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Steven Rose
In the last decade, especially in the context of dramatic advances in the sciences of both genes and brains, the stream of ultra-Darwinist and biologically determinist claims has become a torrent. First the Human Genome Program and then the Decade of the Brain have offered not merely vastly greater knowledge of aspects of human biology, but have also held out the promise of further technological power to manipulate both genes and minds in the interests of individual health and greater social tranquility. Techniques of intervention barely imaginable a decade ago, at best the stuff of science fiction, now rate stock market quotations and turn academic researchers into entrepreneurial millionaires. To judge from headlines in daily newspapers, or the titles of academic papers in major scientific journals, the issues of a decade ago have been settled. Vulgar sociobiology may be out, but what I have called neurogenetic determinism is strongly entrenched. There are genes available to account for every aspect of our lives, from personal success to existential despair: genes for health and illness, genes for criminality, violence and 'abnormal' sexual orientation - even for 'compulsive shopping'. And genes too to explain, as ever, the social inequalities that divide our lives along lines of class, gender, race, ethnicity..... And where there are genes, genetic and pharmacological engineering hold hopes for salvation that social engineering and politics have abandoned.
The challenge to the opponents of biological determinism is that while we have been may have been effective in our critique of its reductionist claims, we have not offered a coherent alternative framework within which to interpret living processes. We may reply that we have been too busy attempting to rebut the determinists, but sooner or later it becomes necessary to spell out more coherently our contrasting biological case. Lifelines originated as an attempt to meet that challenge. First, to try to convey what it means to 'think like a biologist' about the nature of living processes. Second, to analyse both the strengths and limitations of the reductionist tradition which dominates much of biology. And third, to offer a perspective on biology which transcends genetic reductionism, by placing the organism, rather than the gene, at the centre of life - this is the perspective that I call homeodynamic. To stress my positive case, it has also in places been necessary to set it against the counter-case made at its rhetorically strongest. To do so, I have had to choose appropriate foils. The two authors who have most clearly served me in this way are the sociobiologist Richard Dawkins, whose several books speak with a single ultra-Darwinist voice, and the philosopher Daniel Dennett, whose Darwin's Dangerous Idea carries ultra-Darwinism to the furthest reaches of excess.
Note to the Precis.
Because Lifelines is written as a book for a general audience, several sections, notably those on genetics and development, include a substantial amount of explanatory material which will be familiar to most readers of this Journal, and I have therefore omitted them from the Precis, or abbreviated them to summary statements of the examples employed.
The power of western science derived from its capacity to explain, and later to control aspects of the non-living world studied by physics and chemistry. Only subsequently were the methods and theories shaped by the success of these older sciences turned towards the study of living processes themselves. The past successes of science have been based not so much on observation and contemplation but on active intervention into the phenomena they wish to explain. Biologists are now beginning to lay claims to universal knowledge, of what life is, how it emerged, and how it works. Throughout all life forms, all living processes certain general principles hold; certain mechanisms, certain forms of chemistry, exist in common. But intervention into living processes confronts us with moral dilemmas, because biology impinges directly on how we live. Its technologies transform our personal, social and natural environments and make claims as to who we are, about the forces that shape the deepest aspects of our personalities, and even about our purposes here on earth.
The science we do, the theories we prefer, the technologies we use and create as part of that science, can never be divorced from the social context in which they are created, the purposes of those who fund the science, the world views within which we seek and find appropriate answers to the great what, why and how questions that frame our understanding of life's purposes. So with modern biology, whose multifarious answers to these questions are imbued with social and political significance. The dominant fashion for giving genetic explanations to account for many if not all aspects of the human social condition, from the social inequalities of race, gender and class to individual propensities such as sexual orientation, use of drugs or alcohol or the failures of the homeless or psychologically distressed to survive effectively in modern society, is the ideology of biological determinism. I offer an alternative vision of living systems which recognises the power and role of genes without subscribing to genetic determinism, which recaptures an understanding of living organisms and their trajectories through time and space as lying at the centre of biology. It is these trajectories that I call lifelines.
Themes: biological questions. There is commonly supposed to be a hierarchy of sciences, ranging from physics through chemistry, biology and the human sciences. In this convention, physics is seen as the most fundamental of the sciences to which the others must aspire, or be reduced. But biological sciences raise themes which cannot be reduced to physics. To show why, consider a frog jumping into a pool. The cause of the jump may be described as the contraction of the leg muscles, preceded by nerve impulses, etc. Or one could explain the jump in terms of intention - to escape a predator - or in terms of ontogeny, or of phylogeny - or in terms of the actin and myosin fibres of which the muscle is composed. All are necessary and valid parts of description; only the last is reductionist. Which explanation one finds satisfying depends on the purposes for which it is intended.
Themes: time. The concept of time, and the direction of `time's arrow,' are central to biology. Living processes are complex, often irreproducible because historically contingent, and hence also practically irreversible. Dobzhansky asserted that 'nothing in biology makes sense except in the light of evolution.' I claim nothing in biology makes sense except in the light of history. , of life in general, of individual development, and of the history of our own science and its concerns. The past is the key to the present.
Themes: space. The second deep theme with which biologists are concerned is that of structure. To the three dimensions of space must be added the one of time. Organisms have forms which change but also persist throughout their life's trajectory, despite the fact that every molecule in their body has been replaced thousands of times over. How is form achieved and maintained? Cells, organisms, are more than simple lists of chemicals. Neither their three dimensional structures nor their lifelines, can simply be read off from the one dimensional strand of DNA. Today the task of a biology of structure has become one of understanding how to reassemble these components, to explain both form and its transformation and persistence through time.
Themes: dynamics. Homeostasis is a dominating motif of biological thought. But the metaphor of homeostasis constrains our view of living systems. Lifelines are not purely homeostatic, they have a beginning, at conception, and an end, at death. Organisms, and indeed ecosystems, develop, mature and age. The set points of homeostatic theory are not themselves constant during this trajectory but change over time. To put the organism and its lifeline back at the core of biology means replacing the static, reductive, DNA-centred view of living systems which currently pervades biological thinking by an emphasis on dynamics, process, the relationships between object and fields, the paradox of development by which any organism has simultaneously to be and to become.
Themes: autopoiesis. These processes of development transcend the crude dichotomies of nature and nurture, gene and environment, determinism and freedom. Instead we must speak of the dialectic of specificity and plasticity during development through which the living organism constructs itself. The central property of all life is autopoiesis, the capacity and necessity to build, maintain and preserve itself.
Science begins with observation, but no-one observes neutrally. We construct our world. Observation demands sampling, categorising events and processes, distinguishing object from field. And most sciences are also interventive, requiring that experimental conditions are constrained and manipulated - and hence reduced (Example: my own work on memory in chicks).
This example also points to another feature of science, the use of resemblance (chick memory as equivalent to human memory). Metaphors occur when we liken some process or phenomenon observed in one domain to that in a quite different one. Metaphors are not meant to imply identity of process or function, but should serve to cast light on the phenomenon one is studying. Analogy implies a surface resemblance between two phenomena, perhaps in terms of the function of a particular structure. By contrast, homology implies a deeper identity, derived from an assumed common evolutionary origin. Thus homology carries with it an assumption of shared history and origins, and, by inference, implies common mechanisms.(Example: forelimb feet of a horse and the human hand; chick and human memory).
Does memory consitute a Platonic natural kin? Are there indeed 'natural kinds' in biology? Neither individuals, nor species, nor complex biological molecules such as proteins can be so regarded. Each is defined operationally, and has a unity given by process, not by composition.
The purpose of observing and experimenting is to derive knowledge of the world and its workings; to enable us to predict and control it. This action imperative characterises modern science. Bacon understood this when he described experiments as of two kinds, those that brought light and those that brought fruit. For Bacon, knowledge came through induction. Popper replaced induction with hypothesis-making. Kuhn argued instead for paradigms, frameworks within which the problem-solving of normal science was set. But where do paradigms come from? For Kuhn the question was an individualistic, almost psychological one. However, following both the older Marxist tradition and the newer insights of the sociologists of science, Kuhn's question allows the social into science. We frame our questions of the world in ways which are constrained both by the material reality of that world, and the paradigm blinkers -our social expectations and the history of how our science chooses to ask its questions. Here the power of metaphor in biology - often derived from technological or social artefacts - becomes important (examples: ATP as a currency system, DNA as a code, brains as computers; social organisms as conforming to monetarist cost-benefit economics). Favoured paradigms and hypotheses are rarely simply disconfirmed (example; an experiment of mine done jointly with Sheldrake to test so-called morphic resonance). Nor does the fact that a technology `works' mean that the framework in which it is based is true (examples: claims that children who misbehave at school suffer from attention deficit disorder, and can be treated with the drug ritalin; ritalin may indeed make a child more tractable, but that doesn't confirm the original diagnosis).
A further constraints on science is the available technology. The questions that we ask of the living processes we study are not merely not answerable without the technology, they are unthinkable. Before the development of light microscopes, in the seventeenth century, the existence of bacteria and other single-celled organisms was wholly unsuspected. So was tbe `unit' of life, the cell, until the microscopists of the mid 19th century. Until the advent of the electron microscope in the early 1950s, the internal constituents of cells were unobservable and hence unknown. It was impossible either to build theories about the partition of cellular functions which such subcellular particles might embody.
Technology solves certain problems and suggests others. But it also constrains the way we view the world. Example: electron microscopy. To prepare living tissues for em it is necessary to fix, embed, stain and section. The apprentice electron microscopist is taught how and what to see, what to regard as `real' and what as `artefact' - the unwanted consequences of one or more of the procedures through which the living tissue has been put. Thus the new observer is initiated into the conventional wisdom developed by forty years of work in the artificial world of electron microscopy. This fixed pattern of the electron micrograph which forms the basis for drawing of cells in biology textbooks and provides the convention within which even experienced biologists mainly think of them. So powerful is the technology that it becomes hard to move beyond it, to think in three, let alone four dimensions. (Other examples: X-ray diffraction patterns; gel separation of proteins).
These are the sciences made possible by technology, the technologies made possible by science. The world-view we create is derived from the intimate interaction of technology and science with the eye of craft experience, shaped by the theoretical expectations within which we as biological researchers must live. It is a world which presents challenges which go deeper than Popperian hypothesis making, Kuhnian paradigms, and truth versus performance with which those studying the epistemology of science attempt to make their own sense of what we do. Wresting reliable knowledge from the world we biologists study is, as Koestler described it, an Act of Creation.
So what justification can there be for claiming that it is possible to obtain reliable knowledge of the living world? The evolutionary lineage which led to humans has been characterised by the development of more flexible organisms with bigger and more powerful brains, able to adapt to respond to rapidly changing circumstances. To survive and succeed our evolutionary forebears had to rely on our brains, to make reliable hypotheses about the world around us and to act appropriately upon them. If the mental world which we construct in this way did not reasonably accurately correspond to the way the world outside 'really' is, we could not survive. Such hypothesis-making may be seen as the starting point for science. But science is socially organised hypothesis making. Hypotheses must be shared, tested and agreed amongst a community. Nothing that occurs in the non-human animal world matches the cumulative nature of hypothesis making which constitutes human science. We are able to build on the tested and seemingly validated hypotheses not merely of those currently alive but of all previous generations.
However, humans are more than just scientific hypothesis makers. We live in communities shaped by many other cultural and economic forces, that provide strong guidance as to how we should view the world around us and our fellow-humans. In Britain in the 1990s, where the gap between rich and poor is greater than it has been for a generation, the world is seen from a very different perspective by the directors of the privatised utilities to that of the people they have sacked. In a society in which there is a strong division of labour and power between men and women in every field of work from science to child care, their viewpoints on the world will also differ. A white racist football fan will be unlikely to make the same hypotheses about the world as will the black player he abuses.
For many fields of scientific hypothesis-making these rather crudely drawn distinctions may be irrelevant but biology lays claims to be in a position to tell us, as humans, who we are, where we came from, where we are going to, how we must live and relate to our fellow living creatures. The metaphors and analogies we find attractive are laden with cultural values and expectations that come from outside our science. Those who deny this are ignorant of the hard work done by philosophers and sociologists in developing an understanding of the nature of science and the knowledge it creates.
Despite this doubt at the very core of the scientific endeavour, we are not in a position to assert that 'anything goes'. Although the observations we make about the world are theory- and ideology-laden before we start, and the joints into which we carve nature are provided less by a priori definitions than by operational need, nonetheless they must make some more-or-less good fit with the world or we could not proceed. Our hypotheses would fail. However great their budget, genetic engineers will not be able to turn humans into angels, nor cryogenicists restore the memories of the past owner of a severed and frozen head.
Reductionism to many scientists is first not second nature. As an example, an exchange between Popper, who argued that biochemistry is irreducible to chemistry, and Perutz, who drew on the role of haemoglobin to claim that it could be so reduced. But knowledge of the molecular structure of haemoglobin explains how it serves as an oxygen carrier, and cannot answer the biological question of what function such a capacity serves in a living organism.
Reductionism as methodology. We find it easier to understand phenomena if we can hold them relatively isolated from the rest of the world and alter potential variables singly, simplifying and enabling one to generate seemingly linear chains of cause and effect. (Example: studying enzyme kinetics by altering either temperature or pH. Altering both simultaneously makes mathematisation almost impossible.) Hence the attraction of reductionism and why it has served science so well. But living systems are not simple. Variables interact. Parameters are not fixed. Properties are non-linear. And the living world is highly non-uniform. We fail if we are not careful to remember that what happens in the test-tube may be the same, the opposite of, or bear no relationship at all to what happens in the living cell, still less the living organism in its environment. It all depends.
Theory reduction. One of the aims of science is to simplify, to embrace a maximal description of the world within the minimum possible number of laws and variables. The history of science contains a number of examples of what were originally believed to be different phenomena, and were only later discovered to be identical. (Examples: The morning and evening stars, regarded as distinct in previous cosmologies, now understood to be a single entity, the planet Venus; the sciences of heat and light were once regarded as distinct; today both heat and light are seen as forms of electromagnetic radiation.)
Some unifications have been immensely powerful, particularly at the interface between biochemistry and chemistry. Example: Lavoisier's recognition that the body's 'burning' of the sugar glucose to carbon dioxide and water, with the concomitant production of utilisable energy, was in chemical terms the equivalent of oxidation. This understanding, that living processes did not depend on some mysterious life force but involved chemical reactions which followed the same rules as those of chemistry and could be studied in isolation, was one of the great reductionist triumphs of the nineteenth and early twentieth century. More than mere metaphor, homology or analogy, it was an exact description. Yet there are dangers inherent in such theory reduction, which led to a philosophy of mechanical materialism amongst physiologists.
Modern textbooks offer the reduction of 'gene' to 'DNA' as a parallel case to the identity of the morning and evening stars. But 'Gene' and 'DNA' are not (just) two names for the same object. And it is at this point that theory reduction tips over into its problematic, philosophical form which claims that ultimately chemical theory is reducible to a special case of physics, biochemistry to chemistry, physiology to biochemistry, psychology to physiology, and ultimately sociology to psychology and hence to physics.(Example: EO Wilson's claim that neurobiology will cannibalise sociology.)
To see the implications of this type of reductionism, consider biochemistry and physiology. Although the two sciences may speak different languages, use different instruments and read different journals, the phenomena they are studying are the same, but at different levels - also an ambiguous term. But what would the elimination of physiology for biochemistry etc imply? Are we trying to describe a causal relationship - that biochemistry -say of a muscle twitch - is causally responsible for the physiological event? If so this is a very different use of the word cause from the way in which we normally employ it to describe the relationship in time between cause and effect - one event necessarily and specifically following from another. But the sliding of the actin and myosin filaments - the biochemist's description - does not precede the muscle contraction; it is the muscle contraction - or at least part of it. That is, the relationship between the events described in the two languages is one of identity, not cause - but a non-reductive identity; there are features of the muscle twitch, such as function, which physiology describes but biochemistry cannot. To put it formally, ontological unity permits epistemological diversity. The key feature which distinguishes a lower 'level' from those above it is that at each level new interactions and relationships appear between the component parts, relationships which cannot be inferred simply by taking the system to pieces.
Furthermore philosophical reductionism implies that whatever the emergence of higher order properties, they are somehow secondary to the lower order ones. Parts come before wholes. Yet the nature of evolutionary and developmental processes in biology means that there is no such necessary primacy. Wholes, emerging, may in themselves constrain or demand the appearence of parts.To understand the world's ontological unity we need the epistemological diversity that the different levels of explanation offer.
The trajectory of any organism through time and space - its personal lifeline - is unique. Although each individual resembles all others of the same species, and resembles more closely still its parents and siblings, no two are identical. What confers these similarities, these identities and differences, on the space-time trajectories of life? These questions are the objects of study of genetics and developmental biology, which began by asking rather similar questions about the nature of life, but at a key point in their history became damagingly separated one from the other. This has resulted in conceptual confusions which have persisted well into the present days. But to appreciate the consequences of these confusions we have to go back into the history of genetic and developmental thinking. Biology's own history is centrally engaged within these current disputes.
Genetics genesis. Mendel not only showed that certain characters were transmitted independently, but introduced quantitative measures, observing that they appeared in successive generations in simple and reproducible ratios. Inheritance was discrete; each surface property was represented by an unobservable particle or store of information, on the basis of which the colour and shape of the succeeding generations was determined (hence eg 3/1 ratios). Mendel was lucky. By contrast the characters that interested Galton - human features such as height, or strength of handgrip, or head circumference or intelligence - varied continuously across a broad range and offspring tended to occupy middle territory between their parents. Such continuously varying characteristics seemed to blend. Indeed Mendel's ratios turn out to be very special cases, even though, following their rediscovery in 1900, they formed the cornerstone of genetics. The individual hidden determinants of surface characters became genes, and the total of an individual's genes formed its genotype (nowadays genome). The surface characters themselves comprised the individual's phenotype. It is important to recognise that none of these terms were very precisely defined, and practically from the beginning meant different things to different researchers, varying from the specific features of any individual of a species to some Platonically idealised 'species-type' to which all actually existing members of the species approximated. Genes were essences: the ultimate, indivisible units on which the outward forms depended; the unmoved movers, unchanged changers, within each organism.
'Phenotype' is similarly ambiguous, and is used to refer to any or all observable or measurable features of an organism, from the presence of a particular enzyme to hair colour or body feature or even a piece of characteristic behaviour such as gait whilst walking. Dawkins even goes so far as to describe aspects of the external environment of an organism as part of its phenotype - for instance, he sees the dam that a beaver constructs as part of that beaver's phenotype. Yet the dam is not the product of the activity of a single individual, but of the collective labours of many beavers. It also harbours a multitude of other species. If the dam is a phenotype, it is the phenotype of a community, not of an individual, and its relationship to any individual's genes, genotype or genome is thus tenuous.
The distinction between discontinuous variation and continuous variation remained problematic through the 1920s. Pearson developed many of the statistical methods still in use today to analyse complex data. Indeed the histories of genetics and of statistics have been thoroughly interlocked ever since. The resolution of the conflict depended on the recognition that continuous variation, in features such as height, could be regarded as a consequence of the interaction of many genes of small effect. Divergences from simple Mendelian ratios steadily accumulated (eg sex-linked characters) Other divergences from the ratios are less straightforward, and the models became more and more complex to account for them. However complicated and varied the observed phenotypes, the modellers were still determined to explain them on the basis of the interaction of the indivisible causal particles which they conceived genes to be. If the ratios didn't work it was because some other factors were obscuring the proper functioning of the genes. ( Partial dominance; incomplete penetrance). Once these possibilities are admitted, there is virtually no distribution of phenotypes found in the population to which a genetic model cannot be fitted. In the traditional Popperian sense, such genetic models are strictly unfalsifiable. Given enough assumptions, any model can be 'fixed.' (eaxample: schizophrenia).
Whilst the Mendelian rediscoverers were busy defining the phenotypic features they observed as the products of hypothesized genes, other biologists were looking at organisms from quite a different perspective. How does the union of egg and sperm ultimately produce an organism which may consist of 1014 such cells, differentiated into tissues and organs, precisely located in space? Embryologists described cell division, from fertilisation to the formation of the blastula and gastrulation, and identified a role for the chromosomes. This rhythm of cell division unrolling in a seamless sequence operates according to rules which the early embryologists found hard to fathom. For some, the only explanation was that the developing embryo was imbued by an irreducible life force. To most this conclusion was unacceptable; they were observing a complex piece of living clockwork. Whichever philosophy one adopted, the dividing ball of cells was splendidly accessible to experimental manipulation. What would happen, for instance, if one removed a portion of the dividing cell ball, or cut it neatly in half? The results confused researchers for decades, for the conclusion seemed to be 'it all depends.' Depends on the organism, depends on how many divisions the ball of cells has made prior to the cut; depends from where in the ball one removes the sample. (Example; contrast between Roux, Driesch and Loeb). Depending on the organism, at early stages in the cell division process, each cell still retains all the determinants - genes - to make an entire offspring; at later stages some regions of the developing ball of cells retains this capacity and others do not; later still the capacity is entirely lost, and the developmental fate of each region of the cell ball is fixed and cannot be modulated.
Tranplant studies revealed more. Sometimes its fate is determined by the environment into which it has been transplanted, in others it carries its own fate with it. (Example: transplant a group of cells from the region of a developing insect destined to become a leg, and insert it into the head region. Depending on the age of the embryo, the number of divisions it has undergone since fertilisation, the transplanted tissue may be incorporated into the developing head, or may develop into an additional leg projecting anomolously from the head). During mitotic division each cell receives an identical set of determinants or genes and is totipotent. Later although all the genes are still present in all the cells, which genes are expressed depends on the developmental history of the particular cell. Thus gene expression depends on both time and space.
The major concern of developmental biology remained that unrolling programme which led from a single fertilised egg to the fully formed organism. How is it that what seem at first sight to be very similar cell masses, going through seemingly similar transformations, end up in the one case producing a mouse and in the other a human? Why do the daughters of a cell from one part of the dividing embryonic cell mass end up as liver and from another as brain or bones? How is it that all individual humans end up so astonishingly similar? Developmental biology is the science of the rules which produce regularities, similarities between organisms. Genes are part of a harmonious dialectic of interaction with the environment by which fertilised cells become mature adults through a trajectory described as ontogeny. And the constraints on this trajectory are only in part genetic.
By contrast, genetics was and is concerned with differences. Why is one Drosophila red eyed, the other white eyed? Why do people differ in height; why do some have blood cells which carry a haemoglobin molecule which seems unable to bind and carry oxygen as efficiently as is normal? The question is to be answered in terms, ultimately, of the modern descendants of Mendelian determinants, the genes. Thus for genetics, genes are discrete units which lead in linear fashion to red versus white eyes or any other character of interest. Ontogeny is of interest only insofar as genetic differences may produce abnormalities in development. Otherwise, the geneticists' organisms are empty of time and internal content; there are only genes and phenotypes. They have no trajectory, no lifeline.
Using Drosophila, Morgan and his group showed that unusual mutations were transmitted in a Mendelian manner and increased by X-rays. Genes had a physical location in the cell, on chromosomes, and were thus distributed to daughter cells during mitosis, making possible the beginning of gene mapping. The term gene now had two different meanings. On the one hand it was still an abstract entity, the determinant of a particular phenotypic character. On the other it had a clear location, a map reference, and could be shown to be physically transmitted between cells and their offspring during both division and sex. The step which took genetics beyond Morgan's location of genes to chromosomes also brought it into conjunction with biochemistry for the first time. Mutations in Neurospora were even easier to induce and study than in fruit flies, but now the consequences were metabolic. Mutants lack specific enzymes which play a crucial role in the pathways which lead to missing metabolites. Each specific mutation leads to the absence of a specific enzyme. Hence Beadle and Tatum's formulation: one gene equals, or produces, one enzyme.
Genes themselves had taken a further step away from being hidden entities. They no longer determined characters, but instead, in a yet-to-be understood manner, were responsible for the production of enzymes. So what is a gene 'for' a character? Consider eye colour, which depends on the presence in the cells of particular pigments. In their absence, the eye is blue, increasing quantities of the pigments provide colours which range from green to brown. Ignoring the developmental processes that lead to the formation of the eye, and within the eye the iris, and the biochemical steps whereby the necessary precursors to the synthetic pathway are produced, the direct pathway that leads to the synthesis of the eye pigments involves many different enzymes. Hence to biochemists there is no longer any gene 'for' eye colour. Instead there is a difference in the biochemical pathway that leads to brown and to blue eyes. A gene 'for' blue eyes means 'one or more genes in whose absence the metabolic pathway which leads to pigmented eyes terminates at the blue eye stage.' This rephrasing yet again exposes the distinction between a developmental and a genetic approach. For the developmental biologist, what is of interest is the route which leads to pigmented eyes. But the geneticist is still interested in the difference between brown and blue eyes and retains the misleading shorthand of genes 'for' such colour differences. Dawkins, in The Extended Phenotype explicitly makes the same point, before going on to discount it as irrelevant, provided the system behaves as if such `genes for' existed. That is, his genes are purely theoretical constructs, combinations of properties which may or may not be embedded in specific enzymes or lengths of DNA, but which can be used to play mathematical modelling games. But sloppy terminology abets sloppy thinking. And it has implications for gene technology too. As more is learned about the human genome, so early simplicities, such as the existence of a single gene responsible 'for' a particular disease, retreat. Many ostensibly 'single gene disorders' are now known to result from different gene mutations in different people. All may show a similar clinical picture but the gene mutation and hence enzyme malfunction which results in the disorder may be very different in each case. This also means that drugs effective in ameliorating the condition in one person may be simply ineffective in another.
The history of how genes became DNA, culminating in the famous Nature papers of Crick, Watson, Franklin, Wilkins et al in 1953 is too well known to need retelling. But what made a length of DNA a gene? Genes now coded for polypeptides, and the 19690s saw the breaking of this code and the formulation of Crick's Central Dogma:
DNA-------->RNA--------->protein
'..once `information' has passed into the protein it cannot get out again.'
A formulation which is as central to ultra-Darwinian theory as it is to molecular biology. DNA had become the master-molecule, and the nucleus in which it was located had assumed its patriarchal role in relationship to the rest of the cell. It is hard to know which had more impact on the future directions of biology, the determination of the role of DNA in protein synthesis, or the organising power of the metaphor within which it was framed (Example: Dawkins' description of willow seeds as floppy discs)..
Periods of great unifying simplicity in science are frequently followed by times in which simplicity dissolves once more into complexity. Not all DNA is coding; much is concerned with regulation (operons, etc). And much more seems `junk or 'selfish' - Crick's term. (Note that Crick's DNA's selfishness is demonstrated by the fact that it doesn't do anything for the cell or the organism in which it is embedded; it simply allows itself to be copied. Dawkins' selfish genes on the other hand are so because they specifically aid the succesful reproduction of the organism which contains them and hence their own replication.) Nor are the coding sequences for any particular polypeptide aligned along the DNA; they are separated by introns, and can be spliced, edited, read in different ways. The result is that far from being able to speak of one gene/one protein, both genes and proteins are disarticulated. Genes can be assembled from alternative pieces of DNA or rearranged so that their codes are read differently. And proteins take on multiple forms as a result of cellular processes distal to DNA itself. 'Genes' are no longer coterminous with DNA-beads-on-a-chromosome. Nor are even these segments stably located on the chromosome; as McClintock showed, genes could jump. Hence the modern concept of the fluid genome.
Far from being isolated in the cell nucleus, magisterially issuing orders by which the rest of the cell is commanded, genes, of which the phenotypic expression lies in lengths of DNA distributed along chromosomes, are in constant dynamic exchange with their cellular environment. The gene as a unit determinant of a character remains a convenient Mendelian abstraction, suitable for armchair theorists and computer modellers with digital mindsets. The gene as an active participant in the cellular orchestra in any individual's lifeline is a very different proposition.
DNA is a stable molecule; what brings it to life is the cellular environment in which it is embedded. Genetic theorists have been misled by the metaphors that Crick provided into describing DNA (and RNA) as 'self-replicating' molecules or replicators, as if they could do it all by themselves. But they aren't and they can't. Replication isn't an inevitable chemical mechanism. Copying requires the precursor molecules - which themselves must be synthesized - enzymes to unwind the two DNA strands, and others to insert the new nucleotides in place and zip them up again. And the whole process requires energy. Further, the histones surrounding the relevant region or regions of the double helix must be unwrapped, the DNA strands separated, enzymes must transcribe the 'sense' strand into its matched length of RNA, individual RNA lengths spliced, edited and further manipulated in the cell nucleus, and if and only if so permitted, leave the nucleus to be inserted into the copying machinery in the cell cytoplasm. Without the complex biochemical environment the cell provides, 'genes' in the DNA sense of the term, simply can't function.
This is why an individual's lifeline requires more than merely the mixing of parental DNAs at the moment of fertilisation. Sperm provide only DNA. But an egg contains more than just the maternal complement of DNA to match that provided by the paternal sperm. It has in addition all the cellular apparatus required to bring both sets of the DNA together to play their part in the cellular orchestra, as well as the mitochondria with their own independent DNA. From this moment of conception on, the maternal cellular machinery is responsible for directing the activation of particular genes (DNA-sequences) and hence the synthesis of specific proteins. These proteins in turn include some whose function is to act as switches, regulators to turn on, and in due course turn off, other DNA-sequences. A continuous cycle of synthetic activity begins in which DNA-sequences are uncovered, transcribed into RNA, processed, spliced, edited, translated into proteins which then provide feedback control to the DNA, perhaps switching off their own synthesis, perhaps switching on the synthesis of other proteins by uncovering other DNA-sequences or influencing the splicing and editing steps. This exquisitely timed and subtly orchestrated cellular symphony culminates in due course in the synthesis of those proteins which begin the process of replicating and segregating the chromosomes once more, enabling the cell to divide and the cycle to recommence.
In the digital information metaphor all these cellular mechanisms are dumb, because they dont't carry `information.' But it is the cellular machinery which times and edits the synthetic processes. Insofar as the information metaphor is valid at all, it can be expressed only in the dynamic interaction between the DNA and the cellular system in which it is embedded. Cells make their own lifelines.
Thus in both the Mendelian and the biochemical senses genes are only partially determinate entities within genomes. How, when and to what extent any gene is expressed - that is, how its sequence is translated into a functioning protein - depends on signals from the cell in which it is embedded, and as this cell is itself at any one time in receipt of and responding to signals not just from a single gene but from many others which are simultaneously switched on or off, the expression of any single gene is influenced by what is happening in the whole of the rest of the genome.
When we talk about the development of an organism as being a product of the interaction of genes and environment therefore, the phrase masks as much as it reveals. Neither gene nor environment are unproblematic terms. A 'gene' as abstract determinant is quite different from the complex processing mechanisms which put together particular DNA sequences which define the primary sequences of proteins. Nor are proteins merely defined as their primary sequences; they have complex secondary and tertiary structures which depend not just on their amino acid sequence but on their environment, on the presence of water, ions and sometimes other small molecules, on acidity and alkalinity. The path from primary structure to fully fledged protein does not involve as many regulatory steps as that from DNA to protein, but it contains orders of complexity which move us yet further away from the one gene-one protein heuristic. And as proteins themselves become assembled into higher order structures within the cell, yet further constraints come into play.
The school textbooks which start with Mendel and his ratios have it wrong. Without Mendel genetics would never have got off to such a start. and he deserves honour for his experiments. But the founders of a field, by choosing experimental systems which seem to give clearcut answers, often also produce an appearence of simplicity which is ultimately misleading. The famous and paradigmatic Mendelian ratios are the results of rather special cases, the phenotypic expressions of enzyme pathways rather little influenced by environmental circumstance, perhaps just because they reflect relatively trivial features of that phenotype. By contrast the expression of most genes is modified at several levels. It is affected by which other genes are present in the genome of the particular organism, by the cellular environment, the extracellular environment and, in the case of multicellular organisms, by the extra-organismic environment Example: the ambiguous consequences of knockout mutations. In many cases in which genes coding for proteins which are supposed to have vital functions within the cellular economy have been deleted the absence both of the gene and of the protein whose synthesis it codes for seem to make little observable difference to the life of the animal. It has ` no phenotype'. This does not mean that the protein concerned does not play a vital role in the cellular economy; rather it is a demonstration of the power of developmental plasticity, of functional redundancy in the organism. Redundancy assists stability; it means that there may be many alternative routes that the cell and the organism can adopt during development which can lead to an essentially identical end-point. In the presence of a particular gene and protein, one route is adopted, and in their absence another is taken. Once again, there is no necessary linear path between gene and organism. Such plasticity is not infinite; there are sharp limits to the tolerance of any gene - or any phenotype - to environmental change. Outside these limits, the response is to curl up and die. But within them, the expression of any gene may be defined in terms of Dobzhansky's concept of norm of reaction - rather out of fashion amongst today's theorists who prefer a modern version of preformationism, in which genes are prime movers.
At the heart of modern biology lies the issue of the nature of individual living units - organisms. Their lifelines may range over many orders of magnitude in both time and space. Some arise esssentially fully developed, like a newly budded yeast, others grow to a reasonably stable adulthood before ageing and decaying, others incrementally throughout their lives. Yet others go through a series of radical transformations in which entire bodyplans become reconstructed, as when eggs become caterpillars become chrysalises become butterflies. Life persists not in three but in four dimensions - persistence which is above all dependent upon the maintenance of order, order within the cell, order within the organism, and order in the relationship of the organism to the world outside it. Genes and genomes neither contain the future of the organism, nor are they to be regarded, as in modern metaphors, as architects' blueprints or information theorists' codebearers. They are no more and no less than an essential part of the toolkit with and by which organisms construct their own futures.
Neither cells nor organisms can be considered in isolation from their own external environments. The boundary between cell and environment is its semipermeable membrane across which all trafficking must occur. For single-celled organisms, the environment of the cell is obviously also that of the organism, the ever fluctuating external world, inherently patchy. Some regions may be antithetical to survival - too hot, too dry, too acid.....Some may be rich in food sources, others poor. Faced with such patchiness, many single-celled organisms can take steps to seek out more favourable conditions (Example; cilia and flagella). But their power to choose a favourable environment is limited by the range of environments available, and survival will also depend on the ability of the organism to adapt to less than optimum conditions (Hence the operon, which is the mechanism whereby the organism in interaction with its environment determines which of its available genes are to be active at any one time.)
Such interactions between cells and environments become more complex for a multicellular organisms. Buffered by a regulated internal environment cells no longer need the operon mechanism, but instead lose their autonomy within the greater unity of the organism, they have surrendered their capacity for replication and their totipotency. They become specialised, as liver or brain, leaf or root. In the course of this specialisation, as ontogeny proceeds, particular DNA-sequences are switched on or off in defined temporal sequences. It is no longer only a case of proceeding through the cell cycle to division but of establishing cells with an appropriate structure, shape and pattern of enzymes to function as part of a particular organ. To ensure harmony at a multicellular rather than a cellular level, each cell has to be able to respond to the presence of its neighbours and to signals from distant parts of the organism (hence hormones, transmitters, modulators...) arriving at its membrane surface. The cellular lifeline has become subordinated to that of the organism.
Like the term gene, the term environment is thus complex and many-layered. For individual gene-sized sequences of DNA, the environment is constituted by the rest of the genome and the cellular machinery in which it is embedded; for the cell, the buffered milieu in which it floats; for the organism, the external physical, living and social worlds. Which features of the external world constitute 'the environment' differ from species to species; every organism thus has an environment tailored to its needs. Even for the individual gene, the genomic background against which it is expressed differs during the cell cycle as other genes are switched on and off. Outside the organism, change is virtually the only constancy. Stasis is death.
Boundaries between organism and environment are not fixed. Organisms are constantly absorbing parts of their environment into themselves as food, and as constantly modifying their surroundings by working on them, by excreting waste products, or by modifying the world to suit their needs, from birds nests to beaver dams and termite mounds. Organisms and environment interpenetrate. Abstracting an organism from its environment, ignoring this dialectic of interpenetration, is a reductionist step which methodology may demand but which will always mislead. Nor are organisms are passive responders to their environments. They actively choose, and work to change them.
The first phases of the life cycle are those of development. From the moment of fertilisation, cells grow, divide and hence multiply. Daughter cells begin to align themselves with respect one to the other, to migrate to specific regions within the developing embryo. Within each cell, particular genes are switched on, others off, in intricate sequences, as originally totipotent cells become specialised and the mature form of the organism unrolls from its undifferentiated state. From very early on in their development organisms have to be capable simultaneously of quasi-independent existence, and of growing further towards maturity. Moreover, the properties that enable them at any one moment to maintain their existence are not always merely miniature forms of those they will need in adulthood. This is obvious for some life forms. Frogs' eggs become tadpoles become frogs. Each stage requires a radical transformation of body plan, yet one during which the functions necessary to life must be preserved. But it is also true in quite subtle ways for organisms which seem to show linear developmental trajectories. When a new born baby suckles at its mother's breast, the suckling reflex is not simply an undeveloped form of the chewing technique that will be needed when the child switches to solid food; quite different neural and mechanical processes are involved. Life demands of all its forms that they are able simultaneously to be and to become.
The unrolling processes of development are best understood in terms of specificity and plasticity.. Many ontogenetic processes are relatively unmodifiable by experience (Example: relatively fixed development of the visual system). But plasticity is also necessary. (Example, alterations to visual cortex neuronal connectivity dependent on rearing environment). Specificity and plasticity are embedded properties of the organism; both are completely made possible by the genes, and completely made possible by the environment. They cannot be partitioned.
Two contrasting metaphors have been used to describe the process by which multicellular organisms develop: selection and instruction. Consider the human brain, with its highly ordered pattern of characterisitcally shaped and located neurons. From conception to birth requires the generation of about a million cells an hour, whilst during postnatal development some 30,000 synapses a second will be created under each square centimetre of cortex, until the full complement are present. Development requires the ordered birth and migration of these cells. To arrive at the correct both distant and local signals must be involved. (Example: role of trophic factors). However, the migrating cells or growing axons also need to keep in step with one another; each has to know who its neighbours are. The diffusion of a local gradient molecule, together with the presence of some type of chemosensors on the axon surface, could enable each to determine whether it has neigbours to its right and left and to maintain step with them.
Part of this process - the achievement of long-range order - is compatible with a cooperative, instructionist model, but the overproduction of neurons and synapses implies also ultimate selection amongst cells or connections competing for targets. Selection in this sense can account for local but not distant processes. Instructive and selective mechanisms are only part of the picture of development. The maintenance of stable order requires the collective, cooperative properties of the entire ensemble of cells. Each depends on the others in the creation and preservation of the dynamic pattern of connections which impose new patterns on the world beyond the organism. Development is essentially a constructivist process; the developing organism, in its being and its becoming, in its specificity and its plasticity, constructs its own future.
Even the constructivist model of development discussed above however implies a degree of determinism, albeit a richer concept than that of the unidimensional gene. But we need to go beyond this in emphasising the role of chance, of contingency, at all levels of analysis of living systems. Consider the micro level of the individual cell and its subcellular components. Biochemists deal not with individual cells or molecules but with aggregates of millions, and on this scale properties become relatively predictable. But what is predictable for the mass does not apply to the individual (Example: there are only about 30 hydrogen ions in any single mitochondrion). Chance, contingency affects all cellular processes (Examples: numbers of bristles on Drosophila legs; different foetal circumstances for identical twins depending on placental relationships).
Organisms arte supposed to maintain homeostasis. But in fact the set points around which conditions fluctuate are not constant but vary momentarily, diurnally, monmthly, and over a lifetime. Furthermore they are maintained dynamically, not statically. Hence homeodynamics. Seeing organisms as merely homeostatic is to deny them lifelines. Each of our presents is shaped by and can only be understood by our pasts, our personal, unique, developmental history as an organism. Even the moment-to-moment stability of the organism is maintained not statically but dynamically; molecules and cells turnover on timescales varying from minutes to months. Why this ceaseless flux?
The answer is simple: living systems need to be dynamic to survive, able to adjust themselves to the fluctuations which even in the best-buffered internal milieu, their cooperative existence as part of the greater unity of the organism demands. It is to this irreducible dynamism as the generator of stable order that we must turn in order to understand how, having constructed itself through the processes of development, the organism is able to preserve its integrity and act upon the external world. These are the phenomena of autopoeisis.
Internal cellular stability depends on two features. First, cells and organisms are thermodynamically open systems far from equilibrium, which for their existence depend on a continuous energy flow, generated through the catabolic/anabolic cycle which results in the synthesis of ATP, ultimately through the activities of autotrophic organisms (primarily photosynthesis). Equations relevant to closed equilibrium systems are largely inapplicable to living processes.
Second, the existence of an interacting metabolic web. Individual reactions are catalysed by enzymes; sequences of reactions, like glycolysis, by chains of enzymes whose overall rates are seemingly controlled by individual enzyme kinetic properties, so that in a chain the slowest reaction becomes the controller. However, just as in a living cell one cannot abstract an individual enzyme reaction from the metabolic dance of the molecules, so one cannot abstract any single reaction pathway. Most of its components are involved in many different reaction pathways, knitted together by multiple interconnections. Once such a web reaches a sufficient degree of complexity, it becomes strong, stable and capable of resisting change; the stability no longer resides in the individual components, the enzymes, their substrates and products, but in the web itself. The more interconnections, the greater the stability and the less its dependence on any individual component.
Further, the cellular web has a degree of flexibility which permits it to reorganise itself in response to injury or damage. Self-organisation and self-repair are its essential autopoietic properties. These properties of stability and self-organisation are the key to the fundamental irreducibility of living cells. The stability is dynamic, and depends in part on metabolic oscillatory processes (Example: calcium waves). Metabolic organisation is not merely the sum of cellular parts, and cannot be predicted from individual enzyme reactions and substrate concentrations..
Cells are not simply bags containing semi-random mixes but contain many internal structures (nucleus, mitochondria, etc). Each represents a separate compartment within which relatively segregated sets of reactions can occur. Communication between these compartments, in terms of exchange of substances and signals between them, takes place through selective membranes, which act as gatekeepers across which specialised signalling molecules and small inorganic ions control access. Homeodynamic order with the cell is thus maintained not merely through the self-stabilising properties of metabolic webs, but through internal structural constraints provided by semi-permeable lipid membranes in which are embedded proteins which recognise and regulate the entry and exit of key metabolites. Ionic changes also modulate the microenvironment within which protein structure is modulated, complex structures such as microtubules and ribosomes can self-assemble, and enzyme-linked reactions occur.
Lifelines, then, are not embedded in genes. Their existence is posited on homeodynamics. Their four dimensions are autopoietically constructed through the interplay of physical forces, the intrinsic chemistry of lipids and proteins, the self-organising and stabilising properties of complex metabolic webs, and the specificity of genes which permit the plasticity of ontogeny. The organism is both the weaver and the pattern it weaves, the choreographer and the dance that is danced.
`Darwinism' has become an almost universal - and often abused - term. Darwinian protagonists offer a 'tough-minded' ultra-Darwinism as a universal mechanism to explain all phenomena of life. Philosophers follow them; Dennett writes a book entitled Darwin's Dangerous Idea in which Darwinian mechanisms are described as a 'universal acid' which eats away at everything it touches. Edelman interprets the brain processes concerned with experience, memory and consciousness as representing 'neural Darwinism.' Hull claims scientific theories themselves win or lose the struggle for acceptance according to Darwinian mechanisms. One reads of Darwinian psychology, Darwinian medicine, Darwinian economics. Dawkins, caps the lot with his claim that human culture itself operates on Darwinian principles in which the units of transmission are not genes but 'memes.' It may be time to try to rescue Darwin from some of his over-solicitous modern friends, if we are to do justice, but no more than justice, to the part he and his ideas have played in the history of biology and in our understanding of living processes.
Before Darwin, the interpretation of life on earth was trapped within a mode of thinking imposed by biblical traditions. Species were immutable, linked in a great chain of being, beginning with the lowliest and ending with that acme of god's creation, Humankind (Man) himself. The industrial revolution shattered this stability; change (and evolution means simply change over time) became acceptable. The discovery of fossils implied extinct species, whose history could be dated. Before Charles, both Erasmus Darwin and Lamarck had sought to describe, and account for such changes. It was Charles who offered the mechanism by way of a simple syllogism:-
1. Like breeds like, with variations.
2. Some of these varieties are more favourable (to the breeder, or to nature)
than others.
3. All creatures produce more offspring than can survive to breed in their
turn.
4. The more favoured varieties are more likely to survive long enough to
breed.
5. Hence there will be more of the favoured variety in the next generation, and
6. Thus species will tend to evolve over time.
This process is natural selection. As a syllogism it has an inexorable logicality. If 1, 2 and 3 are true, 4, 5 and 6 follow inevitably. This is why philosophers such as Dennett are able to describe it as a universal mechanism. Yet for Darwin there were major theoretical difficulties at the heart of the theory; the mechanism of transmission both of similarities and variations; the classic argument from design; and the problem of speciation.
Darwin's achievement was to demolish the idea of the immutability of species, and, even more importantly, of a great chain of being. Humans are no longer at the pinnacle of life. Instead living forms can be drawn as related to one another as the branches and twigs of a bush. All of us currently alive, amoebae as well as humans, are in this respect equal, the succesful survivors of evolutionary history. There is no scale of life on the basis of which one can judge some currently living forms as `lower' and others as `higher,' more or less `evolutionary successful.' A further crucial feature of Darwinism is its insistance on the role of chance. Natural selection abolishes purpose from evolution, and, some felt in consequence, from human life itself.
Variation. The problem of transmission was resolved with the theory of the gene, although when Mendel was rediscovered at the turn of the century mutational change seemed to replace natural selection, and it wasn't until the `neo-Darwinian synthesis' of Fisher, Haldane and Sewall Wright around 1930 that it was seen that the two theories supported rather than contradicted eachother.
Heritability. Fisher's synthesis was directed at trying to understand the contributions of genes and environment to variation in populations. In a uniform environment all the variance would be contributed by the genes, and with identical genes, all the variance would be contributed by the environment. But genotypes and environments both vary and the purpose of heritability estimates is to try to tease them apart. To do so however, it is necessary to make some simplifying assumptions. Variance describes the way in which any particular measure of a trait in a population is distributed about the mean value for that population, made up of a component contributed by the genes and a component contributed by the environment, which together can be added to give a total of nearly 100%. The remainder, which to make the mathematics work has to be a rather small proportion, is considered to be the product of an interaction between genes and environment. If genotypes are distributed randomly across environments, it is possible to estimate heritability, which defines the proportion of the variance which is genetically determined. However, the mathematics only works if all the relevant simplifying assumptions are made. If there is a great deal of interaction between genes and environment, that is if genes behave according to Dobzhansky's vision of norms of reaction, if genes interact with each other, and if the relationships are not linear and additive but interactive, the entire mathematical apparatus of heritability estimates falls apart. Thus the meaningful application of heritability estimates is only possible in very special cases, from which the majority of traits of interest outside the special world of artificial selection are likely to escape. Furthermore the figure derived for the heritability is itself dependent on the environment - that is, if you change the environment, the heritability estimate changes.
These caveats perhaps help to explain why heritability estimates have been so persistently misunderstood. It becomes wholly misleading when applied to aspects of human behaviour. Milk yield is a phenotype which is reasonably straightforward to measure. But intelligence? Political tendency? Likelihood of getting divorced? Religiosity? Job satisfaction? As one can't treat human populations quite like breeding experiments with wheat or cattle, and distribute genotypes across environments, one has to make do with what between them nature and society provide. The standard techniques have involved comparing traits in siblings, MZ and DZ twins, and the use of adoption studies. The problems are manifold. To mention just two, separated twins tend to be placed in rather similar environments; whilst adoptive parents are unlikely to treat their adoptive child `exactly' as they do a natural one, and are far more likely to be anxiously on the lookout for tendencies which reveal the child to be `taking after' some undesirable character of its natural parent. Such real life problems are simply swept aside in the process of fitting the numbers obtained into the complex statistical manipulations required to generate the seemingly objective heritability estimate.
As a result seemingly bizarre traits turn out to have `high heritability', for which the most parsimonious explanation is that they demonstrate the inappropriateness of attempting to apply a mathematical formalism devised for plant and animal breeding to such dubious phenotypic characters as the diversity of human social behaviour and attitudes. Yet some behaviour geneticists argue that even such high heritabilities underestimate the true influence of the genes. Bouchard proposes that our genes `predispose' us to seek enviroments congenial to the genetic imperatives. Thus genes create environments, and `environment' - whatever that term may mean - ceases to be a truly independent variable in the heritability equations. It is their genes therefore, which are a major cause of everything from childhood accidents to divorce in midlife, for such genes lead their owners to place themselves in situations in which the probability of accident or divorce increases. Like the claims for the `extended phenotype' this argument perversely swallows the four dimensional universe of lifelines entirely into the double helix of DNA.
Adaptation. The argument from design is confronted head-on in Dawkins' The Blind Watchmaker and its successors: `What use is half an eye' he asks, and answers `One percent better than 49% of an eye, and the difference is significant.' The trouble with this argument is that there is no way of determining whether, amongst our evolutionary ancestors, 50% of an eye was really significantly better in Darwinian terms - that is, contributed significantly more to reproductive success -than 49%. It would depend what other costs the organism accrued in achieving this 1% advantage, and how much having eyes contributed to its success in finding food, and avoiding predators so as to increase its chances of finding a mate and hence reproducing. There is of course no evidence on these issues, and so the claim must remain an undemonstrable assertion, although one which most biologists will find reasonably convincing. In the classical Popperian sense such stories about evolution are unfalsifiable. All that we can do is to offer plausible accounts of how a process may have occurred or a structure evolved.
Sexual selection If all adaptation serves the function of enhancing survival, how come so many animals - especially males - have traits which seem on the face of it to be inimical to long and efficient life? (Example: the peacock's train). Darwin's interpretation of sexual selection was that females were motivated to choose, and hence select beauty. More modern versions argue instead that seemingly dysfunctional adornments are markers of good health and hence good genes. Whichever version of the theory is adopted, sociobiologists have sought to press it into service to provide an evolutionary `Darwinian' explanation for the preferences expected in human sexual choice, once again treating metaphor as if it were homology. For example, competition amongst human males for mates is discussed as the macro-version of what is said to be the micro-level competition amongst individual sperm to be 'the one' to succesfully penetrate and fertilise the egg. Males and their sperm compete, females and their ova quiescently await their fate. The problem is that, as with most human extensions of evolutionary mechanisms, but in an even more extreme form, such accounts simply cannot encompass the rich diversity of human experience, and instead have recourse to traditional and often sexist caricatures which ignore the historical and anthropological evidence of variation in social practices across time and space and instead treat current western norms - or rather, assertive restatements of what the authors perceive as those norms, for they show as little respect for sociology as they do for history or anthropology - as if they were human universals.
Altruism. With the claims for the genetic mechanism and evolutionary significance of altruistic behaviour, we are at the heart of sociobiological thinking.If organisms seek to maximise their reproductive success, then how do we account for birds which on detecting a predator, draw attention to it, and simultaneously to themselves by uttering warning cries? Ought they not instead try to make themselves as inconspicuous as possible, so as to diminish the chance of being picked off? Earlier group-selectionist ides, once discarded, are now creeping back into the literature once more, but the dominant mode of explanation is kin selection, a mathematical formulation which, if one grants its basic assumptions - that is, that living forms exist primarily to perpetuate their genes - is as inevitable a syllogism as the original Darwinian formulation of natural selection. Although I see no reason to doubt the principle, proving it is harder. Certainly, behaviour which might be defined as altruistic does occur amongst group-living animals, although equally there is no shortage of evidence as to competitiveness amongst them. The empirical question is whether apparently altruistic behaviour can be shown to benefit preferentially the kin of the altruist rather than the group as a whole. Perhaps in response to the relative weakness of the data, Trivers offered an alternative version:reciprocal altruism - an act performed to benefit non-kin, but which is performed in expectation of a subsequent return of the compliment. And once again, human sociobiologists have sought, on the slightest of evidence, to deprive human unselfish behaviour of any function other than one of these forms of selectionist altruism, once again reducing metaphor to homology.
Speciation. It may seem extraordinary, but the Darwinian syllogism provides no mechanism for the formation of new species, which was after all ostensibly what The Origin was all about. All that is claimed is that in any given circumstances, external conditions (the environment, Nature) will favour the perpetuation of varieties which can do their species-thing a bit better than the rest. Example: Kettlewell's peppered moths, which also demonstrate another fundamental point. A 'more favoured variety' is one which is favoured under current circumstances. Evolution by natural selection can respond only to the current situation. It cannot predict the future. At one point of the species trajectory in time it is the peppered form which has the greater survival value, at a later time the melanic, and then again the peppered. The environmental change occurs, and natural selection trails along behind, following, responding, but never leading and never predicting. Such evolutionary processes could obviously modify a species over time to such a degree that its members would no longer be able to mate fertilely with their ancestors could these be brought back to life. In this sense, species can gradually be transformed through processes of natural selection steadily tracking environmental change. But this still doesn't explain how natural selection alone can result in one preexisting species splitting into two. For this, additional mechanisms are required; primarily presumably geographical separation and founder effects, of which the most famous example is Darwin's own, the Galapagos finches. But could this be all? For the orthodox ultraDarwinian, there is nothing else available.
Ultra-Darwinism has a metaphysical foundation: the purpose of life is reproduction of the genes embedded in the `lumbering robots' which constitute living organisms. There follow two premises: (1) the unit of life is an individual gene whose sole activity is to create the conditions for their own reproduction by directing the development and physiological function of the organism; (2) most aspects of the phenotype are adaptive, selected for by the honing force of natural selection. This metaphysic derives from a combination of Hobbes and Smith. Life is a war of all against all, but the invisible hand of the market generates even cooperative behaviour from competitive individualism. A further element is a restatement in scientific form of the theology of preformationism. Our task is to preserve and transmit copies of our DNA.
It follows that the prime function of every living organism is to maximise its inclusive fitness - that is, to ensure the maximal spread of its own and its close relative's genes in succeeding generations. This determinism worries Dawkins and others, who therefore claim that we have the capacity to rebel against the tyranny of our genes. But if the power to rebel does not itself come from our genes, then the argument implies a sort of Cartesian dualism, and the mechanical materialism of selfish genery trips over into a type of idealism.
The case against ultra-Darwinism rests on the following claims.
1. The individual gene is not the only level at which selection occurs.
2. Natural selection is not the only force driving evolutionary change.
3. Organisms are not indefinitely flexible to change; selection is `table
d'hote' and not `a la carte.'
4. Organisms are active players in their own destiny.
1. Any individual gene can only be expressed against the background of the whole of the rest of the genome. Genes produce gene products which in turn influence other genes, switching them on and off, modulating their activity and function. If selection ultimately determines whether a particular gene survives or not, it can only do so in context. A gene is only selected if it results in a selectable phenotypic change - yet what is required to produce such a change is not one but many actual biochemical gene-size lengths of DNA. Furthermore, Weismann's barrier is not as impermeable as implied, so developmental processes also affect transgenerational gene transmission. Waddington argued that developmental processes in multicellular organisms could help both direct and, as he put it, canalise, potentially favourable mutations. Bonner identified two routes round Weismann's barrier. Thus both plants, and animals such as Hydra, retain the capacity either to differentiate into somatic cells, or to become sequestered as gametes, or to remain totipotent. Those cells which remain totipotent retain the prospect of becoming gametes after an indefinite number of cell divisions - and this means that any genetic variation occurring during those divisions will be heritable. That totipotency is available even to mammals is now proven by Dolly and her successors. Further, during development, originally totipotent cells divide, become determined, and migrate to appropriate positions within the developing embryo, resulting in competive/selective mechanisms operating at the cellular level; cellular variation will affect the outcome of such competition.
So selection acts on genes, on genomes, and on cells, notably during development. But for multicellular organisms it is ultimately the organism as an integral unit which will or will not reproduce and hence dispatch copies of its genes into subsequent generations. So natural selection in the sense that Darwin originally conceived it can only act through the actions and properties of the entire organism, its phenotype. For ultra-Darwinists that is not a problem; the phenotype is merely a proxy for the genes it contains, the gene's way of making copies of itself. But this implies a direct relationship, one-for-one, between gene and phenotype, and this `empty phenotype' view ignores development.
The fact that selection occurs at many levels dampens the effects of change at any one level. For instance, mutation rates in DNA are relatively constant, yet these are not necessarily reflected in phenotypic change (hence Eldredge and Gould's pnctuated equilibrium). Furthemore there is a vast amount of hidden phenotypic diversity (Example; isoenzymes) which is likely to be neutral so far as selection pressures are concerned.
Finally in this context, organisms do not exist in isolation, but in populations, and populations in ecological communities involving many hundreds or thousands of different species locked into relationships which may be competitive or cooperative. Thus within species, evolutionary stable strategies (Maynard Smith) mean that any individual's character may or may not be selectively favourable depending on the balance between that individual and others in the population, whilst the facts that any species' niche is defined in the context of all other species within an ecosystem (predator or pray, mutualistic or commensal or even, in Margulis' term, symbiogenic, like mitochondria) and that all species are evolving, mean that the evolution of any one is shaped and constrained by that of many others. Evolution means coevolution, built on both competitive and cooperative mechanisms.
2. Selection mechanisms include competition for scarce resource, sexual and kin selection, founder effects, expansion of populations into new niches, selective predation and coevolution of populations and species. Selection at any given level of the hierarchy between individual genes and ecosystems, does not automatically imply selection and evolutionary change at any other; there is sufficient flexibility and redundancy within living systems to make such tight coupling unnecessary. But not all phenotypic variation is adaptive, and not all change is selective. Contingency also applies (Examples: Gould's account of the Burgess Shale fossils; dinosaur extinction following climate change). And what constitutes an adaptation is itself problematic and evolutionary accounts become Panglossian Just-So stories (example; flamingo legs as pink to confuse predators rather than as a consequence of the colour of blood). Gould and Lewontin used the famous spandrels of San Marco as an example of how adaptationist assumptions could be misleading; their account has been criticised by Dennett; however, architectural reassessment of the role of spandrels (pendentives) favours the original interpretation.
3. Within the adaptationist programme, the trajectory that any lifeline can take is ultimately limited only by the question of whether it is adaptive. Of course, evolution is cumulative, and has to build on whatever materials it has at hand. So to arrive at any adaptive structure, behaviour or molecular property there has to be a legitimate route from where the present state of the system to some presumably more adapted place elsewhere. And these constraints determine what is or is not evolutionarily possible. (Examples: limits on the size of single cells, and of multicellular organisms - surface area/volume and mass relationships, skeletal properties etc, set by chemistry and physics). But there are deeper prospects opened by discussion of `laws of form' (Examples: Darcy Thompson's topological transformations; radiolaria crystalline forms, pentadactyl limbs; pinecone patterns in Fibonacci series; the role of morphogenetic fields).
4. The metaphor of natural selection is one in which Nature sets a series of challenges which organisms either pass, in which case they are privileged enough to pass copies of their genes on to a successor generation, or they fail. By contrast, the autopoietic vision implies that organisms actively choose and transform their environments, to adjust and appropriate them to their own ends (Examples: unicells moving to food rich environments, growing axons finding and modifying targets, etc.) Organisms change environments, and environments have their own trajectories constantly transformed not merely by the workings out of the inanimate forces of weather, temperature and cosmic history, but above all by the interactions of myriad lifeforms.
Where once the definition of being alive was to be a breathing, metabolising, environment-sensing and responding organism, molecular biologists tend to see the basic function of life as the power to replicate, and the basic unit of life is therefore a molecule with this power, a naked nucleic acid polymer. There are religious undertones to his view that in the beginning was the word. But could life have begun with a naked molecule of DNA or RNA? So-called self-replicating experimental procedures are already quite complex. They must occur in a test-tube which serves as a surrogate cell, including all the necessary mix of enzymes, ions and controlled temperatures. It follows that accurate replication could only have emerged long after the development of cell-like structures capable of such crucial living processes as metabolism, growth and division. What characterises all living organisms, including ancient fossils, is the presence of a cell membrane, and such cells must precede replicators.
Origin of life theorists and experiments have shown how abiotic synthesis of amino acids and other organic precursors is possible. The biochemical parsimony which characterises modern living forms suggests that these substances must have appeared prior to their organisation into replicating organisms. Life consists primarily of arrangements of the elements carbon, hydrogen, oxygen and nitrogen together with smaller quantities of phosphorus and sulphur, ions of calcium, magnesium, sodium, potassium and some heavy metals. Compounds of these most abundant elements are thermodynamically unstable but, capable of relatively long life in watery solution; their synthetic chemistry requires energy but they trap energy easily in the form of sugars; they readily combine to form long chain molecules, lipids, polysaccharides, proteins and nucleic acids, especially in a reducing atmosphere (Miller-Urey experiment). The earth's early atmosphere provided this environment; it is life itself which has subsequently modified it by trapping carbon and releasing oxygen. Oparin and Haldane proposed that droplets of concentrated organic chemicals could concentrate out of a prebiotic soup (coacervate drops). Other concentration mechanisms coulds include clay surfaces. Lipids spontaneously form micelles and droplets surrounded by bimolecular membranes, within which the soup would be concentrated. These represent protocells. Such cells would have another property seemingly fundamental to life in that there would be an electrochemical gradient across their membranes.
The next evolutionary step would be to stabilise the myriad potential chemical reactions that could occur within the proto-cells. Kauffman's models suggest that given enough metabolic interactions in due course catalytic and autocatalytic relationships would arise, especially granted the possibility of catalytic surfaces such as that provided by clay. Computer models of such processes show that a random set of chemicals in a constrained area soon settle into a robust and autopoietic metabolic web in which stable balances of constituents result. Traffic across the liposome membrane will bring new materials into the cell and excrete waste products, and cells which increase in size will simply split into two.
Thus cell formation and division, and sophisticated metabolic stability, have all been achieved by originally abiotic processes, in which the properties which are characteristic of life are embedded not in a single molecular substituent but in the entire system which constitutes the cell, and without replicators. The metabolic web must have extended beyond any individual proto-cell, to embrace the entire population. If chemicals were to be exchanged between cells, by ingestion or by cell division, the reactions within each cell must have tended to converge.
Even before the problem of accurate replication had been resolved, there would have been another more pressing problem, that of energy. An evolutionary bottleneck would have been produced until the energy-generation problem could be solved. Early chemoautotrophes would in due course have been replaced by photosynthesizing organisms, which in turn were responsible for changing earth's atmosphere (and could later be embraced within more complex organisms, as chloroplasts, by symbiogenesis. Only after the development of effective energy-generating and utilising mechanisms, though presumably before the development of the modern cellular systems, would it be possible for nucleic acid based replication - probably initially RNA - to emerge.
Once these molecules had been incorporated within the metabolic web of the cell, they would offer a whole new range of properties. For they would now achieve a level of fidelity in copying and reproduction which would have been unobtainable by mere random division without them. Just how this mechanism settled down into its present day form, based as it is on the trinity of DNA, RNA and protein, is a matter of intense speculation. Contingency, rather than laws of molecular form or adaptation, may rule at this point in the story. But once a particular set of nucleic acid-amino acid correspondences had emerged, convergence within the web would be likely to help ensure its universality. In any event, the essential point is that once cells containing these mechanisms had arisen, they would multiply rapidly and swamp out all others, as only they could produce exact copies of themselves. Evolution, having generated nucleotide polymers within the primitive cells, had now also produced a mechanism which could be relied upon to amplify them, and before long to conquer the earth - yet another reason why whatever the processes by which life forms were first generated, so far as life on this planet is concerned, they cannot repeat themselves.
This chapter shifts gears, to focus on reductionism as ideology in human affairs. The primacy given to reductionist explanations of human behaviour leads to claims, made by scientists but trumpeted by the media, that the origins of everything from sexual orientation to violence, criminality and `compulsive shopping' lie in the genes. Neurogenetics claims to be able to answer the question of where, in a world full of individual pain and social disorder, we should look not merely to explain but even more potently to change our condition. Although this is not a new debate, the apparent power of modern genetics gives it new force, and the ideologues of neurogenetic determinism claim that their science will in due course render sociology, economics and even philosophy, redundant.
Neurogenetic determinism, is based on a faulty reductive sequence whose steps include: reification; arbitrary agglomeration; improper quantification; belief in statistical 'normality;' spurious localisation; misplaced causality; dichotomous partitioning between genetic and environmental causes; and confounding metaphor with homology. The issue at stake the appropriate level of organisation of matter at which to seek causally effective determinants of the behaviour of individuals and societies. The structure of the argument is similar whether the discussion focusses on intelligence, sexuality or violence.
Reification converts a dynamic process into a static phenomenon. Example: violence as an interaction between people becomes `aggressive behaviour,' the property of an individual).
Arbitrary agglomeration lumps together many different reified interactions as if they were all exemplars of the one character. Thus aggression becomes the term used to describe processes as disparate as a man abusing his lover or child, fights between football fans, strikers resisting police, racist attacks on ethnic minorities, civil and national wars as if in fact they were all examples of the same underlying mechanism of `anti-social behaviour' (Example, the claim that a genetic abnormality in monoamine oxidase predisposes to variants of these activities). Yet the identical act performed in different contexts (eg war or peace) may be socially desirable or undesirable (example: British troops in Northern Ireland).
Improper quantification argues that reified and agglomerated characters can be given numerical values (Example: the IQ scale which reifies `intelligence', agglomerates many different processes within the term, and then claims to be able to provide a single number which defines where an individual lies in the intelligence hierarchy). Belief in statistical normality then assumes that in any given population the distribution of such behavioural scores takes a Gaussian, normal distribution. Yet such curves are a product of the test design. There is no biological necessity for such a unidimensional distribution, nor for one in which the population shows such a convenient spread. Yet the power of this reified statistic is that it conflates two different concepts of 'normality'; it has normative implications, and to lie more than two standard deviations from the mean is to be abnormal (Example: The Bell Curve).
Having reified processes into objects and arbitrarily quantified them, the reified object ceases to be a property even of the individual, but instead becomes that of a part of the person. (Example: schizophrenic brains, genes - or even urine - rather than of brains, genes or urine derived from a person diagnosed as suffering from schizophrenia). This shorthand of 'gay brains' or 'selfish genes' does more than merely sell books for their scientific authors; it both reflects and endorses the modes of thought and explanation that constitute neurogenetic determinism, for it disarticulates the complex properties of individuals into isolated and localised lumps of biology.
Misplaced causation. During aggressive encounters people show dramatic changes in, for instance the levels of circulating steroid hormones and adrenalin in their bloodstream and the release of neurotransmitters in their brains, all of which can be affected by drug treatments. People whose life history includes many such encounters are likely to show lasting differences in a variety of brain and body markers. But to describe such changes as if they were the causes of particular behaviours is to mistake correlation or even consequence for cause. Drugs such as ritalin may make children more tractable at school; the cause of their so-called attention deficit disorder is unlikely to be too little amphetamine in their brains. The search for `first causes' seems to lead inevitably to genes.
Confounding metaphor with homology. If first causes are genetic, then they must have evolved and similar behaviours should be found in non-human animals. Example: `aggression,' measured in rats by measuring how long they take to kill mice, and taking this as a surrogate for `violent behaviour' in humans.
Reductionist ideology not only hinders biologists from thinking adequately about the phenomena we wish to understand; it has two important social consequences: it serves to relocate social problems to the individual, thus 'blaming the victim' rather than exploring the societal roots and determinants of a phenomenon; and second, it diverts attention and funding from the social to the molecular (Example: alcoholism research in the US or Russia). For any aspect of the living world, multiple forms of explanation, are possible. But for any such phenomenon there are also determining levels of explanation - those which most clearly account for the specificity of the phenomenon and also point to potential sites of intervention into it. Effective science requires a better recognition of determining explanation and hence the determining level at which to intervene. Failing this it becomes a waste of human ingenuity and resource, a powerful ideological strategy of victim-blaming and a distraction from the real tasks that both science and society require.
This chapter summarises the main arguments of the book in the form of ten slogans, as follows:
1. Our history shapes our knowledge
2. One world, many ways of knowing
3. Levels of organisation
4. It all depends
5. Being and becoming
6. Stability through dynamics
7.Organism and environment interpenetrate
8. Structure constrains evolution
9. The past is the key to the present
10.Life constructs its own future
To conclude: for humans as for all other living organisms, the future is radically unpredictable. This means that we have the ability to construct our own futures, albeit in circumstances not of our own choosing. And that it is therefore our biology that makes us free.