Before we consider the impact of the double bind hypothesis upon genetics and evolutionary theory, it is necessary to examine the relationship between theories of
94 C. L. Hull, et al., Mathematico-deductive Theory of Rote Learning: A Study in Scientific Methodology, (Yale University Institute of Human Relations), New Haven, Yale University Press, 1940; also H. F. Harlow, "The Formation of Learning Sets," Psychol. Review, 1949, 56: 51-65.
learning and these two other bodies of knowledge. I referred earlier to the three subjects together as a triad. The structure of this triad we must now consider.
Genetics, which covers the communicational phenomena of variation, differentiation, growth, and heredity, is commonly recognized as the very stuff of which evolutionary theory is made. The Darwinian theory, when purged of Lamarckian ideas, consisted of a genetics in which variation was presumed to be random, combined with a theory of natural selection would impart adaptive direction to the accumulation of changes. But the relation between learning and this theory has been a matter of violent controversy which has raged over the so-called "inheritance of acquired characteristics."
Darwin's position was acutely challenged by Samuel Butler, who argued that heredity should be compared with—even identified with—memory. Butler proceeded from this premise to argue that the processes of evolutionary change, and especially adaptation, should be regarded as the achievements of a deep cunning in the ongoing flow of life, not as fortuitous bonuses conferred by luck. He drew a close analogy between the phenomena of invention and the phenomena of evolutionary adaptation, and was perhaps the first to point out the existence of residual organs in machines. The curious homology whereby the engine is located in the front of an automobile, where the horse used to be, would have delighted him. He also argued very cogently that there is a process whereby the newer inventions of adaptive behavior are sunk deeper into the biological system of the organism. From planned and conscious actions they become habits, and the habits become less and less conscious and less and less subject to voluntary control. He assumed, with-out evidence, that this habitualization, or sinking process, could go so deep as to contribute to the body of memories, which we would call the genotype, and which determine the characteristics of the next generation.
The controversy about the inheritance of acquired characteristics has two facets. On the one hand, it appears to be an argument which could be settled by factual material. One good case of such inheritance might settle the matter for the Lamarckian side. But the case against such inheritance, being negative, can never be proved by evidence and must rely upon an appeal to theory. Usually those who take the negative view argue from the separation between germ plasm and somatic tissue, urging that there can be no systematic communication from the soma to the germ plasm in the light of which the genotype might revise itself.
The difficulty looks like this: conceivably a biceps muscle modified by use or disuse might secrete specific metabolites into the circulation, and these might conceivably serve as chemical messengers from muscle to gonad. But (a) it is difficult to believe that the chemistry of biceps is so different from that of, say, triceps that the message could be specific, and (b) it is difficult to believe that the gonad tissue could be equipped to be appropriately affected by such messages. After all, the receiver of any message must know the code of the sender, so that if the germ cells are able to receive the messages from the somatic tissue, they must already be carrying some version of the somatic code. The directions which evolutionary change could take with the aid of such messages from the soma would have to be prefigured in the germ plasm.
The case against the inheritance of acquired characteristics thus rests upon a separation, and the difference between the schools of thought crystallizes around philosophic reactions to such a separation. Those who are willing to think of the world as organized upon multiple and separable principles will accept the notion that somatic changes induced by environment may be covered by an explanation which could be totally separate from the explanation of evolutionary change. But those who prefer to see a unity in nature will hope that these two bodies of explanation can somehow be interrelated.
Moreover, the whole relationship between learning and evolution has undergone a curious change since the days when Butler maintained that evolution was a matter of cunning rather than luck, and the change which has taken place is certainly one which neither Darwin nor Butler could have foreseen. What. has happened is that many theorists now assume learning to be fundamentally a stochastic or probabilistic affair, and indeed, apart from nonparsimonious theories which would postulate some entelechy at the console of the mind, the stochastic approach is perhaps the only organized theory of the nature of learning. The notion is that random changes occur, in the brain or else-where, and that the results of such random change are selected for survival by processes of reinforcement and extinction. In basic theory, creative thought has come to resemble the evolutionary process in its fundamentally stochastic nature. Reinforcement is seen as giving direction to the accumulation of random changes of the neural system, just as natural selection is seen as giving direction to the accumulation of random changes of variation.
In both the theory of evolution and the theory of learning, however, the word "random" is conspicuously undefined, and the word is not an easy one to define. In both fields, it is assumed that while change may be dependent upon probabilistic phenomena, the probability of a given change is determined by something different from probability. Underlying both the stochastic theory of evolution and that of learning, there are unstated theories regarding the determinants of the probabilities in question.95 If, however, we ask about change in these determinants, we shall again be given stochastic answers, so that the word "random," up-on which all of these explanations turn, appears to be a word whose meaning is hierarchically structured, like the meaning of the word "learning," which was discussed in the first part of this lecture.
Lastly, the question of the evolutionary function of acquired characteristics has been reopened by Waddington's work on phenocopies in Drosophila. At the very least, this work indicates that the changes of phenotype which can be achieved by the organism under environmental stress are a very important part of the machinery by which the species or hereditary line maintains its place in a stressful and competitive environment, pending the later appearance of some mutation or other genetic change which may make the species or line better able to deal with the ongoing stress. In this sense at least, the acquired characteristics have important evolutionary function. However, the actual experimental story indicates something more than this and is worth reproducing briefly.
What Waddington works with is a phenocopy of the phenotype brought about by the gene bithorax. This gene has very profound effects upon the adult phenotype. In its presence the third segment of the thorax is modified to resemble the second, and the little balancing organs, or halteres, on this third segment become wings. The result is a four-winged fly. This four-winged characteristic can be produced
95 In this sense, of course, all the theories of change assume that the next change is in some degree prefigured in the system which is to undergo that change.
artificially in flies which do not carry the gene bithorax by subjecting the pupae to a period of intoxication with ethyl ether. Waddington works with large populations of Drosophila flies derived from a wild strain believed to be free of the gene bithorax. He subjects the pupae of this population in successive generations to the ether treatment, and from the resulting adults selects for breeding those which show the best approximation to bithorax. He has continued this experiment over many generations, and already in the twenty-seventh generation he finds that the bithorax appearance is achieved by a limited number of flies whose pupae were withdrawn from the experimental treatment and not subjected to ether. Upon breeding from these, it turns out that their bithorax appearance is not due to the presence of the specific gene, bithorax, but is due to a constellation of genes which work together to give this effect.
These very striking results can be read in various ways. We can say that in selecting the best phenocopies, Wadding-ton was in fact selecting for a genetic potentiality for achieving this phenotype. Or we can say that he was selecting to reduce the threshold of ether stress necessary to produce this result.
Let me suggest a possible model for the description of these phenomena. Let us suppose that the acquired characteristic is achieved by some process of fundamentally stochastic nature—perhaps some sort of somatic learning—and the mere fact that Waddington is able to select the "best" phenocopies would lend support to this assumption. Now, it is evident that any such process is, in the nature of the case, wasteful. To achieve a result by trial and error which could have been achieved in any more direct way necessarily consumes time and effort in some sense of these words. Insofar as we think of adaptability as achieved by stochastic process, we let in the notion of an economics of adaptability.
In the field of mental process, we are very familiar with this sort of economics, and in fact a major and necessary saving is achieved by the familiar process of habit formation. We may, in the first instance, solve a given problem by trial and error; but when similar problems recur later, we tend to deal with them more and more economically by taking them out of the range of stochastic operation and handing over the solutions to a deeper and less flexible mechanism, which we call "habit." It is, therefore, perfectly conceivable that some analogous phenomenon may obtain in regard to the production of bithorax characteristics. It may be more economical to produce these by the rigid mechanism of genetic determination rather than by the more wasteful, more flexible (and perhaps less predictable) method of somatic change.
This would mean that in Waddington's population of flies there would be a selective benefit for any hereditary line of flies which might contain appropriate genes for the whole—or for some part—of the bithorax phenotype. It is also possible that such flies would have an extra advantage in that their somatic adaptive machinery might then be available for dealing with stresses of other kinds. It would appear that in learning, when the solution of the given problem has been passed on to habit, the stochastic or exploratory mechanisms are set free for the solution of other problems, and it is quite conceivable that a similar advantage is achieved by passing on the business of determining a somatic characteristic to the gene-script96
96 These considerations alter somewhat the old problem of the evolutionary effect of use and disuse. Orthodox theory could only suggest that a mutation reducing the (potential) size of a disused organ had survival value in terms of the resulting economy of tissue. The present theory
It may be noted that such a model would be characterized by two stochastic mechanisms: first, the more superficial mechanism by which the changes are achieved at the somatic level, and, second, the stochastic mechanism of mutation (or the shuffling of gene constellations) at the chromosomal level. These two stochastic systems will, in the long run under selective conditions, be compelled to work together, even though no message can pass from the more superficial somatic system to the germ plasm. Samuel Butler's hunch that something like "habit" might be crucial in evolution was perhaps not too wide of the mark.
With this introduction we can now proceed to look at the problems which a double bind theory of schizophrenia would pose for the geneticist.
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