. In recent years, cognitive biology has gained momentum as an independent research field. Cognitive biology builds on the concepts of EEM and understands knowledge as a biogenic phenomenon. Its main objective is also the formulation of substantiated interrelations between cognition and evolution but it focuses on cognitive functionality at all levels of biological organization. It thus employs a “vertical” approach that encompasses nested hierarchies which span from single molecules, cells, and tissues to the organismal level, communities, and societies. In contrast to cognitive biology, EEM is here understood to adopt a “horizontal” approach that focuses on phylogenetic explanations of cognition and knowledge acquisition. Linking EEM with the key ideas of cognitive biology could make EEM’s research program stronger as it can more easily accommodate phylogenetic and ontogenetic questions within a hierarchical, multilevel perspective. This is of particular importance for a more comprehensive account of cognition since living systems are subject to context-dependent causal influences from different organizational levels. In addition to EEM, there is a second program of EE. This program has been labeled evolutionary epistemology of theories and understands the increase in human knowledge, such as scientific theories, as naturalistic accounts of evolution. Both, EEM and EET initially drew from the core concepts of the Modern Synthesis. Several scholars have severely criticized the analogies made between EET and the Neo-Darwinian key processes of evolution. In particular processes of random mutation, the rate of variation, natural selection as the unique driving force, and the adaptationist agenda are believed to reveal disanalogies. In contrast to the Modern Synthesis, the Extended Evolutionary Synthesis not only recognizes developmental processes but also ecological interactions and systems dynamics as well as social and cultural evolutionary reciprocity as important evolutionary processes. Concepts of the Extended Evolutionary Synthesis are therefore expected to be more fruitful for re-conceptualizing parallels between scientific theorizing and biological evolution. (shrink)

The scientific community believes in the theory of evolution with a passion that rivals that of any religious belief. This passion extends beyond the irrefutable evidence of the fossil record to the familiar claims of 'survival of the fittest 'and random mutation. Yet the theory of natural selection has,to the knowledge of the present author,never been tested against the alternative hypothesis that evolution is, in fact, the ongoing development of a single, world-spanning super-organism. Just what kind of evidence (...) would settle this question is not clear, so this paper is intended to begin the discussion. It does so by suggesting how a new, quantitative theory of 'pragmatic information' could analyze the widespread temporal and inter-species connections that a developmental view of evolution would imply. (shrink)

Erect posture and large brain are two of the most significant anatomical traits that distinguish us from nonhuman primates. But humans are also different from chimpanzees and other animals, and no less importantly, in their behavior, both as individuals and socially. Distinctive human behavioral attributes include tool-making and technology; abstract thinking, categorizing, and reasoning; symbolic (creative) language; self-awareness and death-awareness; science, literature, and art; legal codes, ethics and religion; complex social organization and political institutions. These traits may all be said (...) to be components of human culture, a distinctively human mode of adaptation to the environment that is far more versatile and successful than the biological mode. Cultural adaptation is more effective than biological adaptation because its innovations are directed, rather than random mutations; because it can be transmitted "horizontally", rather than only "vertically", to descendants; and because cultural heredity is Lamarckian, rather than Mendelian, so that acquired characteristics can be inherited. I explore ethics as a distinctive human trait. The question whether ethical behavior is biologically determined may refer either to the capacity for ethics (i.e., the proclivity to judge human actions as either right or wrong), or to the moral norms accepted by human beings for guiding their actions. I will propose: (1) that the capacity for ethics is a necessary attribute of human nature; and (2) that moral norms are products of cultural evolution, not of biological evolution. (shrink)

This paper draws on the philosophy of Karl Popper to present a descriptive evolutionary epistemology that offers philosophical solutions to the following related problems: ‘What happens when learning takes place?’ and ‘What happens in human learning?’ It provides a detailed analysis of how learning takes place without any direct transfer of information from the environment to the learner, and it significantly extends the author's earlier published work on this topic. She proposes that learning should be construed as a special case (...) of ‘problem solving’ and as a fundamentally critical and creative process in which learning organisms develop ‘expectations’ that are not purely an outcome of genetic inheritance or random mutation. Human learning is then characterised with reference to: objectified knowledge; descriptive and argumentative language; theoretical problems; the search for error and specific limitation. If the author's evolutionary analysis of learning is valid, it would suggest that we should, if we wish to promote learning, be wary of corralling children and older students in environments that inhibit autonomous activity, that discourage criticality and creativity and generally limit opportunities for trial and error‐elimination. But education institutions, particularly those for older children and adolescents, are very often environments of this constraining kind. Traditionally, educationists have vastly underestimated the human potential for imaginative criticism—because in general they have not recognised the extent to which it lies at the heart of what humans, including the youngest children, do in order to succeed at even the most basic tasks. (shrink)

The general inorganic nature of traditional selection theory (based on differential growth between any two systems) is pointed out, wherefrom it follows that this theory cannot provide explanations for the characteristics of organic evolution. Specific biophysical aspects enter with the complexity of macro-molecules: vital physical conditions for the perpetuation of the system, irrevocable extinction (= death) and random change leading to novelty, are the result of complexity per se. Further biophysical properties are a direct function of the pathway along (...) which random mutation in nucleic acids is converted into continuous protein — (specifically enzyme) — function, from there into organismic phenotype with fitness components which may, or may not, correspond to identifiable structural units in DNA. The general machine-like properties of enzymes, in that there is no additive relationship between structural (amino acid) composition and functional output, is discussed in more detail. The continuous growth functions of molecular concentrations, directed by enzyme turnover, determine simple laws of growth and morphogenesis in the organic hierarchy and thus of phenotype. Thus, the combined effect of DNA-structure and of environmental parameters (temperature, pressure, pH, etc.) on protein function determines ultimately the actual phenotype and hence, quality and intensity of genotypic selection. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Alzheimer's Disease, Mild Cognitive Impairment, and the Biology of Intrinsic AgingThomas B. L. Kirkwood (bio)Keywordsaging, Alzheimer’s disease, genetic mutation, mild cognitive impairment, telomereThe article by Gaines and Whitehouse (2006) raises key questions about the uncertain relationship between (i) the intrinsic, "normal" aging process, and (ii) the clinicopathologic states represented by the labels of Alzheimer's disease (AD) and mild cognitive impairment (MCI). This short commentary offers a perspective on (...) this debate that is drawn from a consideration of underlying biological mechanisms.Because age is unquestionably the greatest single risk factor associated with AD and MCI, I begin by asking what we know about the intrinsic processes of aging. The central feature of current understanding of intrinsic aging is that it consists of the gradual, lifelong accumulation of a wide variety of molecular and cellular faults that begins very early in life and eventually leads to overt functional impairments resulting in age-related frailty, disability, and disease (Kirkwood 2005). This is an essentially bottom-up process. A strong consensus has emerged in recent years that there is no active program for aging and that there are no genetic factors that have evolved specifically to cause aging or age-related diseases. Unquestionably, there are genes that influence susceptibility to disease and even length of life, but these genes are genes for maintenance and repair functions, not for aging. It is the limitation in the past evolutionary pressure to invest in greater longevity than was required, within an environment where life was usually truncated by hazards such as starvation, injury, or infection, that means that our maintenance systems—good as they are—are insufficient to keep us going indefinitely. Added to this is the idea that there are probably also genes that program processes that are good for the young organism, but which may in later life have harmful effects. Processes like inflammation and apoptosis, which are seen to occur extensively in aged tissues, including brain, surely evolved to help cope with infection and cellular damage arising earlier in life. That they are called into play in aged tissues is a direct, but secondary, consequence of accumulated damage.With this general framework to understand the intrinsic biology of aging, let us now ask what we might expect a priori for the aging of an organ such [End Page 79] as the brain. Although we cannot pretend complete ignorance of how the brain actually does age, our enquiry can be based entirely on data from other organ systems, so we can develop our predictions about brain aging without prejudice.Aging begins very early during human development, faults accumulating from the first stages of embryonic development. Each time a cell divides, each of the daughter cells is likely to acquire a few new mutations. We know this from the estimates for the error rate in DNA replication and the size of the human genome. It is confirmed by direct evidence that at individual gene loci where mutations have been measured, mutation frequency increases with age (Morley 1998; Vijg 2000). In addition to replication errors, DNA is damaged on a daily basis to a very considerable degree by agents such as reactive oxygen species (free radicals), which are formed as byproducts of normal cellular metabolism. Although most of this damage is corrected by repair, the repair mechanisms themselves are not error free and additional mutations accumulate through this route. If a mutation is lethal to the cell, the cell dies and thus the mutation is eliminated. However, the majority of mutations are nonlethal, either because the mutation is recessive and the cell carries an intact gene copy on the other chromosome, because the gene is not currently required, or because the mutation produces only a delayed deleterious effect. Examples of genes that produce delayed deleterious effects include the genes responsible for familial AD. It is interesting to reflect that on statistical grounds alone, it is almost certain that each of us carries a randomly determined fraction of cells in our brains that bear amyloid precursor protein or presenilin mutations associated with AD. We also carry a heterogeneous array of random mutations that compromise essential cell maintenance functions. How many such... (shrink)

There is an argument that has recently been deployed in favor of thinking that the mind is mostly (or even exclusively) composed of cognitive modules; an argument that draws from some ideas and concepts of evolutionary and of developmental biology. In a nutshell, the argument concludes that a mind that is massively composed of cognitive mechanisms that are cognitively modular (henceforth, c-modular) is more evolvable than a mind that is not c-modular (or that is scarcely c-modular), since a cognitive mechanism (...) that is c-modular is likely to be biologically modular (henceforth, b-modular), and b-modular characters are more evolvable (e.g., Sperber 2002, Carruthers 2005). In evolutionary biology, the evolvability of a character in an organism is understood as the “organism’s capacity to facilitate the generation of non-lethal selectable phenotypic variation from random mutation” with respect to that character. Here I will argue that the notion of cognitive modularity needed to make this argument plausible will have to be understood in terms of the biological notion of variational independence; that is, it will have to be understood in such a way that a cognitive feature is c-modular only if few or no other morphological changes (cognitive and not) are significantly correlated with variations of that feature arising in members of the relevant population. I will also argue that all –except for (possibly) one—of the connotations contained in a cluster of notions of cognitive modularity widely accepted in some of the mainstream currents of thought in classical cognitive science, are simply irrelevant to the argument. In order to argue for this, I will have to examine the question as to whether there are any strong theoretical connections between (1) those connotations and (2) notions of modularity accepted in biology, specially in evolutionary and in developmental biology, that are thought to be most relevant to arguments to the effect that biological modularity enhances evolvability. (shrink)

Most of us believe everything happens for a reason. Whether it is "God's will","karma", or "fate," we want to believe that nothing in the world, especially disasters and tragedies, is a random, meaningless event. But now, as never before, confident scientific assertions that the world embodies a profound contingency are challenging theological claims that God acts providentially in the world. The random and meandering path of evolution is widely used as an argument that God did not create life.Abraham's (...) Dice explores the interplay between chance and providence in the monotheistic religious traditions, looking at how their interaction has been conceptualized as our understanding of the workings of nature has changed. This lively historical conversation has generated intense ongoing theological debates, and provocative responses from science: what are we to make of the history of our universe, where chance and law have played out in complex ways? Or the evolution of life, where random mutations have challenged attempts to find purpose within evolution and convinced many that human beings are but a "glorious accident"? The enduring belief that everything happens for a reason is examined through a conversation with major scholars, among them holders of prestigious chairs at Oxford and Cambridge Universities and the University of Basel, as well as several Gifford lecturers, and two Templeton prize winners. Organized historically, Abraham's Dice provides a wide-ranging scientific, theological, and biblical foundation to address the question of providence and divine action in a world shot through with contingency. (shrink)

Since more than hundred years the attempts to explain biological adaptations constitute the main current of evolutionary thinking. In 1901 C. LI. Morgan wrote: „The doctrine of evolution has rendered the study of adaptation of scientific importance. Before that doctrine was formulated, natural adaptations formed part of the mystery of special creation, and played a great role in natural theology through the use of the argument from 'design in nature’". The modem doctrine of biology stresses the importance of the environment (...) in „shaping" the inner properties of every living being. This means an obvious although tacit refusal to assume or recognize any single, integrated agent in the origin of main functional biological traits and in the genesis of new kinds of life. The role ascribed to random mutations, and to „pressures of the environment" is just one aspect of the neodarwinian theory. Another aspect of this doctrine is the widespread conviction that all phenomena of life are a natural, both random and necessary result of interactions between constantly changing material objects. (shrink)

In this wide-ranging collection of essays on origins, mathematician Granville Sewell looks at the big bang, the fine-tuning of the laws of physics, and the evolution of life. He concludes that while there is much in the history of life that seems to suggest natural causes, there is nothing to support Charles Darwin’s idea that natural selection of random mutations can explain major evolutionary advances. Sewell explains why evolution is a fundamentally different and much more difficult problem than others (...) solved by science, and why increasing numbers of scientists are now recognizing what has long been obvious to the layman, that there is no explanation possible without design. This book summarizes many of the traditional arguments for intelligent design, but presents some powerful new arguments as well. (shrink)

The archaeological record is very limited and its analysis has been contentious. Hence, molecular biologists have shifted their attention to molecular dating techniques. Recently on April 2013, the prestigious Cell Press Journal Current Biology published an article (Fu et al. 2013) entitled “A Revised Timescale for Human Evolution Based on Ancient Mitochondrial Genomes”. This paper has twenty authors and they are researchers from the world’s top institutes like Max Planck Institute, Harvard, etc. Respected authors of this paper have emphatically accepted (...) that the fossil record is inadequate and unreliable. These statements clearly substantiate that now biologists are agreeing that fossil records do not provide any significant evidence at all for conventional evolution theory. Despite the well-recorded fact of the continual grand propaganda of Darwinism based on fossil evidence for more than 150 years, in recent times biologists are surprisingly coming up with such statements, based on their confidence that evolution can be explained purely by the genealogical/genomic record provided by modern molecular biology. Still many respected journals (for example the article in Nature, Retallack, 2013) continue to publish articles on fossil evidence to support Darwinian evolution. These incoherently diverse claims prove that Darwinists are struggling with unscientific ideological approaches to explain biodiversity. Darwinian evolutionary theory is not only the basis of modern biology, but also acts as the guiding principle of science and intellectual reasoning for modern civilization. Hence, a scientific understanding of the breakdown of the Darwinian theory of objective evolution is very important for overcoming the traditional scientific temper of mechanistic intellectualism that characterizes this ideology. In my article “21st Century Biology Refutes Darwinian Abiology” (published in two parts in November and December 2012 issues of The Harmonizer: www.mahaprabhu.net/satsanga/harmonizer) it was noted that several recent findings challenge the credibility that random mutations and natural selection can provide a valid basis for justifying the naturalistic evolution of species. The present article summarizes the problems associated with the fossil record and dating techniques, and its implication on the neo-Darwinian mechanistic misconception of biological life as mere molecular chemistry or abiology. An alternative approach based on the Vedāntic view for explaining biodiversity in the light of 21st century biology is also discussed in the end of the article. (shrink)

The German synthesis of evolutionary theory that grew out of opposition to idealistic morphology has been anchored in the systematic work at the species level and below pursued by the Berlin School around Erwin Stresemann (involving Bernhard Rensch and Ernst Mayr), in the 1939 German translation of Dobzhansky’s Genetics and the Origin of Species, and in a 1943 anthology on evolution edited by Gerhard Heberer. The latter volume opened with a philosophical essay written by Hugo Dingler that was intended to (...) provide the theoretical foundation for the theory of descent. Dingler and Heberer not only shared a commitment to the Darwinian evolutionary mechanisms of random mutation and natural selection, but also drew from Darwinism the justification for racial hygiene and eugenics. Dingler’s “unequivocal-methodological system” is a meta-scientific construct that offers no ontological grounding of evolutionary theory. Dingler’s voluntarism is subjectivist and stipulative and for those reasons ineffective in a critique of idealistic morphology. Dingler claimed descent with modification as a historical fact, but dealt only marginally with evolutionary mechanisms, and did not touch on issues of phylogeny reconstruction. (shrink)

It is commonly thought that evolution is a chance process, an idea found in popular writings on evolution, but also in academic writing in a broad range of scientific disciplines: scientific, philosophical and theological. One problem is that words such as ‘chance’ and ‘random’ are used with a range of different meanings according to context, and in evolutionary biology the word ‘chance’ is sometimes used in a way that is different from its use in mathematics and philosophy. The present (...) article aims to clarify the range of meanings and to argue the case that the evolutionary process is far from being a ‘theory of chance’ from biological, mathematical, or indeed philosophical and theological perspectives. (shrink)

The 1940s and 1950s were marked by intense debates over the origin of drug resistance in microbes. Bacteriologists had traditionally invoked the notions of ‘training’ and ‘adaptation’ to account for the ability of microbes to acquire new traits. As the field of bacterial genetics emerged, however, its participants rejected ‘Lamarckian’ views of microbial heredity, and offered statistical evidence that drug resistance resulted from the selection of random resistant mutants. Antibiotic resistance became a key issue among those disputing physiological vs. (...) genetic explanations of variation in bacteria. Postwar developments connected with the Lysenko affair gave this debate a new political valence.Proponents of the neo-Darwinian synthesis weighed in with support for the genetic theory. However, certain features of drug resistance seemed inexplicable by mutation and selection, particularly the phenomenon of ‘multiple resistance’—the emergence of resistance in a single strain against several unrelated antibiotics. In the late 1950s, Tsutomu Watanabe and his collaborators solved this puzzle by determining that resistance could be conferred by cytoplasmic resistance factors rather than chromosomal mutation. These R factors could carry resistance to many antibiotics and seemed able to promote their own dissemination in bacterial populations. In the end, the vindication of the genetic view of drug resistance was accompanied by a recasting of the ‘gene’ to include extrachromosomal hereditary units carried on viruses and plasmids. (shrink)

Genetic drift (variously called “random drift”, “random genetic drift”, or sometimes just “drift”) has been a source of ongoing controversy within the philosophy of biology and evolutionary biology communities, to the extent that even the question of what drift is has become controversial. There seems to be agreement that drift is a chance (or probabilistic or statistical) element within population genetics and within evolutionary biology more generally, and that the term “random” isn’t invoking indeterminism or any technical (...) mathematical meaning, but that’s about where agreement ends. Yet genetic drift models are a staple topic in population genetics textbooks and research, with genetic drift described as one of the main factors of evolution alongside selection, mutation, and migration. Some claim that genetic drift has played a major role in evolution (particularly molecular evolution), while others claim it to be minor. This article examines these and other controversies. -/- In order to break through the logjam of competing definitions of drift, this entry begins with a brief history of the concept, before examining various philosophical claims about the proper characterization of drift and whether it can be distinguished from natural selection; the relation of drift to debates over statisticalism; whether drift can be detected empirically and if so, how; and the proper understanding of drift as a model and as a (purported) law. (shrink)

Evolutionary biology since Darwin has seen a dramatic entrenchment and elaboration of the role of chance in evolution. It is nearly impossible to discuss contemporary evolutionary theory in any depth at all without making reference to at least some concept of “chance” or “randomness.” Many processes are described as chancy, outcomes are characterized as random, and many evolutionary phenomena are thought to be best described by stochastic or probabilistic models. Chance is taken by various authors to be central to (...) the understanding of fitness, genetic drift, macroevolution, mutation, foraging theory, and environmental variation, to take but a few examples. And for each of these notions, there are yet more stories to tell. Each weaves itself into the various branches of evolutionary theory in myriad different ways, with a wide variety of effects on the history and current state of life on Earth. Each is grounded in a particular trajectory in the history of philosophy and the history of biology, and has inspired a variety of responses throughout science and culture. This book endeavors to offer a cross-section of biological, historical, philosophical, and theological approaches to understanding chance in evolutionary theory. (shrink)

In his theory of evolution, Darwin recognized that the conditions of life play a role in the generation of hereditary variations, as well as in their selection. However, as evolutionary theory was developed further, heredity became identified with genetics, and variation was seen in terms of combinations of randomly generated gene mutations. We argue that this view is now changing, because it is clear that a notion of hereditary variation that is based solely on randomly varying genes that are unaffected (...) by developmental conditions is an inadequate basis for evolutionary theories. Such a view not only fails to provide satisfying explanations of many evolutionary phenomena, it also makes assumptions that are not consistent with the data that are emerging from disciplines ranging from molecular biology to cultural studies. These data show that the genome is far more responsive to the environment than previously thought, and that not all transmissible variation is underlain by genetic differences. In Evolution in Four Dimensions (2005) we identify four types of inheritance (genetic, epigenetic, behavioral, and symbol-based), each of which can provide variations on which natural selection will act. Some of these variations arise in response to developmental conditions, so there are Lamarckian aspects to evolution. We argue that a better insight into evolutionary processes will result from recognizing that transmitted variations that are not based on DNA differences have played a role. This is particularly true for understanding the evolution of human behavior, where all four dimensions of heredity have been important. (shrink)

This chapter contains sections titled: * Introduction * 1 The Word “Evolution” Is Ambiguous * 2 Certain Aspects of the Theory of Evolution Are Problematic * Notes * Bibliography.