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Applying evolutionary epistemology: from immunity to intelligence
J. Social
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1988 11, 399-408
Applying evolutionary epistemology: from immunity to intelligence Ian J. Deary
Department of Psychology, University of Edinburgh, 7 George Square, Edinburgh EH8 9JZ, Scotland A formal description of the process of knowledge accretion has been accepted in three areas: somatic evolution, adaptive enzyme formation and adaptive immunity. Random variation followed by natural selection is the method by which all three processeslead to an organism’s increased fitness to its environment. This paper gives a detailed account of the discovery that adaptive immunity is better described in selectionist rather than instruction& terms. It is argued that, since other biological adaptation systemsare best described by an evolutionary epistemology, selectionist approaches to brain development and cognition are liable to be more helpful than instructionist accounts.
Introduction The problem of how organisms gain in knowledge and become better adapted to their
environment is central in psychology. A general theory which describes the structure of all knowledge-gain processes might appear over-ambitious, yet that is the purpose of the enterprise called evolutionary epistemology. Although the ideas which drive evolutionary epistemology are not new, it is generally accepted that the explicit beginning of the movement was Campbell’s 1974 paper (at that time, Campbell supplied a large bibliography acknowledging many precursors). The core ideas in evolutionary epistemology are: that evolution-even in its biological aspects-is a knowledge process: and that all knowledge-gain systems follow a random variation followed by natural selection process; and this is what is known as the evolutionary analogy. Critics of evolutionary epistemology have remarked that, while this might be a sticient outline for the process of somatic evolution, it fails to capture the processes of mental development, learning and scientific progress in man, let alone the development of culture. Nevertheless, there have been several attempts to develop an ‘evolutionary analogy’ in these areas (see, for example, Plotkin & Odling-Smee, 198 1) but, to date, evolutionary epistemology remains a philosophical or metapsychological rather than a scientific discipline. In this paper, I will describe how an evolutionary epistemological approach has led to success in advancing the understanding of one knowing system: adaptive immunity. The more general purpose .of the paper is to suggest that selectionist thinking will lead to the adoption of more promising approaches in understanding all aspects of animal cognition. We tend to use knowledge to refer to the primarily human, process of forming and storing regularities about the world. But, following Campbell, I will use knowledge 0140-1750/88/040399
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gain to refer to any change in an organism’s structure that leads to an improvement in adaptive fit to its niche at the time it comes about (it may be maladaptive later). This paper will focus on adaptive changes found in organisms over their own life-span. The problem of innate knowledge will not be addressed, although in Campbell’s scheme a genotype represents knowledge of the world and may be seen as the physical embodiment of what Popper has called ‘innate hypotheses’. [Again, the statement that a genome is knowledge might stretch the patience of some but, as a developing foetus forms muscles, red blood cells and eyes, it is difficult to deny that it knows about (or is hypothesizing the existence of) gravity, atmospheric composition and the existence of light reflecting and absorbing bodies in a transparent medium. That it does not consciously know these phenomena is of little concern, it comes into the world preadapted to certain aspects of a niche.] The rules and expectations provided by the genome cannot prepare the complex organism for all possible environmental challenges. For humans, the problem is particularly severe. The time lapse between birth and reproduction in humans ranges from about 16 to about 40 years. In other words, the human structure has to be maintained for this length of time in order that it may reproduce. The correlation between intergenerational time lapse and the complexity of the adaptive capacities may, therefore, be expected to be high. Unless an organism exists in a very isolated and rich niche with few competitors or predators, the ability to respond successfully to environmental challenges will be important for survival at least until the age of reproduction and care of the young. These challenges are anything that will affect adversely the integrity of the organism leading to reduced or absent reproductive or nurturing abilities. In fact, the main challenges are chemical (due to micro-organisms and toxins) and physical (due to predators, climate, accidents, etc). In response to these challenges, animals have developed adaptive immunity and, for want of a better term, intelligence, respectively. Just as intelligence deals with the physical and social environment, so does the immune system adapt to aspects of the chemical environment. It does this by surveying and perceiving aspects of the chemical environment; discriminating between self and not self; making appropriate effector responses to stimuli; and remembering or storing ‘percepts over many years in order to facilitate responses at a second or subsequent presentation of the same stimulus (i.e. it learns). I shall demonstrate that, by using a selectionist approach (i.e. the evolutionary analogy), immunologists were able to predict some of the rules of immune functioning. The analogy provided a description of adaptive immunity as a knowledge-gain process that excluded blind alleys in research and theory. If we take the lessons of this theoretical resolution in immunity into the area of cognition, we may save time and effort. Template theory in immunity From before 1940 until the 196Os, immunologists were, in effect, debating a problem of epistemology. The problem was that of adaptive immunity. Higher animals are able to manufacture circulating antibody that reacts specifically with certain micro-organisms or their products (or parts of either that serve as identifiers for the invaders and are refered to as antigens). The immunologists faced several problems: if the host organism has never met a particular antigen before, how does it recognize it as foreign? How does the recognition lead to antibody formation (and the effective elimination of the antigen)? And how does the host remember the antigen’s structure so that when it meets it on a subsequent occasion it is able to respond more quickly and with more antibodies than
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the first time? Clearly, it does not do violence to meaning to describe this as a problem of knowing. As a result of an environmental event, the organism has effected a specific response and retained a specific memory-this is a broad description of both adaptive immune and intelligent functioning. How is it done? At about the middle of the present century, there were two main theories. The earlier, and the one that held general sway until the 1960s was the ‘template’ theory. There was no single author of this theory, but it received its most complete exposition in the paper by Nobel laureate Linus Pauling (1940). Pauling became interested in how the immune system modelled antigen structure and posed the question, ‘. . . what is the simplest reasonable process of formation of such a molecule?’ Pauling’s answer was that, . . . the antigen causes the polypeptide chain to assume a configuration complementary to the antigen. The number of configurations accessibleto the polypeptide chain is so great as to provide an explanation of the ability of the animal to form antibodies with considerable specificity for an apparently unlimited number of different antigens (Pauling, 1940).
Intuitively, this appealed to many immunologists. There was agreement that what identified antigens was the ‘shape’ or configuration of their, primarily surface, determinants. Therefore, a system that existed to intercept, discriminate and respond to these shapes would do well to use the antigens as templates for the formation of a specific antibody response. There were two improbabilities of this ‘instructionist’ system that were not discussed. By supposing that the same globulin molecule could take on the shape of almost any antigen, Pauling was demanding that these proteins not only adopt many unstable configurations but that they also retain them when they leave the template. It is known that proteins tend to adopt a configuration of lowest energy that is relatively specific and is held together by many reversible bonds as well as some covalent disulphide linkages. The number of covalent bonds in any one protein the size of a globulin molecule would be incapable of adopting and retaining an indefinite number of specific shapes. Yet this is just what Pauling’s theory demanded: that the globulin was a tabula rasa, with no innate predisposition to any one shape, that could be modelled like clay upon antigen. Apart from the chemical improbability of such a proposal, the system also appears evolutionarily unlikely. What Pauling was suggesting was that, perhaps at a single step, evolution provided a single, open-ended and undirected modelling system for foreign antigens, a Royal Mint capable of manufacturing a die for any coin imaginable. If template theory was correct, it is hard to imagine the system being built in a piecemeal way. Since it hypothesized the existence of an uncommitted general capacity to mould antigens, it seemed to suggest that the whole structure was built, unlike Rome, in a day. Template theory was anthropomorphic: it reflected the way humans go about constructing factories but did not appear to resemble the blind progression of evolution. Moreover, this instructionist model required that the antigen be present for the manufacture of subsequent antibody, The antigen molecule, after its desertion by the newly-formed antibody molecule, may serveas the pattern for another . . (Pauling, 1940).
In this scheme, so-called immunological memory was not explained because the ‘instructor’ was eliminated by the antibody, thus removing the template for further production. In the most obvious way Pauling was suggesting that the immune system ‘wrapped its mind round the problem’. Some of the ideas did fit the experimental data at the time, but the driving force of the theory was an instructionist epistemology. There were other implications of template theory that were not noted at the time. If an antibody modelled
I. J. Deary the antigen why was this, by definition, novel shape not then treated as antigen and set upon by the immune system? It is known that the antibody of one animal may act as an antigen in another species, there is nothing protective about being an antibody per se, and Pauling’s theory could not explain why each new antibody did not then become an antigen in its own system. (It is interesting to note that if new antibody was formed using the original antibody as a template, it would have the shape of the original antigen and be attacked once more!) Clonal selection theory
The theory that challenged template theory had less intuitive force. It developed from an analogy with somatic evolution and adaptive enzyme formation in bacteria. Two Nobel laureates were involved in propagating what started as the ‘natural selection’ theory and was refined to become the ‘clonal selection’ theory of antibody formation. Jeme (1955) suggested that the role of antigen was not that of a template for antibody formation but that, Among the population of circulating globulin molecules there will, spontaneously, be fractions possessingaffinity toward any antigen to which the animal can respond. . . . The introduction of an antigen into the blood or into the lymph leads to the selectiveattachment to the antigen of those globulin molecules which happen to have a complementary configuration (Jerne, 1955).
Thus, animals happened to have, naturally,
the immense numbers of configurations
needed to fit most antigens. The evolutionary analogy was explicit: by generating, somehow, antigen recognizers of many different shapes spontaneously or randomly, the
best fit to the antigen would not have to be modelled but simply selected from the alternatives. Although Jerne got much of the subsequent detail wrong, his theoretical shift was able to explain the so far puzzling phenomena of booster effects, immunological memory and the relative importance of the antigens on the surface of an organism vs their internal antigens. The first two of these were unresolved anomalies in
template theory. The suggestions of Jerne were developed by Sir Macfarlane Burnet in a series of books and articles. Bumet, like Jerne, looked to the structure of biological change in somatic evolution and bacterial adaptive enzyme formation to inform his understanding of adaptive change in acquired immunity. Bumet’s (1959) introduction to the clonal selection theory of acquired immunity did not begin, as most texts would have done, with an account of the immune system’s cells or their origins but with a discussion of the way that bacteria adapt by producing novel enzymes to destroy, say, antibiotics. The explanations for the adaptive enzyme production included, again, instructionist and selectionist theories: either the bacterium formed a new enzyme after a genetic change that was brought on by the antibiotic; or a single bacterium, by chance, had developed the enzyme by a mutation (bacteria have high mutation rates and very short generation times) and was selectively retained as the non-enzyme producers were destroyed. The latter explanation was correct: bacteria got to ‘know’ about antibodies by the process of random change followed by natural selection. Burnet ended, These considerations of the processes of change in populations of bacteria and viruses were designed to act as an introduction to the discussion of clonal selection amongst the cells of the vertebrate organism, more specifically amongst human mesenchymal cells. Throughout, a single theme has been dominant-the potency of mutation and selectivesurvival to change the character of a population of cells to bring it into more appropriate relationship to its environment. The remainder of these lectures are concerned to show that this is as relevant to cell populatons within the mammalian body as to populations of viruses and bacteria (Bumet, 1959).
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Burnet’s message was that two knowledge processes had voted in favour of a Darwinian vs a Lamarckian mechanism, and he doubted whether this new problem of adaptation would be any different. Burnet reviewed theories with regard to two main problems in immunity: (1) how does the immune system discriminate between self and not self? (Either self is not attacked because it is recognized or not self is attacked because it is recognized. Either way, wrote Burnet, the body required a, ‘library of information to be stored’.) (2) How does immunity last a life time, and how do daughter cells carry the antibody production information of the parent cells (since immunological memory was far greater than the life-span of lymphocytes)? The template theory of HaurowitzPauling was explained, and a modification by Burnet & Fenner examined. In his modified template theory, Burnet had tried to solve the above problems using template ideas. The problem of self-recognition, the earlier Burnet had suggested, existed because there exist ‘self markers’. Further, a recognition unit was involved in antibody production to deflect the possibility of immune response to self. Of course, there was no empirical evidence for the existence of these structures except for the fact that the self was not attacked: the supposed answer was a restatement of the problem. The answer to the second problem was Lamarckian: immunological memory came about because a genocopy of the antigen was incorporated in the genome. It did not take long for Burnet to see the inelegance and theoretical poverty of his indirect template theory which, when tested against these problems in a rigorous way, was clearly incapable of dealing with many important empirical facts. Burnet called the self-marker/ recognition unit ideas ‘clumsy and ‘only a rough paraphrase of the actual mechanism’. In fact, they were only a rough paraphrase of the original question. Burnet then dealt with Jerne’s natural selection theory. After dealing with some errors of fact (for instance, Jerne’s mistaken guess that recognition sites for foreign antigens were on circulating gamma globulin molecules), Burnet drew the core idea.from Jerne’s theory, that the body had, . . a population comprising carriers of all the reactive sites needed to unite with any potential antigenic determinant except those already existing in accessiblecomponents of the body (Burnet, 1959). The insight of Jerne’s solved one more problem for template theories that was never stated explicitly. In template theory it was proposed that the immune system first recognized the foreignness of the antigen and then made a specific antibody to it, so that is would be recognized in the future. Thus, it required two recognition processes: one for foreignness and one for specificity. Two considerations make this scheme unlikely. First, antigens constitute a wide range of macromolecules, proteins and carbohydrates that have no single shared identifier. Second, many antigens are very similar in conformation to the host macromolecules. Thus, no one discriminator would do for foreignness. Many different discriminators were needed and, because some antigens were very like the host’s body surface markers, they would have to be very specific. The template theory then, when pushed, had to posit that, to make a template of an antigen, the host had to be able to recognize the antigen in a specific way in advance. Template theory was untenable in this form, which was essentially a form of selectionist theory. Burnet gave Jerne’s insight a firmer physical basis, . . . any tenable form of Jerne’s theory must involve the existence of multiple clones of globulin producing cellseach responsible for one genetically determined type of antibody globulin (Bumet, 1959). Burnet put the recognition sites for antigens on the surface of cells, and with this tweak of Jerne’s theory much fell into place. Here was a mini scientific revolution which
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was well documented only because a single man was driven by a belief in the broad applicability of Darwinian explanation. Yet, empirically there were no compelling reasons for immunologists to accept his clonal selection theory. He wrote, The reasons for temporarily or permanently discarding the ‘indirect template’ hypothesis in favour of the clonal selection approach were cumulative and largely indirect (Burnet, 1959).
Burnet listed five points that led to his theoretical switch. Three were experimental findings that had only a tenuous relation to the theories. Of the two most compelling reasons, one was an analogy and one was a theoretical point. First, adaptive enzyme
production by bacteria was known to be genetically determined and not a transcript of a pattern introduced by, say, an antibiotic. For Burnet, This destroyed the significance of any analogy between adaptive enzyme production and the indirect template hypothesis of antibody formation (Bumet, 1959).
He reckoned that if this adaptive change did not work in a template or instructionist fashion then, by reference to his Darwinist principles, it was unlikely that another should. If bacteria adapted by random variation and natural selection, then so, probably, did the immune system. Second, Burnet saw that his notion of self-markers was vacuous and dubbed the idea, ‘semi-mystical in character and generally unattractive’. For template theory, it was a case of theory immunization leading, eventually, to theory collapse. With the gradual acceptance of clonal selection theory, immune phenomena became more amenable to explanation. Self-tolerance was due to the elimination of selfrecognizing cells in early life. Bumet paused, though: in choosing a clonal selection hypothesis, he still had no proof that at some stage the antigen did not shape the antibody. As was shown above, the logic of this notion leads to unsolvable problems but Burnet had a more general reason to throw out any vestige of the template hypothesis: There seems no reason to engraft such a grossly Lamarckian qualification on what might be described as a strictly Darwinian process at the cellular level. .The theory differs from the standard interpretation of antibody production in replacing the concept that in one way or another the antigen actively enforces production of a new pattern of specific globulin, by the view that somatic mutation and selection within the mesenchymal cell populations can have the same overall effect (Burnet, 1959).
Burnet’s concluding theoretical remarks cleared much confusion. He was able to articulate the fact that, once an antibody was developed, the two theories differed very little: the key difference was an epistemological one, that of how the body came to be informed of the structure of a foreign antigen. Burnet’s book remains an unusual one in biology. He took concepts that had served well in other areas and offered them as a structure for resolving a debate in a new area. Further, he did it at a time when the majority of his profession held an opposing view. He produced no single piece of evidence that could decide between the two approaches, but Bumet did make a single specific prediction. He felt that clonal selection theory would be validated, . . . if it could be shown that cellsfrom a non-immune animal gave rise to clones, each cell of which under proper physiological conditions contained, or could liberate, antibody-type globulin of a single pattern. . . (Bumet, 1959).
The empirical research that led to the general acceptance of clonal selection theory is documented by two key workers in a recent article (Ada & Nossal, 1987). Bumet offered his approach to other biologists, Irrespective of what field we are considering, as the environment changes the natural population changes, and in the present state of our knowledge the changes are best understood in terms of mutation and selective survival (Bumet, 1959).
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The relationship between the knower and the known was no longer, in the field of immunity, thought to be, ‘something almost as definite as the relation between the pattern on the face of a coin and that on the die which stamped it’ (Bumet, 1962). A decade later (Burnet, 1969), the immunologists had accepted the clonal selection theory and investigated the problem of how the ‘vast repertoire of specific antibodies [can] . . . be produced more or less on demand’. As with any good new theory, it was able to ‘ . . . absorb in natural fashion the various concepts as they arose from the new experimental approaches. . . ‘. But it was neither this ability nor the unifying structure of Darwinian selection that swung most practioners round; it was empirical results such as the discovery that patients with the illness multiple myeloma were producing a great excess of a single immunoglobulin. The immune system, concluded Burnet, had all . . the elements of a Darwinian situation. . . The numbers of essentially autonomous genetic elements, the lymphoid cells, are large, perhaps around 10” in man, giving adequate opportunity for mutation, and the selective advantage of an accidentally appropriate pattern is enormous and extremely rapidly expressed (Burnet, 1959).
From immunity to intelligence If the Darwinian scheme of random variation followed by natural selection has informed thinking about adaptive fit (or knowing) in somatic evolution, bacterial adaptive enzyme production and adaptive immunity, there might be lessons for those working on those areas of knowing that apply to animal nervous systems. In the three systems that have been successfully described using selectionist thinking, one clear message is that organisms are not moulding responses to environmental information. Instead, knowing systems in nature tend to have a generator of alternatives that are selected by the environment for fitness. The extension of the insights in immunological adaptation have been applied to nervous system adaptation occasionally over the last 20 years. In 1970 Burnet offered that, The general structure of the central nervous system must be determinative but there are hundreds of situations in which large numbers of similar cells move to distribute themselves or their axons more or less uniformly over a defined region. Further, there is a great deal to suggest that the functional structure of a working brain is built up by something which may represent essentially a form of natural selection of circuits arising by random processes(Bumet, 1970). In this short quote, Burnet anticipated the key concepts of an evolutionary epistemology as applied to the nervous system. For instance, Plotkin & Odling-Smee’s (1981) selectionist multi-level hierarchy of knowing processes involves somatic evolution (Burnet’s general central nervous system structure), brain development (where Bumet anticipated the success of the now popular selective stabilization theories) and brain function (the process of learning and what we generally refer to as knowing). Jerne (1985), too, has devoted some attention to bringing immunological concepts to the problems of cognition. In a recent address, he used the example of the immune system explicitly as a knowing system and compared it with human language. Both immune and language capacities, said Jerne, were ‘complete’ or open-ended in their repertoire: i.e. the 10’ or so B lymphocytes, means that the immune system can respond, by the formation of specific antibodies, to any molecule existing in the world, including molecules that the system has never before encountered (Jerne, 1985).
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Jerne was impressed by the fact that most languages make do with 100,000 words or less, and that antibody variable regions (two per antibody molecule of about 100 amino acid residues confer the specificity for particular antigens) appear to function like sentences in a language, although the alphabet of the immune system is still unknown. Jerne remarked that Chomsky’s notion of a generative grammar works well as a description of adaptive immunity. Burnet and Jerne, then, may be seen as allies of Campbell in construing the problems of knowing as biological problems that should be guided by selectionist principles. Popper (1975), too, saw that the success of selectionist over template theory in immunity should be used as a guide to the structure of knowledge growth, I suggest therefore that we conceive the way scienceprogresses somewhat on the lines of Niels
Jerne’s and Sir Macfarlane Bumet’s theories of antibody formation. . The fundamental idea of Jerne was that the instruction or information which enables the antibody to recognise the antigen is, literally, inborn . these cells [antibody production cells] are selected with the help of the invading environment (that is, with the help of the antigen), rather than instructed (Popper, 1975).
Selectionist theories in intelligence
The main problem with sorting out the selectionist theories in brain function is that the brain is examined at many levels. There are theories that describe the process of development, at one level, and those that attempt to give an account of learning and memory. Nevertheless, there exist template and clonal selection theories at different levels of description. Two examples of template theory will suffice to draw a parallel with immunity. The theory of memory and intelligence devised by Hendrickson & Hendrickson (1980) proposed that, for every percept, an RNA molecule was constructed according to the pattern of electrical impulses invoked by the stimulus. Like Pauling’s theory, the notion was that the environment shaped a physical record in the organism. This theory was based on empirical evidence but, while subsequent findings concerning cell membrane receptors and ion channels have disproved the theory, its template nature indicated its non-viability earlier. Another template theory was the frame-system theory of Minsky (1977). Minsky’s account of perception demanded that a very general, uncommitted capacity existed to construct frames for any set of percepts. Here, again, the emphasis was on the malleable organism with a nervous system that was able to model the environment. A more selectionist account of perception would ask questions such as: is there evidence of early over-connection in nervous systems? What elements of the environment are perceived by organisms? And is there evidence for the selection of useful connections in brain development and learning? There is a growing body of opinion which conceptualizes brain development and memory formation within a similar framework; i.e. the formation of excess connections and the later selection or selective stabilization of those units that are useful. The ideas of Mark (1974), Changeux & Danchin (1976), Singer (1986) and Edelman & Reeke (1982) cover the fields of memory, brain development and artificial intelligence but all have the common tie of being selectionist theorists. A description of the psychological environment that accords with these views on development and learning was given by Gibson (1966). Here, again, there is a useful analogy with immunity. Perception of the chemical environment by the immune system is limited to those chemical configurations for which the organism already has
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recognizers (antigen recognition sites exist on various immune system cells). Thus, organisms have innate predispositions to recognize certain aspects of the chemical environment, and it is almost certain that this repertoire was shaped by natural selection. Gibson’s theory of visual perception takes a similar approach. The physical environment, according to Gibson, is perceived by an organism in terms of affordances. The concept of affordances succeeds in describing the environment in terms of recognition units for organisms’ perceptual systems. The immune system never really ‘sees’ a salmonella bacterium when it attacks it; it simply recognizes and responds to antigens which render the bacterium attackable by selected immune system antibodies. Antigens afford the possibility of response. Gibson’s perceptual affordances offer the possibility of behavioural responses. Certain ground textures afford, say, walkability or sinkability. Characteristics of objects afford, say, eatability or throwability. Gibson’s description of perception is selectionist. In his account, perceptual systems develop as organisms are selected for their ability to detect the affordances that the environment offers. Again, it is almost certain that the repertoire of affordances that the organisms perceive was shaped by a natural selection process. The epistemology of the selectionist theorists in both immunity and in intelligence/ cognition is an evolutionary epistemology. They follow the pattern of evolution by positing that states of affairs tend to be thrown up in profusion while those most appropriate are retained. In the field of artificial intelligence, Edelman is rare in using Darwinian theory as a starting point. His recognition automata have the following characteristics which make their intelligence more biological than artificial: their connectivity is set but experience alters preset connection strengths; there are networks which detect local features while others detect, simultaneously, global features; and re-entrant interactions between the two networks allow associative memory. Indeed, Edelman’s automaton would make as good an immune system as it would a visual recognition system. Conclusion
Perhaps one of the less helpful aspects of evolutionary epistemology is the appearance it gives as being a new movement. The bibliographies of Campbell show that selectionist thinking as applied to cognition is not new. Two important unresolved issues might be helped by the above discussion. First, it has been difficult to decide whether evolutionary epistemology is philosophy or science. Plotkin (1987) has reckoned that less than 10% of evolutionary epistemology published represents science. Second, the problem of what may legitimately be called knowledge remains. The development of ideas in adaptive immunity suggests that evolutionary epistemologists should look beyond cognition, culture and scientific progress, which occupy all their energies at present, for data to support their hypotheses. Processes which are simpler (adaptive enzyme formation in bacteria) or better understood (adaptive immunity) provide additional support for the evolutionary analogy and serve to make the links between somatic evolution and cognition appear less premature. Campbell’s (1974) opening shot succeeded in expanding the concept of ,knowledge well beyond that of central nervous system knowing. Resolution of the theoretical problems and the subsequent development of immunological knowledge should be seen as a success for evolutionary epistemology: an example of selectionist thinking that guided the outcome of a practical problem of adaptation to a novel environment.
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Acknowledgements The author thanks Dr Henry Plotkin, Dr John Stewart, Professor Jerre Levy and Mr Chris Brand for their helpful comments on earlier drafts of this article.
References Ada, G. L. & Nossal, Sir G. (1987). Sci. Am. 257, August, pp. 50-57. Burnet, Sir M. (1959). The Clonal Selection Theory of Acquired Immunity. Cambridge: Cambridge University Press. Burnet, Sir M. (1962). The Integrity of the Body. London: Oxford University Press. Burnet, Sir M. (1969). Cellular Immunology. Cambridge: Cambridge University Press. Burnet, Sir M. (1970). Immunological Surveillance. Oxford: Pergamon. Campbell, D. T. (1974). In (P. A. Schlipp, Ed.): The Philosophy of Karl Popper, vol. I. La Salle, Open Court. Changeux, J. P. & Danchin, A. (1976). Nature 264, 705-712. Edelman, G. M. & Reeke, G. N., Jr (1982). Proc. nut1 Acad. Sci. USA 79, 2091-2095. Gibson, J. J. (1966). The Senses Considered as Perceptual Systems. Boston: Houghton Mifflin. Hendrickson, D. E. & Hendrickson, A. E. (1980). Pers. indiv. 02% 1, l-33. Jerne, N. K. (1955). Proc. nut1 Acad. Sci. USA 41, 849. Jerne, N. K. (1985). Science 229, 1057-1059. Mark, R. (1974). Memory and Nerve Ceil Connections. Oxford: Oxford University Press. Minsky, M. (1977) In (P. N. Johnson-Laird & P. C. Wason, Ed.): Thinking: Readings in Cognitive Science. Cambridge: Cambridge University Press. Pauhng, L. (1940). J. Am. them. Sot. 26, 2643-2648. Plotkin, H. C. (1987). Biof. Phil. 2, 295-313. Plotkin, H. C. & Odling-Smee, F. J. (1981). Behav. Brain Sci. 4, 225-268. Popper, Sir K. R. (1975). In (R. Harre, Ed.): Problems of Scientific Revolution. Oxford: Oxford University Press. Singer, W. (1986). Eur. Arch, Psych. neurol. Sci. 236, 4-9.
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Applying evolutionary epistemology: from immunity to intelligence Ian J. Deary
Department of Psychology, University of Edinburgh, 7 George Square, Edinburgh EH8 9JZ, Scotland A formal description of the process of knowledge accretion has been accepted in three areas: somatic evolution, adaptive enzyme formation and adaptive immunity. Random variation followed by natural selection is the method by which all three processeslead to an organism’s increased fitness to its environment. This paper gives a detailed account of the discovery that adaptive immunity is better described in selectionist rather than instruction& terms. It is argued that, since other biological adaptation systemsare best described by an evolutionary epistemology, selectionist approaches to brain development and cognition are liable to be more helpful than instructionist accounts.
Introduction The problem of how organisms gain in knowledge and become better adapted to their
environment is central in psychology. A general theory which describes the structure of all knowledge-gain processes might appear over-ambitious, yet that is the purpose of the enterprise called evolutionary epistemology. Although the ideas which drive evolutionary epistemology are not new, it is generally accepted that the explicit beginning of the movement was Campbell’s 1974 paper (at that time, Campbell supplied a large bibliography acknowledging many precursors). The core ideas in evolutionary epistemology are: that evolution-even in its biological aspects-is a knowledge process: and that all knowledge-gain systems follow a random variation followed by natural selection process; and this is what is known as the evolutionary analogy. Critics of evolutionary epistemology have remarked that, while this might be a sticient outline for the process of somatic evolution, it fails to capture the processes of mental development, learning and scientific progress in man, let alone the development of culture. Nevertheless, there have been several attempts to develop an ‘evolutionary analogy’ in these areas (see, for example, Plotkin & Odling-Smee, 198 1) but, to date, evolutionary epistemology remains a philosophical or metapsychological rather than a scientific discipline. In this paper, I will describe how an evolutionary epistemological approach has led to success in advancing the understanding of one knowing system: adaptive immunity. The more general purpose .of the paper is to suggest that selectionist thinking will lead to the adoption of more promising approaches in understanding all aspects of animal cognition. We tend to use knowledge to refer to the primarily human, process of forming and storing regularities about the world. But, following Campbell, I will use knowledge 0140-1750/88/040399
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gain to refer to any change in an organism’s structure that leads to an improvement in adaptive fit to its niche at the time it comes about (it may be maladaptive later). This paper will focus on adaptive changes found in organisms over their own life-span. The problem of innate knowledge will not be addressed, although in Campbell’s scheme a genotype represents knowledge of the world and may be seen as the physical embodiment of what Popper has called ‘innate hypotheses’. [Again, the statement that a genome is knowledge might stretch the patience of some but, as a developing foetus forms muscles, red blood cells and eyes, it is difficult to deny that it knows about (or is hypothesizing the existence of) gravity, atmospheric composition and the existence of light reflecting and absorbing bodies in a transparent medium. That it does not consciously know these phenomena is of little concern, it comes into the world preadapted to certain aspects of a niche.] The rules and expectations provided by the genome cannot prepare the complex organism for all possible environmental challenges. For humans, the problem is particularly severe. The time lapse between birth and reproduction in humans ranges from about 16 to about 40 years. In other words, the human structure has to be maintained for this length of time in order that it may reproduce. The correlation between intergenerational time lapse and the complexity of the adaptive capacities may, therefore, be expected to be high. Unless an organism exists in a very isolated and rich niche with few competitors or predators, the ability to respond successfully to environmental challenges will be important for survival at least until the age of reproduction and care of the young. These challenges are anything that will affect adversely the integrity of the organism leading to reduced or absent reproductive or nurturing abilities. In fact, the main challenges are chemical (due to micro-organisms and toxins) and physical (due to predators, climate, accidents, etc). In response to these challenges, animals have developed adaptive immunity and, for want of a better term, intelligence, respectively. Just as intelligence deals with the physical and social environment, so does the immune system adapt to aspects of the chemical environment. It does this by surveying and perceiving aspects of the chemical environment; discriminating between self and not self; making appropriate effector responses to stimuli; and remembering or storing ‘percepts over many years in order to facilitate responses at a second or subsequent presentation of the same stimulus (i.e. it learns). I shall demonstrate that, by using a selectionist approach (i.e. the evolutionary analogy), immunologists were able to predict some of the rules of immune functioning. The analogy provided a description of adaptive immunity as a knowledge-gain process that excluded blind alleys in research and theory. If we take the lessons of this theoretical resolution in immunity into the area of cognition, we may save time and effort. Template theory in immunity From before 1940 until the 196Os, immunologists were, in effect, debating a problem of epistemology. The problem was that of adaptive immunity. Higher animals are able to manufacture circulating antibody that reacts specifically with certain micro-organisms or their products (or parts of either that serve as identifiers for the invaders and are refered to as antigens). The immunologists faced several problems: if the host organism has never met a particular antigen before, how does it recognize it as foreign? How does the recognition lead to antibody formation (and the effective elimination of the antigen)? And how does the host remember the antigen’s structure so that when it meets it on a subsequent occasion it is able to respond more quickly and with more antibodies than
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the first time? Clearly, it does not do violence to meaning to describe this as a problem of knowing. As a result of an environmental event, the organism has effected a specific response and retained a specific memory-this is a broad description of both adaptive immune and intelligent functioning. How is it done? At about the middle of the present century, there were two main theories. The earlier, and the one that held general sway until the 1960s was the ‘template’ theory. There was no single author of this theory, but it received its most complete exposition in the paper by Nobel laureate Linus Pauling (1940). Pauling became interested in how the immune system modelled antigen structure and posed the question, ‘. . . what is the simplest reasonable process of formation of such a molecule?’ Pauling’s answer was that, . . . the antigen causes the polypeptide chain to assume a configuration complementary to the antigen. The number of configurations accessibleto the polypeptide chain is so great as to provide an explanation of the ability of the animal to form antibodies with considerable specificity for an apparently unlimited number of different antigens (Pauling, 1940).
Intuitively, this appealed to many immunologists. There was agreement that what identified antigens was the ‘shape’ or configuration of their, primarily surface, determinants. Therefore, a system that existed to intercept, discriminate and respond to these shapes would do well to use the antigens as templates for the formation of a specific antibody response. There were two improbabilities of this ‘instructionist’ system that were not discussed. By supposing that the same globulin molecule could take on the shape of almost any antigen, Pauling was demanding that these proteins not only adopt many unstable configurations but that they also retain them when they leave the template. It is known that proteins tend to adopt a configuration of lowest energy that is relatively specific and is held together by many reversible bonds as well as some covalent disulphide linkages. The number of covalent bonds in any one protein the size of a globulin molecule would be incapable of adopting and retaining an indefinite number of specific shapes. Yet this is just what Pauling’s theory demanded: that the globulin was a tabula rasa, with no innate predisposition to any one shape, that could be modelled like clay upon antigen. Apart from the chemical improbability of such a proposal, the system also appears evolutionarily unlikely. What Pauling was suggesting was that, perhaps at a single step, evolution provided a single, open-ended and undirected modelling system for foreign antigens, a Royal Mint capable of manufacturing a die for any coin imaginable. If template theory was correct, it is hard to imagine the system being built in a piecemeal way. Since it hypothesized the existence of an uncommitted general capacity to mould antigens, it seemed to suggest that the whole structure was built, unlike Rome, in a day. Template theory was anthropomorphic: it reflected the way humans go about constructing factories but did not appear to resemble the blind progression of evolution. Moreover, this instructionist model required that the antigen be present for the manufacture of subsequent antibody, The antigen molecule, after its desertion by the newly-formed antibody molecule, may serveas the pattern for another . . (Pauling, 1940).
In this scheme, so-called immunological memory was not explained because the ‘instructor’ was eliminated by the antibody, thus removing the template for further production. In the most obvious way Pauling was suggesting that the immune system ‘wrapped its mind round the problem’. Some of the ideas did fit the experimental data at the time, but the driving force of the theory was an instructionist epistemology. There were other implications of template theory that were not noted at the time. If an antibody modelled
I. J. Deary the antigen why was this, by definition, novel shape not then treated as antigen and set upon by the immune system? It is known that the antibody of one animal may act as an antigen in another species, there is nothing protective about being an antibody per se, and Pauling’s theory could not explain why each new antibody did not then become an antigen in its own system. (It is interesting to note that if new antibody was formed using the original antibody as a template, it would have the shape of the original antigen and be attacked once more!) Clonal selection theory
The theory that challenged template theory had less intuitive force. It developed from an analogy with somatic evolution and adaptive enzyme formation in bacteria. Two Nobel laureates were involved in propagating what started as the ‘natural selection’ theory and was refined to become the ‘clonal selection’ theory of antibody formation. Jeme (1955) suggested that the role of antigen was not that of a template for antibody formation but that, Among the population of circulating globulin molecules there will, spontaneously, be fractions possessingaffinity toward any antigen to which the animal can respond. . . . The introduction of an antigen into the blood or into the lymph leads to the selectiveattachment to the antigen of those globulin molecules which happen to have a complementary configuration (Jerne, 1955).
Thus, animals happened to have, naturally,
the immense numbers of configurations
needed to fit most antigens. The evolutionary analogy was explicit: by generating, somehow, antigen recognizers of many different shapes spontaneously or randomly, the
best fit to the antigen would not have to be modelled but simply selected from the alternatives. Although Jerne got much of the subsequent detail wrong, his theoretical shift was able to explain the so far puzzling phenomena of booster effects, immunological memory and the relative importance of the antigens on the surface of an organism vs their internal antigens. The first two of these were unresolved anomalies in
template theory. The suggestions of Jerne were developed by Sir Macfarlane Burnet in a series of books and articles. Bumet, like Jerne, looked to the structure of biological change in somatic evolution and bacterial adaptive enzyme formation to inform his understanding of adaptive change in acquired immunity. Bumet’s (1959) introduction to the clonal selection theory of acquired immunity did not begin, as most texts would have done, with an account of the immune system’s cells or their origins but with a discussion of the way that bacteria adapt by producing novel enzymes to destroy, say, antibiotics. The explanations for the adaptive enzyme production included, again, instructionist and selectionist theories: either the bacterium formed a new enzyme after a genetic change that was brought on by the antibiotic; or a single bacterium, by chance, had developed the enzyme by a mutation (bacteria have high mutation rates and very short generation times) and was selectively retained as the non-enzyme producers were destroyed. The latter explanation was correct: bacteria got to ‘know’ about antibodies by the process of random change followed by natural selection. Burnet ended, These considerations of the processes of change in populations of bacteria and viruses were designed to act as an introduction to the discussion of clonal selection amongst the cells of the vertebrate organism, more specifically amongst human mesenchymal cells. Throughout, a single theme has been dominant-the potency of mutation and selectivesurvival to change the character of a population of cells to bring it into more appropriate relationship to its environment. The remainder of these lectures are concerned to show that this is as relevant to cell populatons within the mammalian body as to populations of viruses and bacteria (Bumet, 1959).
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Burnet’s message was that two knowledge processes had voted in favour of a Darwinian vs a Lamarckian mechanism, and he doubted whether this new problem of adaptation would be any different. Burnet reviewed theories with regard to two main problems in immunity: (1) how does the immune system discriminate between self and not self? (Either self is not attacked because it is recognized or not self is attacked because it is recognized. Either way, wrote Burnet, the body required a, ‘library of information to be stored’.) (2) How does immunity last a life time, and how do daughter cells carry the antibody production information of the parent cells (since immunological memory was far greater than the life-span of lymphocytes)? The template theory of HaurowitzPauling was explained, and a modification by Burnet & Fenner examined. In his modified template theory, Burnet had tried to solve the above problems using template ideas. The problem of self-recognition, the earlier Burnet had suggested, existed because there exist ‘self markers’. Further, a recognition unit was involved in antibody production to deflect the possibility of immune response to self. Of course, there was no empirical evidence for the existence of these structures except for the fact that the self was not attacked: the supposed answer was a restatement of the problem. The answer to the second problem was Lamarckian: immunological memory came about because a genocopy of the antigen was incorporated in the genome. It did not take long for Burnet to see the inelegance and theoretical poverty of his indirect template theory which, when tested against these problems in a rigorous way, was clearly incapable of dealing with many important empirical facts. Burnet called the self-marker/ recognition unit ideas ‘clumsy and ‘only a rough paraphrase of the actual mechanism’. In fact, they were only a rough paraphrase of the original question. Burnet then dealt with Jerne’s natural selection theory. After dealing with some errors of fact (for instance, Jerne’s mistaken guess that recognition sites for foreign antigens were on circulating gamma globulin molecules), Burnet drew the core idea.from Jerne’s theory, that the body had, . . a population comprising carriers of all the reactive sites needed to unite with any potential antigenic determinant except those already existing in accessiblecomponents of the body (Burnet, 1959). The insight of Jerne’s solved one more problem for template theories that was never stated explicitly. In template theory it was proposed that the immune system first recognized the foreignness of the antigen and then made a specific antibody to it, so that is would be recognized in the future. Thus, it required two recognition processes: one for foreignness and one for specificity. Two considerations make this scheme unlikely. First, antigens constitute a wide range of macromolecules, proteins and carbohydrates that have no single shared identifier. Second, many antigens are very similar in conformation to the host macromolecules. Thus, no one discriminator would do for foreignness. Many different discriminators were needed and, because some antigens were very like the host’s body surface markers, they would have to be very specific. The template theory then, when pushed, had to posit that, to make a template of an antigen, the host had to be able to recognize the antigen in a specific way in advance. Template theory was untenable in this form, which was essentially a form of selectionist theory. Burnet gave Jerne’s insight a firmer physical basis, . . . any tenable form of Jerne’s theory must involve the existence of multiple clones of globulin producing cellseach responsible for one genetically determined type of antibody globulin (Bumet, 1959). Burnet put the recognition sites for antigens on the surface of cells, and with this tweak of Jerne’s theory much fell into place. Here was a mini scientific revolution which
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was well documented only because a single man was driven by a belief in the broad applicability of Darwinian explanation. Yet, empirically there were no compelling reasons for immunologists to accept his clonal selection theory. He wrote, The reasons for temporarily or permanently discarding the ‘indirect template’ hypothesis in favour of the clonal selection approach were cumulative and largely indirect (Burnet, 1959).
Burnet listed five points that led to his theoretical switch. Three were experimental findings that had only a tenuous relation to the theories. Of the two most compelling reasons, one was an analogy and one was a theoretical point. First, adaptive enzyme
production by bacteria was known to be genetically determined and not a transcript of a pattern introduced by, say, an antibiotic. For Burnet, This destroyed the significance of any analogy between adaptive enzyme production and the indirect template hypothesis of antibody formation (Bumet, 1959).
He reckoned that if this adaptive change did not work in a template or instructionist fashion then, by reference to his Darwinist principles, it was unlikely that another should. If bacteria adapted by random variation and natural selection, then so, probably, did the immune system. Second, Burnet saw that his notion of self-markers was vacuous and dubbed the idea, ‘semi-mystical in character and generally unattractive’. For template theory, it was a case of theory immunization leading, eventually, to theory collapse. With the gradual acceptance of clonal selection theory, immune phenomena became more amenable to explanation. Self-tolerance was due to the elimination of selfrecognizing cells in early life. Bumet paused, though: in choosing a clonal selection hypothesis, he still had no proof that at some stage the antigen did not shape the antibody. As was shown above, the logic of this notion leads to unsolvable problems but Burnet had a more general reason to throw out any vestige of the template hypothesis: There seems no reason to engraft such a grossly Lamarckian qualification on what might be described as a strictly Darwinian process at the cellular level. .The theory differs from the standard interpretation of antibody production in replacing the concept that in one way or another the antigen actively enforces production of a new pattern of specific globulin, by the view that somatic mutation and selection within the mesenchymal cell populations can have the same overall effect (Burnet, 1959).
Burnet’s concluding theoretical remarks cleared much confusion. He was able to articulate the fact that, once an antibody was developed, the two theories differed very little: the key difference was an epistemological one, that of how the body came to be informed of the structure of a foreign antigen. Burnet’s book remains an unusual one in biology. He took concepts that had served well in other areas and offered them as a structure for resolving a debate in a new area. Further, he did it at a time when the majority of his profession held an opposing view. He produced no single piece of evidence that could decide between the two approaches, but Bumet did make a single specific prediction. He felt that clonal selection theory would be validated, . . . if it could be shown that cellsfrom a non-immune animal gave rise to clones, each cell of which under proper physiological conditions contained, or could liberate, antibody-type globulin of a single pattern. . . (Bumet, 1959).
The empirical research that led to the general acceptance of clonal selection theory is documented by two key workers in a recent article (Ada & Nossal, 1987). Bumet offered his approach to other biologists, Irrespective of what field we are considering, as the environment changes the natural population changes, and in the present state of our knowledge the changes are best understood in terms of mutation and selective survival (Bumet, 1959).
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The relationship between the knower and the known was no longer, in the field of immunity, thought to be, ‘something almost as definite as the relation between the pattern on the face of a coin and that on the die which stamped it’ (Bumet, 1962). A decade later (Burnet, 1969), the immunologists had accepted the clonal selection theory and investigated the problem of how the ‘vast repertoire of specific antibodies [can] . . . be produced more or less on demand’. As with any good new theory, it was able to ‘ . . . absorb in natural fashion the various concepts as they arose from the new experimental approaches. . . ‘. But it was neither this ability nor the unifying structure of Darwinian selection that swung most practioners round; it was empirical results such as the discovery that patients with the illness multiple myeloma were producing a great excess of a single immunoglobulin. The immune system, concluded Burnet, had all . . the elements of a Darwinian situation. . . The numbers of essentially autonomous genetic elements, the lymphoid cells, are large, perhaps around 10” in man, giving adequate opportunity for mutation, and the selective advantage of an accidentally appropriate pattern is enormous and extremely rapidly expressed (Burnet, 1959).
From immunity to intelligence If the Darwinian scheme of random variation followed by natural selection has informed thinking about adaptive fit (or knowing) in somatic evolution, bacterial adaptive enzyme production and adaptive immunity, there might be lessons for those working on those areas of knowing that apply to animal nervous systems. In the three systems that have been successfully described using selectionist thinking, one clear message is that organisms are not moulding responses to environmental information. Instead, knowing systems in nature tend to have a generator of alternatives that are selected by the environment for fitness. The extension of the insights in immunological adaptation have been applied to nervous system adaptation occasionally over the last 20 years. In 1970 Burnet offered that, The general structure of the central nervous system must be determinative but there are hundreds of situations in which large numbers of similar cells move to distribute themselves or their axons more or less uniformly over a defined region. Further, there is a great deal to suggest that the functional structure of a working brain is built up by something which may represent essentially a form of natural selection of circuits arising by random processes(Bumet, 1970). In this short quote, Burnet anticipated the key concepts of an evolutionary epistemology as applied to the nervous system. For instance, Plotkin & Odling-Smee’s (1981) selectionist multi-level hierarchy of knowing processes involves somatic evolution (Burnet’s general central nervous system structure), brain development (where Bumet anticipated the success of the now popular selective stabilization theories) and brain function (the process of learning and what we generally refer to as knowing). Jerne (1985), too, has devoted some attention to bringing immunological concepts to the problems of cognition. In a recent address, he used the example of the immune system explicitly as a knowing system and compared it with human language. Both immune and language capacities, said Jerne, were ‘complete’ or open-ended in their repertoire: i.e. the 10’ or so B lymphocytes, means that the immune system can respond, by the formation of specific antibodies, to any molecule existing in the world, including molecules that the system has never before encountered (Jerne, 1985).
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Jerne was impressed by the fact that most languages make do with 100,000 words or less, and that antibody variable regions (two per antibody molecule of about 100 amino acid residues confer the specificity for particular antigens) appear to function like sentences in a language, although the alphabet of the immune system is still unknown. Jerne remarked that Chomsky’s notion of a generative grammar works well as a description of adaptive immunity. Burnet and Jerne, then, may be seen as allies of Campbell in construing the problems of knowing as biological problems that should be guided by selectionist principles. Popper (1975), too, saw that the success of selectionist over template theory in immunity should be used as a guide to the structure of knowledge growth, I suggest therefore that we conceive the way scienceprogresses somewhat on the lines of Niels
Jerne’s and Sir Macfarlane Bumet’s theories of antibody formation. . The fundamental idea of Jerne was that the instruction or information which enables the antibody to recognise the antigen is, literally, inborn . these cells [antibody production cells] are selected with the help of the invading environment (that is, with the help of the antigen), rather than instructed (Popper, 1975).
Selectionist theories in intelligence
The main problem with sorting out the selectionist theories in brain function is that the brain is examined at many levels. There are theories that describe the process of development, at one level, and those that attempt to give an account of learning and memory. Nevertheless, there exist template and clonal selection theories at different levels of description. Two examples of template theory will suffice to draw a parallel with immunity. The theory of memory and intelligence devised by Hendrickson & Hendrickson (1980) proposed that, for every percept, an RNA molecule was constructed according to the pattern of electrical impulses invoked by the stimulus. Like Pauling’s theory, the notion was that the environment shaped a physical record in the organism. This theory was based on empirical evidence but, while subsequent findings concerning cell membrane receptors and ion channels have disproved the theory, its template nature indicated its non-viability earlier. Another template theory was the frame-system theory of Minsky (1977). Minsky’s account of perception demanded that a very general, uncommitted capacity existed to construct frames for any set of percepts. Here, again, the emphasis was on the malleable organism with a nervous system that was able to model the environment. A more selectionist account of perception would ask questions such as: is there evidence of early over-connection in nervous systems? What elements of the environment are perceived by organisms? And is there evidence for the selection of useful connections in brain development and learning? There is a growing body of opinion which conceptualizes brain development and memory formation within a similar framework; i.e. the formation of excess connections and the later selection or selective stabilization of those units that are useful. The ideas of Mark (1974), Changeux & Danchin (1976), Singer (1986) and Edelman & Reeke (1982) cover the fields of memory, brain development and artificial intelligence but all have the common tie of being selectionist theorists. A description of the psychological environment that accords with these views on development and learning was given by Gibson (1966). Here, again, there is a useful analogy with immunity. Perception of the chemical environment by the immune system is limited to those chemical configurations for which the organism already has
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recognizers (antigen recognition sites exist on various immune system cells). Thus, organisms have innate predispositions to recognize certain aspects of the chemical environment, and it is almost certain that this repertoire was shaped by natural selection. Gibson’s theory of visual perception takes a similar approach. The physical environment, according to Gibson, is perceived by an organism in terms of affordances. The concept of affordances succeeds in describing the environment in terms of recognition units for organisms’ perceptual systems. The immune system never really ‘sees’ a salmonella bacterium when it attacks it; it simply recognizes and responds to antigens which render the bacterium attackable by selected immune system antibodies. Antigens afford the possibility of response. Gibson’s perceptual affordances offer the possibility of behavioural responses. Certain ground textures afford, say, walkability or sinkability. Characteristics of objects afford, say, eatability or throwability. Gibson’s description of perception is selectionist. In his account, perceptual systems develop as organisms are selected for their ability to detect the affordances that the environment offers. Again, it is almost certain that the repertoire of affordances that the organisms perceive was shaped by a natural selection process. The epistemology of the selectionist theorists in both immunity and in intelligence/ cognition is an evolutionary epistemology. They follow the pattern of evolution by positing that states of affairs tend to be thrown up in profusion while those most appropriate are retained. In the field of artificial intelligence, Edelman is rare in using Darwinian theory as a starting point. His recognition automata have the following characteristics which make their intelligence more biological than artificial: their connectivity is set but experience alters preset connection strengths; there are networks which detect local features while others detect, simultaneously, global features; and re-entrant interactions between the two networks allow associative memory. Indeed, Edelman’s automaton would make as good an immune system as it would a visual recognition system. Conclusion
Perhaps one of the less helpful aspects of evolutionary epistemology is the appearance it gives as being a new movement. The bibliographies of Campbell show that selectionist thinking as applied to cognition is not new. Two important unresolved issues might be helped by the above discussion. First, it has been difficult to decide whether evolutionary epistemology is philosophy or science. Plotkin (1987) has reckoned that less than 10% of evolutionary epistemology published represents science. Second, the problem of what may legitimately be called knowledge remains. The development of ideas in adaptive immunity suggests that evolutionary epistemologists should look beyond cognition, culture and scientific progress, which occupy all their energies at present, for data to support their hypotheses. Processes which are simpler (adaptive enzyme formation in bacteria) or better understood (adaptive immunity) provide additional support for the evolutionary analogy and serve to make the links between somatic evolution and cognition appear less premature. Campbell’s (1974) opening shot succeeded in expanding the concept of ,knowledge well beyond that of central nervous system knowing. Resolution of the theoretical problems and the subsequent development of immunological knowledge should be seen as a success for evolutionary epistemology: an example of selectionist thinking that guided the outcome of a practical problem of adaptation to a novel environment.
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Acknowledgements The author thanks Dr Henry Plotkin, Dr John Stewart, Professor Jerre Levy and Mr Chris Brand for their helpful comments on earlier drafts of this article.
References Ada, G. L. & Nossal, Sir G. (1987). Sci. Am. 257, August, pp. 50-57. Burnet, Sir M. (1959). The Clonal Selection Theory of Acquired Immunity. Cambridge: Cambridge University Press. Burnet, Sir M. (1962). The Integrity of the Body. London: Oxford University Press. Burnet, Sir M. (1969). Cellular Immunology. Cambridge: Cambridge University Press. Burnet, Sir M. (1970). Immunological Surveillance. Oxford: Pergamon. Campbell, D. T. (1974). In (P. A. Schlipp, Ed.): The Philosophy of Karl Popper, vol. I. La Salle, Open Court. Changeux, J. P. & Danchin, A. (1976). Nature 264, 705-712. Edelman, G. M. & Reeke, G. N., Jr (1982). Proc. nut1 Acad. Sci. USA 79, 2091-2095. Gibson, J. J. (1966). The Senses Considered as Perceptual Systems. Boston: Houghton Mifflin. Hendrickson, D. E. & Hendrickson, A. E. (1980). Pers. indiv. 02% 1, l-33. Jerne, N. K. (1955). Proc. nut1 Acad. Sci. USA 41, 849. Jerne, N. K. (1985). Science 229, 1057-1059. Mark, R. (1974). Memory and Nerve Ceil Connections. Oxford: Oxford University Press. Minsky, M. (1977) In (P. N. Johnson-Laird & P. C. Wason, Ed.): Thinking: Readings in Cognitive Science. Cambridge: Cambridge University Press. Pauhng, L. (1940). J. Am. them. Sot. 26, 2643-2648. Plotkin, H. C. (1987). Biof. Phil. 2, 295-313. Plotkin, H. C. & Odling-Smee, F. J. (1981). Behav. Brain Sci. 4, 225-268. Popper, Sir K. R. (1975). In (R. Harre, Ed.): Problems of Scientific Revolution. Oxford: Oxford University Press. Singer, W. (1986). Eur. Arch, Psych. neurol. Sci. 236, 4-9.