The Role of Somatic Change in Evolution

All theories of biological evolution depend upon at least three sorts of change: (a) change of genotype, either by mutation or by redistribution of genes; (b) somatic change under pressure of environment; and (c) changes in environmental conditions. The problem for the evolutionist is to build a theory combining these types of change into an ongoing process which, under natural selection, will account for the phenomena of adaptation and phylogeny.

Certain conventional premises may be selected to govern such theory building: (a) The theory shall not depend upon Lamarckian inheritance. August Weismann's argument for this premise still stands. There is no reason to believe that either somatic change or changes in environment can, in principle, call (by physiological communication) for appropriate genotypic change. Indeed, the little that we know about communication within the multicellular140 individual indicates that such communication from soma to gene script is likely to be rare and unlikely to be adaptive in effect. However, it is appropriate to attempt to spell out in this essay what this premise implies:

Whenever some characteristic of an organism is modifiable under measurable environmental impact or under measurable impact of internal physiology, it is possible to write an equation in which the value of the characteristic in question is expressed as some function of the value of the impacting circumstance. "Human skin color is some function of exposure to sunlight," "respiration rate is some function of atmospheric pressure," etc. Such equations are constructed to be true for a variety of particular observations, and necessarily contain subsidiary propositions which are stable (i.e., continue to be true) over a wide range of values of impacting circumstance and somatic characteristic. These subsidiary propositions are of different logical type from the original observations in the laboratory and are, in fact, descriptive not of the data but of our equations. They are statements about the form of the particular equation and about the values of the parameters mentioned within it.

It would be simple, at this point, to draw the line between genotype and phenotype by saying that the forms and parameters of such equations are provided by genes, while the impacts of environment, etc. determine the actual event within this frame. This would amount to saying, e.g., that the ability to tan is genotypically determined, while the amount of tanning in a particular case depends upon exposure to sun-light.

In terms of this oversimplified approach to the overlapping roles of genotype and environment, the proposition excluding Lamarckian inheritance would read

* This essay appeared in the journal Evolution, Vol 17, 1963, and is reprinted with the editor's permission.

140 The problems of bacterial genetics are here deliberately excluded.

somewhat as follows: In the attempt to explain evolutionary process, there shall be no assumption that the achievement of a particular value of some variable under particular circumstances will affect, in the gametes produced by that individual, the form or parameters of the functional equation governing the relationship between that variable and its environmental circumstances.

Such a view is oversimplified, and parentheses must be added to deal with more complex and extreme cases. First, it is important to recognize that the organism, considered as a communicational system, may itself operate at multiple levels of logical typing; i.e., that there will be instances in which what were above called "parameters" are subject to change. The individual organism might as a result of "training" change its ability to develop a tan under sunlight. And this type of change is certainly of very great importance in the field of animal behavior, where "learning to learn" can never be ignored.

Second, the oversimplified view must be elaborated to cover negative effects. An environmental circumstance may have such impact upon an organism unable to adapt to it, that the individual in question will in fact produce no gametes.

Third, it is expectable that some of the parameters in one equation may be subject to change under impact from some environmental or physiologic circumstance other than the circumstance mentioned in that equation.

Be all that as it may, both Weismann's objection to Lamarckian theory and my own attempt to spell the matter out share a certain parsimony: an assumption that the principles which order phenomena shall not themselves be supposed changed by those phenomena which they order. William of Occam's razor might be reformulated: in any explanation, logical types shall not be multiplied beyond necessity.

(b) Somatic change is absolutely necessary for survival. Any change of environment which requires adaptive change in the species will be lethal unless, by somatic change, the organisms (or some of them) are able to weather out a period of unpredictable duration, until either appropriate genotypic change occurs (whether by mutation or by redistribution of genes already available in the population), or because the environment returns to the previous normal. The premise is truistical, regardless of the magnitude of the time span involved.

(c) Somatic change is also necessary to cope with any changes of genotype which might aid the organism in its external struggle with the environment. The individual organism is a complex organization of interdependent parts. A mutational or other genotypic change in any one of these (however externally valuable in terms of survival) is certain to require change in many others—which changes will probably not be specified or implicit in the single mutational change of the genes. A hypothetical pregiraffe, which had the luck to carry a mutant gene "long neck," would have to adjust to this change by complex modifications of the heart and circulatory system. These collateral adjustments would have to be achieved at the somatic level. Only those pregiraffes which are (genotypically) capable of these somatic modifications would survive.

(d) In this essay, it is assumed that the corpus of genotypic messages is preponderantly digital in nature. In contrast, the soma is seen as a working system in which the genotypic recipes are tried out. Should it transpire that the genotypic corpus is also in some degree analogic — a working model of the soma—premise c (above) would be negated to that degree. It would then be conceivable.that the mutant gene "long neck" might modify the message of those genes which affect the development of the heart. It is, of course, known that genes may have pleiotropic effect, but these phenomena are relevant in the present connection only if it can be shown, e.g., that the effect of gene A upon the phenotype and its effect upon the phenotypic expression of gene B are mutually appropriate in the overall integration and adaptation of the organism.

These considerations lead to a classifying of both genotypic and environmental changes in terms of the price which they exact of the flexibility of the somatic system. A lethal change in either environment or genotype is simply one which demands somatic modifications which the organism cannot achieve.

But the somatic price of a given change must depend, not absolutely upon the change in question, but upon the range of somatic flexibility available to the organism at the given time. This range, in turn, will depend upon how much of the organism's somatic flexibility is already being used up in adjusting to other mutations or environmental changes. We face an economics of flexibility which, like any other economics, will become determinative for the course of evolution if and only if the organism is operating close to the limits set by this economics.

However, this economics of somatic flexibility will differ in one important respect from the more familiar economics of money or available energy. In these latter, each new expenditure can simply be added to the preceding expenditures and the economics becomes coercive when the additive total approaches the limit of the budget. In contrast, the combined effect of multiple changes, each of which exacts a price in the soma, will be multiplicative. This point may be stated as follows: Let S be the finite set of all possible living states of the organism. Within S, let s1 be the smaller set of all states compatible with a given mutation (ml), and let s2 be the set of states compatible with a second mutation (mz). It follows that the two mutations in combination will limit the organism to the logical product of s1 and s2, i.e., to that usually smaller subset of states which is composed only of members common to both s1 and s2. In this way each successive mutation (or other genotypic change) will fractionate the possibilities for the somatic adjustment of the organism. And, should the one mutation require some somatic change, the exact opposite of a change required by the other, the possibilities for somatic adjustment may immediately be reduced to zero.

The same argument must surely apply to multiple environmental changes which demand somatic adjustments; and this will be true even of those changes in environment which might seem to benefit the organism. An improvement in diet, for example, will exclude from the organism's range of somatic adjustments those patterns of growth which we would call "stunted" and which might be required to meet some other exigency of the environment.

From these considerations it follows that if evolution proceeded in accordance with conventional theory, its process would be blocked. The finite nature of somatic change indicates that no ongoing process of evolution can result only from successive externally adaptive genotypic changes since these must, in combination, become lethal, demanding combinations of internal somatic adjustments of which the soma is incapable.

We turn therefore to a consideration of other classes of genotypic change. What is required to give a balanced "theory of evolution is the occurrence of genotypic changes which shall increase the available range of somatic flexibility. When the internal organization of the organisms of a species has been limited by environmental or mutational pressure to some narrow subset of the total range of living states, further evolutionary progress will require some sort of genotypic change which will compensate for this limitation.

We note first that while the results of genotypic change are irreversible within the life of the individual organism, the opposite is usually true of changes which are achieved at the somatic level. When the latter are produced in response to special environmental conditions, a return of the environment to the previous norm is usually followed by a diminution or loss of the characteristic. (We may reasonably expect that the same would be true of those somatic adjustments which must accompany an externally adaptive mutation but, of course, it is impossible in this case to remove from the individual the impact of the mutational change.)

A further point regarding these reversible somatic changes is of special interest. Among higher organisms it is not unusual to find that there is what we may call a "defense in depth" against environmental demands. If a man is moved from sea level to 10,000 feet, he may begin to pant and his heart may race. But these first changes are swiftly reversible: if he descends the same day, they will disappear immediately. If, however, he remains at the high altitude, a second line of defense appears. He will become slowly acclimated as a result of complex physiological changes. His heart will cease to race, and he will no longer pant unless he undertakes some special exertion. If now he returns to sea level, the characteristics of the second line of defense will disappear rather slowly and he may even experience some discomfort.

From the point of view of an economics of somatic flexibility, the first effect of high altitude is to reduce the organism to a limited set of states (si) characterized by the racing of the heart and the panting. The man can still survive, but only as a comparatively inflexible creature. The later acclimation has precisely this value: it corrects for the loss of flexibility. After the man is acclimated he can use his panting mechanisms to adjust to other emergencies which might otherwise be lethal.

A similar "defense in depth" is clearly recognizable in the field of behavior. When we encounter a new problem for the first time, we deal with it either by trial and error or possibly by insight. Later, and more or less gradually, we form the "habit" of acting in the way which earlier experience rewarded. To continue to use insight or trial and error upon this class of problem would be wasteful. These mechanisms can now be saved for other problems. 141

Both in acclimation and in habit formation the economy of flexibility is achieved by substituting a deeper and more enduring change for a more superficial and more reversible one. In the terms used above in discussing the anti-Lamarckian premise, a change has occurred in the parameters of the functional equation linking rate of respiration to external atmospheric pressure. Here it seems that the organism is behaving as we may expect any ultrastable system to behave. Ashby142 has shown that it is a general formal characteristic of such systems that those circuits con-trolling the more rapidly fluctuating variables act as balancing mechanisms to protect the

141 Bateson, "Minimal Requirements for a Theory of Schizophrenia," A.M.A. Archives of General Psychiatry, 1960, 2: 447.

142 W. R. Ashby, "The Effect of Controls on Stability," Nature, 1945, 155: 242; also Ashby, Design for a Brain, New York, John Wiley & Co., 1952.

ongoing constancy of those variables in which change is normally slow and of small amplitude; and that any interference which fixes the values of the changeful variables must have a disturbing effect upon the constancy of the normally steady components of the system. For the man who must constantly pant at high altitudes, the respiration rate can no longer be used as a changeable quantity in the maintaining of physiological balance. Conversely, if the respiration rate is to become avail-able again as a rapidly fluctuating variable, some change must occur among the more stable components of the system. Such a change will, in the nature of the case, be achieved comparatively slowly and be comparatively irreversible.

Even acclimation and habit formation are, however, still reversible within the life of the individual, and this very reversibility indicates a lack of communicational economy in these adaptive mechanisms. Reversibility implies that the changed value of some variable is achieved by means of homeostatic, error-activated circuits. There must be a means of detecting an undesirable or threatening change in some variable, and there must be a train of cause and effect whereby corrective action is initiated. Moreover, this entire circuit must, in some degree, be available for this purpose for the entire time during which the reversible change is maintained—a considerable using up of available message pathways.

The matter of communicational economics becomes still more serious when we note that the homeostatic circuits of an organism are not separate but complexly interlocked, e.g., hormonal messengers which play a part in the homeostatic control of organ A will also affect the states of organs B, C, and D. Any special ongoing loading of the circuit controlling A will therefore diminish the organism's freedom to control B, C, and D.

In contrast, the changes brought about by mutation or other genotypic change are presumably of a totally different nature. Every cell contains a copy of the new genotypic corpus and therefore will (when appropriate) behave in the changed manner, without any change in the messages which it receives from surrounding tissues or organs. If the hypothetical pregiraffes carrying the mutant gene "long neck" could also get the gene "big heart," their hearts would be enlarged without the necessity of using the homeostatic pathways of the body to achieve and maintain this enlargement. Such a mutation will have survival value not be-cause it enables the pregiraffe to supply its elevated head with sufficient blood, since this was already achieved by somatic change but because it increases the overall flexibility of the organism, enabling it to survive other demands which may be placed upon it either by environmental or, genotypic change.

It appears, then, that the process of biological evolution could be continuous if there were a class of mutations or other genotypic changes which would simulate Lamarckian inheritance. The function of these changes would be to achieve by genotypic flat those characteristics which the organism at the given time is already achieving by the uneconomical method of somatic change. Such a hypothesis, I believe, conflicts in no way with conventional theories of genetics and natural selection. It does, however, somewhat alter the current conventional picture of evolution as a whole, though related ideas were put forward over sixty years ago. Baldwin143 suggested that we consider not only the operation of the external environment in natural selection but also what he called "organic selection" in which

143 J. M. Baldwin, "Organic Selection," Science, 1897, 5: 634.

the fate of a given variation would depend upon its physiologic viability. In the same article, Baldwin attributes to Lloyd Morgan the suggestion that there might exist "coincident variations" which would simulate Lamarckian inheritance (the so-called "Baldwin effect").

According to such a hypothesis, genotypic change in an organism becomes comparable to legislative change in a society. The wise legislator will only rarely initiate a new rule of behavior; more usually he will confine himself to affirming in law that which has already become the custom of the people. An innovative rule can be introduced only at the price of activating and perhaps overloading a large number of homeostatic circuits in the society.

It is interesting to ask how a hypothetical process of evolution would work if Lamarckian inheritance were the rule, i.e., if characteristics achieved by somatic homeostasis were inherited. The answer is simple: it would not work, for the following reasons:

(1) The question turns upon the concept of economy in the use of homeostatic circuits, and it would be the reverse of economical to fix by genotypic change all the variables which accompany a given desirable and homeostatically achieved characteristic. Every such characteristic is achieved by ancillary homeostatic changes all around the circuits, and it is most undesirable that these ancillary changes should be fixed by inheritance, as would logically happen according to any theory involving an indiscriminate Lamarckian inheritance. Those who would defend a Lamarckian theory must be prepared to suggest how in the genotype an appropriate selection can be achieved. Without such a selection, the inheritance of acquired characteristics would merely in-crease the proportion of nonviable genotypic changes.

(2) Lamarckian inheritance would disturb the relative timing of the processes upon which evolution must—according to the present hypothesis — depend. It is essential that there be a time lag between the uneconomical but reversible somatic achievement of a given characteristic and the economical but more enduring alterations of the genotype. If we look upon every soma as a working model which can be modified in various ways in the workshop, it is clear that sufficient but not infinite time must be given for these workshop trials before the results of these trials are incorporated into the final blueprint for mass production. This delay is provided by the indirection of stochastic process. It would be unduly shortened by Lamarckian inheritance.

The principle involved here is general and by no means trivial. It obtains in all homeostatic systems in which a given effect can be brought about by means of a homeostatic circuit, which circuit can, in turn, be modified in its characteristics by some- higher system of control. In all such systems (ranging from the house thermostat to systems of government and administration) it is important that the higher system of control lag behind the event sequences in the peripheral homeostatic circuit.

In evolution two control systems are present: the homeostases of the body which deal with tolerable internal stress, and the action of natural selection upon the (genetically) nonviable members of the population. From an engineering point of view, the problem is to limit communication from the lower, reversible somatic system to the higher irreversible genotypic system.

Another aspect of the proposed hypothesis about which we can only speculate is the probable relative frequency of the two classes of genotypic change: those which initiate something new and those which affirm some homeostatically achieved characteristic. In the Metazoa and multicellular plants, we face complex networks of multiple interlocking homeostatic circuits, and any given mutation or gene recombination which initiates change will probably require very various and multiple somatic characteristics to be achieved by homeostasis. The hypothetical pregiraffe with the mutant gene "long neck" will need to modify not only its heart and circulatory system but also perhaps its semicircular canals, its intervertebral discs, its postural reflexes, the ratio of length and thickness of many muscles, its evasive tactics vis-a-vis predators, etc. This suggests that in such complex organisms, the merely affirmative genotypic changes must far outnumber those which initiate change, if the species is to avoid that cul-de-sac in which the flexibility of the soma approaches zero.

Conversely, this picture suggests that most organisms, at any given time, are probably in such a state that there are multiple possibilities for affirmative genotypic change. If, as seems probable, both mutation and gene redistribution are in some sense random phenomena, at least the chances are considerable that one or other of these multiple possibilities will be met.

Finally, it is appropriate to discuss what evidence is avail-able or might be sought to support or disprove such a hypothesis. It is clear at the outset that such a testing will be difficult. The affirmative mutations upon which the hypothesis depends will usually be invisible. From among the many members of a population which are achieving a given adjustment to environmental circumstances by somatic change, it will not be possible immediately to pick out those few in which the same adjustment is provided by the genotypic method. In such a case, the genotypically changed individuals will have to be identified by breeding and raising the offspring under more normal conditions.

A still greater difficulty arises in cases where we would investigate those homeostatically acquired characteristics which are achieved in response to some innovative genotypic change. It will often be impossible, by mere inspection of the organism, to tell which of its characteristics are the primary results of genotypic change and which are secondary somatic adjustments to these. In the imaginary case of the pregiraffe with a somewhat elongated neck and an enlarged heart, it may be easy to guess that the modification of the neck is genotypic while that of the heart is somatic. But all such guesses will depend upon the very imperfect present knowledge of what an organism can achieve in way of somatic adjustment.

It is a major tragedy that the Lamarckian controversy has deflected the attention of geneticists away from the phenomenon of somatic adaptability. After all, the mechanisms, thresholds, and maxima of individual phenotypic change under stress must surely be genotypically determined.

Another difficulty, of rather similar nature, arises at the population level, where we encounter another "economics" of potential change, theoretically distinguishable from that which operates within the individual. The population of a wild species is today conventionally regarded as genotypically heterogeneous in spite of the high degree of superficial resemblance between the individual phenotypes. Such a population expectably functions as a storehouse of genotypic possibilities. The economic aspect of this storehouse of possibilities has, for example, been stressed by

Simmonds.144 He points out that farmers and breeders who demand 100 per cent phenotypic uniformity in a highly select crop are in fact throwing away most of the multiple genetic possibilities accumulated through hundreds of generations in the wild population. From this Simmonds argues that there is urgent need for institutions which shall "conserve" this storehouse of variability by maintaining unselected populations.

Lerner145 has argued that self-corrective or buffering mechanisms operate to hold constant the composition of these mixtures of wild genotypes and to resist the effects of artificial selection. There is therefore at least a presumption that this economics of variability within the population will turn out to be of the multiplicative kind.

Now, the difficulty of discriminating between a characteristic achieved by somatic homeostasis and the same characteristic achieved (more economically) by a genotypic short cut is clearly going to be compounded when we come to consider populations instead of physiologic individuals. All actual experimentation in the field will inevitably work with populations, and, in this work, it will be necessary to discriminate the effects of that economics of flexibility which operates inside the individuals from the effects of the economics of variability which operates at the population level. These two orders of economics may be easy to separate in theory, but to separate them in experimentation will surely be difficult.

Be all that as it may, let us consider what evidential sup-port may be available for some of the propositions which are crucial to the hypothesis:

(1) That the phenomena of somatic adjustment are appropriately described in terms of an economics of flexibility. In general, we believe that the presence of stress A may reduce an organism's ability to respond to stress B and, guided by this opinion, we commonly protect the sick from the weather. Those who have adjusted to the office life may have difficulty in climbing mountains, and trained mountain climbers may have difficulty when confined to offices; the stresses of retirement from business may be lethal; and so on. But scientific knowledge of these matters, in man or other organisms, is very slight.

(2) That this economics of flexibility has the logical structure described above — each successive demand upon flexibility fractionating the set of available possibilities. The proposition is expectable, but so far as I know there is no evidence for it. It is, however, worthwhile to examine the criteria which determine whether a given "economic" system is more appropriately described in additive or multiplicative terms. There would seem to be two such criteria:

(a) A system will be additive insofar as the units of its currency are mutually interchangeable and, therefore, can-not meaningfully be classified into sets such as were used earlier in this paper to show that the economics of flexibility must surely be multiplicative. Calories in the economics of energy are completely interchangeable and unclassifiable, as are dollars in the individual budget. Both these systems are therefore additive. The permutations and combinations of variables which define the states of an organism are classifiable and—to this extent—noninterchangeable. The system is therefore multiplicative. Its mathematics will resemble that of information theory or negative entropy rather than that of money or energy conservation.

144 N. W. Simmonds, "Variability in Crop Plants, Its Use and Conservation," Biol. Review, 1962, 37: 422-62.

145 L M. Lerner, Genetic Homeostasis, Edinburgh, Oliver and Boyd, 1954.

A system will be additive insofar as the units of its currency are mutually independent. Here there would seem to be a difference between the economic system of the individual, whose budgetary problems are additive (or sub-tractive) and those of society at large, where the overall distribution or flow of wealth is governed by complex (and perhaps imperfect) homeostatic systems. Is there, perhaps, an economics of economic flexibility (a metaeconomics) which is multiplicative and so resembles the economics of physiological flexibility discussed above? Notice, however, that the units of this wider economics will be not dollars but patterns of distribution of wealth. Similarly, Lerner's "genetic homeostasis," insofar as it is truly homeostatic, will have multiplicative character.

The matter is, however, not simple and we cannot expect that every system will be either totally multiplicative or totally additive. There will be intermediate cases which combine the two characteristics. Specifically, where several independent alternative homeostatic circuits control a single variable, it is clear that the system may show additive characteristics—and even that it may pay to incorporate such alternative pathways in the system provided they can be effectively insulated from each other. Such systems of multiple alternative controls may give survival advantage insofar as the mathematics of addition and subtraction will pay better than the mathematics of logical fractionation.

(3) That innovative genotypic change commonly makes demands upon the adjustive ability of the soma. This proposition is orthodoxly believed by biologists but cannot in the nature of the case be verified by direct evidence.

(4) That successive genotypic innovations make multiplicative demands upon the soma. This proposition (which involves both the notion of multiplicative economics of flexibility and the notion that each innovative genotypic change has its somatic price) has several interesting and perhaps verifiable implications.

(a) We may expect that organisms in which numerous recent genotypic changes have accumulated (e.g., as a result of selection, or planned breeding) will be delicate, i.e., will need to be protected from environmental stress. This sensitivity to stress is to be expected in new breeds of domesticated animals and plants and experimentally produced organisms carrying either several mutant genes or unusual (i.e., recently achieved) genotypic combinations.

(b) We may expect that for such organisms further genotypic innovation (of any kind other than the affirmative changes discussed above) will be progressively deleterious.

(c) Such new and special breeds should become more resistant both to environmental stress and to genotypic change, as selection works upon successive generations to favor those individuals in which "genetic assimilation of acquired characteristics" is achieved (Proposition 5).

(5) That environmentally induced acquired characteristics may, under appropriate conditions of selection, be replaced by similar characteristics which are genetically determined. This phenomenon has been demonstrated by Waddington146 for the bithorax phenotypes of Drosophila.

He calls it the "genetic assimilation of acquired characteristics." Similar phenomena have also probably occurred in various experiments when the

146 C. H. Waddington, "Genetic Assimilation of an Acquired Character," Evolution, 1953, 7: 118; also Waddington, The Strategy of Genes, London, Allen and Unwin, 1957.

experimenters set out to prove the inheritance of acquired characteristics but did not achieve this proof through failure to control the conditions of selection. We have, however, no evidence at all as to the frequency of this phenomenon of genetic assimilation. It is worth noting, however, that, according to the arguments of this essay, it may be impossible, in principle, to exclude the factor of selection from experiments which would test "the inheritance of acquired characteristics." It is precisely my thesis that the simulation of Lamarckian inheritance will have survival value under circumstance of undefined or multiple stress.

(6). That it is, in general, more economical of flexibility to achieve a given characteristic by genotypic than by soma-tic change. Here the Waddington experiments do not throw any light, because it was the experimenter who did the selecting. To test this proposition, we need experiments in which the population of organisms is placed under double stress: (a) that stress which will induce the characteristic in which we are interested, and (b) a second stress which will selectively decimate the population, favoring, we hope, the survival of those individuals whose flexibility is more able to meet this second stress after adjusting to the first. According to the hypothesis, such a system should favor those individuals which achieve their adjustment to the first stress by genotypic process.

(7) Finally, it is interesting to consider a corollary which is the converse of the thesis of this essay. It has been argued here that simulated Lamarckian inheritance will have survival value when the population must adjust to a stress which remains constant over successive generations. This case is in fact the one which has been examined by those who would demonstrate an inheritance of acquired characteristics. A converse problem is presented by those cases in which a population faces a stress which changes its intensity unpredictably and rather often—perhaps every two or three generations. Such situations are perhaps very rare in nature, but could be produced in the laboratory.

Under such variable circumstances, it might pay the organisms in survival terms to achieve the converse of the genetic assimilation of acquired characteristics. That is, they might profitably hand over to somatic homeostatic mechanisms the control of some characteristic which had previously been more rigidly controlled by the genotype.

It is evident, however, that such experimentation would be very difficult. Merely to establish the genetic assimilation of such characteristics as bithorax requires selection on an astronomical scale, the final population in which the genetically determined bithorax individuals can be found being a selected sample from a potential population of something like 1050. or 1060 individuals. It is very doubtful whether, after this selective process, there would still. exist in the sample enough genetic heterogeneity to undergo a further converse selection favoring those individuals which still achieve their bithorax phenotype by somatic means.

Nevertheless, though this converse corollary is possibly not demonstrable in the laboratory, something of the sort seems to operate in the broad picture of evolution. The matter may be presented in dramatic form by considering the dichotomy between "regulators" and "adjusters."147 Prosser proposes that where internal physiology contains some variable of the same dimensions as some external environmental variable, it is convenient to classify organisms according to the degree

147 C. L. Prosser, "Physiological Variation in Animals," Biol. Review, 1955, 30: 22-262.

to which they hold the internal variable constant in spite of changes in the external variable. Thus, the homoiothermic animals are classified as "regulators" in regard to temperature while the poikilothermic are "adjusters." The same dichotomy can be applied to aquatic animals according to how they handle internal and external osmotic pressure.

We usually think of regulators as being in some broad evolutionary sense "higher" than adjusters. Let us now consider what this might mean. If there is a broad evolutionary trend in favor of regulators, is this trend consistent with what has been said above about the survival benefits which accrue when control is transferred to genotypic mechanisms?

Clearly, not only the regulators but also the adjusters must rely upon homeostatic mechanisms. If life is to go on, a large number of essential physiological variables must be held within narrow limits. It the internal osmotic pressure, for example, is allowed to change, there must be mechanisms which will defend these essential variables. It follows that the difference between adjusters and regulators is a matter of where, in the complex network of physiologic causes and effects, homeostatic process operates.

In the regulators, the homeostatic processes operate at or close to the input and output points of that network which is the individual organism. In the adjusters, the environmental variables are permitted to enter the body and the organism must then cope with their effects, using mechanisms which will involve deeper loops of the total network.

In terms of this analysis, the polarity between adjusters and regulators can be extrapolated another: step to include what we may call "extraregulators" which achieve homeostatic controls outside the body by changing and controlling the environment—man being the most conspicuous example of this class.

In the earlier part of this essay, it was argued that in adjusting to high altitude there is a benefit to be obtained, in terms of an economics of flexibility, by shifting from, e.g., panting to the more profound and less reversible changes of acclimation; that habit is more economical than trial and error; and that genotypic control may be more economical than acclimation. These are all centripetal changes in the location of control.

In the broad picture of evolution, however, it seems that the trend is in the opposite direction: that natural selection, in the long run, favors regulators more than adjusters, and extraregulators more than regulators. This seems to indicate that there is a long time evolutionary advantage to be gained by centrifugal shifts in the locus of control.

To speculate about problems so vast is perhaps romantic, but it is worth noting that this contrast between the overall evolutionary trend and the trend in a population faced with constant stress is what we might expect from the converse corollary here being considered. If constant stress favors centripetal shift in the locus of control, and variable stress favors centrifugal shift, then it should follow that in the vast spans of time and change which determine the broad evolutionary picture, centrifugal shift of control will be favored.

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