Chapter VII: The Inheritance of Acquired Characters as a Factor in Evolution (2)

In this same connection Spencer brings up the familiar _pièce de résistance_ of the Lamarckian school, the giraffe. He recognizes that the chief traits in the structure of this animal are the result of natural selection, since its efforts to reach higher branches could not be the cause of the lengthening of the legs. But “the coadaptation of the parts, required to make the giraffe’s structure useful, is much greater than at first appears.” For example, the bones and the muscles of the hind-legs have been also altered, and Spencer argues that it is “impossible to believe” that all parts of the hind-quarters could have been coadapted to one another, and to all parts of the fore-quarters. A lack of coadaptation of a single muscle “would cause fatal results when high speed had to be maintained while escaping from an enemy.”

Spencer claims that, since 1886, when he first published this argument, nothing like an adequate response has been made; and I think he might have added that an adequate answer is not likely to be forthcoming, since nothing short of a demonstration of how the giraffe really evolved is likely to be considered as sufficient. Wallace’s reply, that the changes in question could have been brought about by natural selection, since similar changes have been brought about by artificial selection, is regarded as inadequate by Spencer, since it assumes a parallel which does not exist. Nevertheless, Wallace’s reply contains, in my opinion, the kernel of the explanation, in so far as it assumes that congenital variation[19] may suffice to account for the origin of a form even as bizarre as that of the giraffe. The ancon ram and the turnspit dog were marked departures from the normal types, and yet their parts were sufficiently coördinated for them to carry out the usual modes of progression. It would not have been difficult, if we adopted Spencer’s mode of arguing, to show that these new forms could not possibly have arisen as the result of congenital variations.

Footnote 19:

Wallace assumes fluctuating variation to suffice, but in this I cannot
agree with him.

Again, it might be argued that the large, powerful dray-horse could not have arisen through a series of variations from the ordinary horse, because, even if variations in the right direction occurred in the fore-quarters, it is unlikely that similar variations would occur in the hind-quarters, etc. Yet the feat has been accomplished, and while it is difficult to prove that the inheritance of acquired characters has not had a hand in the process, it is improbable that this has been the case, but rather that artificial selection of some kind of variations has been the factor at work.

So long as the Lamarckian theory is supported by arguments like these, it can never hope to be established with anything more than a certain degree of probability. If it is correct, then its demonstration must come from experiment. This brings us to a consideration of the experimental evidence which has been supposed by some writers to give conclusive proof of the validity of the theory.

The best direct evidence in favor of the Lamarckian argument is that furnished by the experiments of Brown-Séquard. He found, as the result of injury to the nervous system of guinea-pigs, that epilepsy appeared in the adult animal, and that young born from these epileptic parents became also epileptic. Still more important was his discovery that, after an operation on the nerves, as a result of which certain organs, the ear or the leg, for instance, are affected, the same affection appears in the young born from such parents. These results of Brown-Séquard have been vouched for by two of his assistants, and his results in regard to the inheritance of epilepsy have been confirmed by Obersteiner, and by Luciani on dogs. Equally important is their later confirmation, as far as the main facts go, by Romanes.

Brown-Séquard gives the following summary of his results. I follow Romanes’ translation in his book on “Darwin and after Darwin,” where there is also given a careful analysis of Brown-Séquard’s results, as well as the outcome of the experiments of Romanes himself. The summary is as follows:—

1. “Appearance of epilepsy in animals born of parents which had been rendered epileptic by an injury to the spinal cord.

2. Appearance of epilepsy also in animals born of parents which had been rendered epileptic by section of the sciatic nerve.

3. A change in the shape of the ear in animals born of parents in which such a change was the effect of a division of the cervical sympathetic nerve.

4. Partial closure of the eyelids in animals born of parents in which that state of the eyelids had been caused either by section of the cervical sympathetic nerve, or the removal of the superior cervical ganglion.

5. Exophthalmia in animals born of parents in which an injury to the restiform body had produced that protrusion of the eyeball. This interesting fact I have witnessed a good many times, and seen the transmission of the morbid state of the eye continue through four generations. In these animals modified by heredity, the two eyes generally protruded, although in the parents usually only one showed exophthalmia, the lesion having been made in most cases only on one of the corpora restiformia.

6. Hæmatoma and dry gangrene of the ears in animals born of parents in which these ear alterations had been caused by an injury to the restiform body near the nib of the calamus.

7. Absence of two toes out of the three of the hind-leg, and sometimes of the three, in animals whose parents had eaten up their hind-leg toes, which had become anæsthetic from a section of the sciatic nerve alone, or of that nerve and also of the crural. Sometimes, instead of complete absence of the toes, only a part of one or two or three was missing in the young, although in the parent not only the toes, but the whole foot was absent (partly eaten off, partly destroyed by inflammation, ulceration, or gangrene).

8. Appearance of various morbid states of the skin and hair of the neck and face in animals born of parents having had similar alterations in the same parts as effects of an injury to the sciatic nerve.”

Romanes, who later went over the same ground, in part under the immediate direction of Brown-Séquard himself, has made some important observations in regard to these results, many of which he was able to confirm.

He did not repeat the experiment of cutting the cord, but he found that, to produce epilepsy, it was only necessary to cut the sciatic nerve. The “epileptiform habit” does not appear in the animal until some time after the operation; it lasts for some weeks or months, and then disappears. The attacks are not brought on spontaneously, but by “irritating a small area of the skin behind the ear on the same side of the body as that on which the sciatic nerve had been divided.” The attack lasts for only a few minutes, and during it the animal is convulsed and unconscious. Romanes thinks that the injury to the sciatic nerve, or to the spinal cord, produces some sort of a change in the cerebral centres, “and that it is this change—whatever it is, and in whatever part of the brain it takes place—which causes the remarkable phenomena in question.”

In regard to Brown-Séquard’s statements, made in the 3d and the 4th paragraphs, in respect to the results of the operation of cutting the cervical sympathetic, Romanes had not confirmed the results when his manuscript went to press; but soon afterward, after Romanes’ death, a note was printed in _Nature_ by Dr. Hill, announcing that two guinea-pigs from Romanes’ experiment had been born, “both of which exhibited a well-marked droop of the upper eyelid. These guinea-pigs were the offspring of a male and female in both of which I had produced for Dr. Romanes, some months earlier, a droop of the left upper eyelid by division of the left cervical sympathetic nerve. This result is a corroboration of the series of Brown-Séquard experiments on the inheritance of acquired characters.”

Romanes states that he also found that injury to a particular spot of the restiform bodies is quickly followed by a protrusion of the eye on the same side, and further, that he had “also had many cases in which some of the progeny of parents thus affected have shown considerable protrusion of the eyeballs of both sides, and this seemingly abnormal protrusion has occasionally been transmitted to the next generation. Nevertheless, I am far from satisfied that this latter fact is anything more than an accidental coincidence.” This reservation is made on the ground that the protrusion in the young is never so great as in the parents, and also because there is amongst guinea-pigs a considerable amount of individual variation in the degree of prominence of the eyeballs. Romanes, while unwilling to deny that an “obviously abnormal amount of protrusion, due to the operation, may be inherited in lesser degree,” is also unwilling to affirm so important a conclusion on the basis of these experiments alone.

In regard to Brown-Séquard’s 6th statement, Romanes found after injury to the restiform body that hæmatoma and dry gangrene may supervene, either several weeks after the operation, or at any subsequent time, even many months afterward. The disease usually affects the upper parts of both ears, and may then gradually extend downward until nearly the whole ear is involved. “As regards the progeny of animals thus affected in some cases, but by no means in all, a similarly morbid state of the ears may arise apparently at any time in the life history of the individual. But I have observed that in cases where two or more individuals _of the same litter_ develop this diseased condition, they usually do so at about the same time, even though this may be months after birth, and therefore after the animals are fully grown.” Moreover, the morbid process never extends so far in the young as it does in the parents, and “it almost always affects the middle third of the ear.” Several of the progeny from this first generation, which had apparently inherited the disease, but had not themselves been directly operated upon, showed a portion of the ear consumed apparently by the same disease. Romanes then gives the following significant analysis of this result. Since a different part of the ear of the progeny is affected, and also a “very much less quantity thereof,” it might seem that the result was due either to a mere coincidence, or to the transmission of microbes. But he goes on to say, that he fairly well excluded both of these possibilities, for, in the first place, he has never observed “the very peculiar process in the ears, or in any other parts of guinea-pigs which have neither themselves had the restiform bodies injured, nor been born of parents thus mutilated.” In regard to microbes, Romanes tried to infect the ears of normal guinea-pigs by first scarifying these parts, and then rubbing them with the diseased surfaces of the ears of affected guinea-pigs. In not a single case was the disease produced.

Romanes concludes that these “results in large measure corroborate the statements of Brown-Séquard; and it is only fair to add that he told me they were the results which he had himself obtained most frequently, but that he had also met with many cases where the diseased condition of the ears in parents affected the same parts in their progeny and also occurred in more equal degrees.”

We come now to the remarkable conclusion given in Brown-Séquard’s 7th statement, in regard to the absence of toes in animals whose parents had eaten off their own hind toes and even parts of their legs. Romanes got neuroses in the animals operated upon, and found that the toes might be eaten off; but none of the young showed any defect in these parts. Furthermore, Romanes repeated the same operation upon the descendants through six successive generations, so as to produce, if possible, a cumulative effect, but no inheritance of the mutilation was observed. “On the other hand, Brown-Séquard informed me that he had observed this inherited absence of toes only in about one or two per cent of cases.” It is possible, therefore, Romanes adds, that his own experiments were not sufficiently numerous to have obtained such cases.

In this connection I may give an account of some observations that I made while carrying out some experiments in telegony with mice. I found in one litter of mice that when the young came out of the nest they were tailless. The same thing happened again when the second litter was produced, but this time I made my observations sooner, and examined the young mice immediately after birth. I found that the mother had bitten off, and presumably eaten, the tails of her offspring at the time of birth. Had I been carrying on a series of experiments to see if, when the tails of the parents were cut off, the young inherit the defect, I might have been led into the error of supposing that I had found such a case in these mice. If this idiosyncrasy of the mother had reappeared in any of her descendants, the tails might have disappeared in succeeding generations. This perversion of the maternal instincts is not difficult to understand, when we recall that the female mouse bites off the navel-string of each of her young as they are born, and at the same time eats the afterbirth. Her instinct was carried further in this case, and the projecting tail was also removed.

Is it not possible that something of this sort took place in Brown-Séquard’s experiment? The fact that the adults had eaten off their own feet might be brought forward to indicate the possibility of a perverted instinct in this case also. At least my observation shows a possible source of error that must be guarded against in future work on this subject.

In regard to the 8th statement of Brown-Séquard, as to various morbid states of the skin, Romanes did not test this, because the facts which it alleges did not seem of a sufficiently definite character.

These experiments of Brown-Séquard, and of those who have repeated them, may appear to give a brilliant experimental confirmation of the Lamarckian position; yet I think, if I were a Lamarckian, I should feel very uncomfortable to have the best evidence in support of the theory come from this source, because there are a number of facts in the results that make them appear as though they might, after all, be the outcome of a transmitted disease, as Weismann claims, rather than the inheritance of an acquired character. Until we know more of the pathology of epilepsy, it may be well not to lay too great emphasis on these experiments. It should not be overlooked that during the long time that the embryo is nourished in the uterus of the mother, there is ample opportunity given for the transmission of material, or possibly even of bacteria. If it should prove true that epilepsy is due to some substance present in the nervous system, such substances could get there during the uterine life of the embryo. Even if this were the case, it may be claimed that it does not give an explanation of the local reappearance of the disease in the offspring. But here also we must be on our guard, for it is possible that only certain regions of the body are susceptible to a given disease; and it has by no means been shown that the local defect itself is inherited, but only the disease. Romanes insists that a very special operation is necessary to bring about certain forms of transmission.

It is well also to keep in mind the fact, that if this sort of effect is inherited, then we must be prepared to accept as a possibility that other kinds of injury to the parent may be transmitted to the offspring. It would be of great disadvantage to animals if they were to inherit the injuries that their parents have suffered in the course of their lives. In fact, we might expect to find many plants and animals born in a dreadful state of mutilation as a result of inheritances of this sort. Thus, while the Lamarckians try to show that, on their principle, characters for the good of the species may be acquired, they must also be prepared, if they accept this kind of evidence, to grant that immense harm may also result from its action. I do not urge this as an argument against the theory itself, but point it out simply as one of the consequences of the theory.

It has been shown quite recently, by Charrin, Delamare, and Moussu, that when, after the operation of laparotomy on a pregnant rabbit or guinea-pig, the kidney or the liver has become diseased, the offspring sometimes show similar affections in the corresponding organs (kidney or liver). The result is due, the authors think, to some substance set free from the diseased kidney of the parent that affects the kidney of the young in the uterus. By injecting into the blood of a pregnant animal fresh extracts from the kidney of another animal, the authors believe that the kidney of the young are also affected. It will be observed that this transmission of an acquired character appears to be different from that of transmission through the egg; for it is the developing, or developed organ itself, that is acted upon. The results throw an interesting light on the cases of epilepsy described by Brown-Séquard, since they show that the diseased condition of the parent may be transmitted to the later embryonic stages. May not, therefore, Brown-Séquard’s results be also explained as due to direct transmission from the organs of the parent to the similar organs of the young in the uterus?

There is another series of experiments of a different sort that has been used as an argument in favor of the Lamarckian view. These are the results that Cunningham has obtained on young flatfish. He put the very young fish, while still bilaterally symmetrical (in which stage the pigment is equally developed on both sides of the body) into aquaria lighted from below. He found that when the young fish begins to undergo its metamorphosis, the pigment gradually disappears on one side, as it would have done under normal conditions, _i.e._ when they are lighted from above. If, however, the fish are kept for some time longer, lighted from below, the pigment begins to come back again. “The first fact proves that the disappearance of the pigment-cells from the lower side in the metamorphosis is an hereditary character, and not a change produced in each individual by the withdrawal of the lower side from the action of light. On the other hand, the experiments show that the absence of pigment-cells from the lower side throughout life is due to the fact that light does not act upon that side, for, when it is allowed to act, pigment-cells appear. It seems to me that the only reasonable conclusion from these facts is, that the disappearance of pigment-cells was originally due to the absence of light, and that the change has now become hereditary. The pigment-cells produced by the action of light on the lower side are in all respects similar to those normally present on the upper side of the fish. If the disappearance of the pigment-cells were due entirely to a variation of the germ-plasm, no external influence could cause them to reappear, and, on the other hand, if there were no hereditary tendency, the coloration of the lower side of the flatfish when exposed would be rapid and complete.”[20]

Footnote 20:

_Natural Science_, October, 1893.

This evidence might be convincing were it not weakened by two or three assumptions. In the first place, it is not shown that if the loss of color on the lower side had been the result of the inheritance of an acquired character that the results seen in Cunningham’s experiment would follow as a consequence. Thus one of the starting-points of the argument really begs the whole question. In the second place, it is unproven that, had the loss of color of the lower side been the result of a variation of the germ-plasm, no external influence could cause it to reappear. In this connection there is another fact that has a bearing on the point here raised. In some species of flatfish the right side is turned down, and in other species the left. Occasionally an individual is found in a right-sided species that is left-sided, and in such cases the color is also reversed. Now, to explain this in the way suggested by Cunningham, we should be obliged to assume that some of the ancestors acquired the loss of pigment on one side of the body, and others on the other side according to which side was turned down. This supposition might be appealed to to give us an explanation of the occasional reversal of the symmetry as a rare occurrence at the present time; but the argument is so transparently improbable that, I believe, the Lamarckian school would hesitate to make use of it, yet, in principle, it is about the same as that Cunningham has followed above.

If, on the other hand, we suppose the difference in color of the two sides to have been the result of a germ-variation, we need only suppose that this was of such a kind that the color of the under side is only in a latent condition, and if an external factor can cause a reaction to take place on the light side, it is not surprising that this should call forth the latent color patterns. The result can be given at least a formal explanation on the theory that the original change was a germ-variation.

We come now to the evidence derived from paleontology. A number of evolutionists, more especially of the American school, have tried to show that the evolution of a number of groups can best be accounted for on the theory of the inheritance of acquired characters. A point that we must always bear in mind is that evolution in a direct line need not necessarily be the outcome of Lamarckian factors. Some of our leading paleontologists, Cope, Hyatt, Scott, Osborn, have been strongly impressed by the paleontological evidence in favor of the view that evolution has often been in direct lines; and some, at least, of these investigators have been led to conclude that only the Lamarckian factor of the inheritance of acquired characters can give a sufficient explanation of the facts. Paleontologists have been much impressed by the fact that evolution has been along the lines which we might imagine that it would follow if the effects of use and of disuse are inherited. There is, however, no proof that this is the case, although there are a number of instances to which this mode of explanation appears to give the readiest solution. But, as has been said before, it is not this kind of evidence that the theory is in need of, since Lamarck himself gave an ample supply of illustrations. What we need is clear evidence that this sort of inheritance is possible, and, from the very nature of the case, it is just this evidence that fossil remains can never supply.

The same criticism may be made of the work of Ryder, Packard, Dali, Jackson, Eimer, Cunningham, Semper, De Varigny, and others of the Lamarckian school. Despite the large number of cases that they have collected, which appear to them to be most easily explained on the assumption of the inheritance of acquired characters, the proof that such inheritance is possible is not forthcoming. Why not then spend a small part of the energy, that has been used to expound the theory, in demonstrating that such a thing is really possible? One of the chief virtues of the Lamarckian theory is that it is capable of experimental verification or contradiction, and who can be expected to furnish such proof if not the Neo-Lamarckians?

We may fairly sum up our position in regard to the theory of the inheritance of acquired characters in the verdict of “not proven.” I am not sure that we should not be justified at present in claiming that the theory is unnecessary and even improbable.

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