Loeb states, on the authority of Eigenmann, that all those forms which live in caves were adapted to life in the dark before they entered the cave, because they are all negatively heliotropic and positively stereotropic, and with these tropisms would be forced to enter a cave whenever they were put at the entrance. Even those among the Amblyopsidae which live in the open have the tropisms of the cave dweller. But these latter are not blind, and the argument only tends to show that the blind fish Amblyopsis entered the caves before it was blind. Nocturnal animals generally must be said to be negatively heliotropic, but these usually have larger and more sensitive eyes than the diurnal.
It is said, however, that Chologaster agassizii, which is not blind, lives in the underground streams of Kentucky and Tennessee, but I think it is open to doubt whether it is a species entirely confined to darkness.
Another point which Loeb omits to mention is the absence of pigment in cave animals, especially Vertebrates such as Amblyopsis and Proteus. If absence of light is not the cause of blindness in these cases, how is it that the blindness is always associated with absence of pigment, since we know that the latter in Fishes and Amphibia is due to the absence of light? It has been shown that Proteus when kept in the light develops some amount of pigment, although it does not become pigmented to the same degree as ordinary Amphibia. We have here, I think, an example of the essential difference between mutations and somatic modifications. Absence of the gametic factor or factors for pigmentation results in albinism, and no amount of exposure to light produces pigmentation in albinos, e.g. albino Axolotls which are well known in captivity. Absence of light, on the other hand, prevents the development of pigment. The question therefore is whether the somatic modification is inherited. The fact that Proteus does not rapidly become as deeply coloured when exposed to light as ordinary Amphibia shows that the gametic factors for pigmentation have been modified as well as the somatic tissues.
Loeb attributes the blindness of cave fishes to a disturbance in the circulation and mutation of the eyes originally occurring as a mutation. But how could an explanation of this kind be applied to the case of Anableps tetrophthalmus, in which each eye is divided by a partition of the cornea and lens into an upper half adapted for vision in air and a lower half for vision in water? This fish lives in the smooth water of estuaries in Central America, and swims habitually with the horizontal partition of the lens level with the surface of the water. It is impossible to understand in this case, firstly, how a mutation could cause the eyes to be divided and doubly adapted to two different optic conditions, and, secondly, how at the same time a convenient 'tropism' should occur which caused the animal to swim with its eyes half in and half out of water. Are we to suppose that the upper half of the body or eye had a positive heliotropism and the lower half a negative heliotropism? The fact is that the fish swims at the surface in order to watch for and feed on floating particles. The tropism concerned is the food tropism, but what is gained by calling the search for food common to all active animals a tropism, and how is the search for food before the food is perceptible to the senses, before it can act as a stimulus on a food-sensitive substance in the body, to be compared to a tropism at all?
Loeb undertakes to prove that the organism as a whole acts automatically according to physicochemical laws. But he misses the question of evolution altogether. For example, he quotes Gudernatsch as having proved that legs can be induced to grow in tadpoles at any time, even in very young specimens, by feeding them with thyroid gland. Loeb writes: 'The earlier writers explained the growth of the legs in the tadpole as a case of an adaptation to life on land. We know through Gudernatsch that the growth of the legs can be produced at any time by feeding the animal with the thyroid gland.' Obviously he thinks that these two propositions are contradictory to each other, whereas there is no contradiction, between them at all. Loeb actually supposes that the thyroid is the cause of the development of the legs. Logically, if this were the case it would follow that if we fed an eel or a snake with thyroid it would develop legs like those of a frog, and if a man were injected with extract of the testes of a stag he would develop antlers on his forehead. It will be obvious to most biologists that the thyroid, whether that of the tadpole itself or that which is supplied as food, only causes the development of legs because the hereditary power to develop legs is already present. The question is how this hereditary power was evolved. Legs are an adaptation to life on land. What we have to consider and to investigate is whether the legs arose as a gametic mutation or as a direct result of locomotion on land.
The general result of clinical and experimental evidence is to show that the hormone of the thyroid is necessary to normal development. The arrest of development in cretinous children is due to some deficiency of thyroid secretion, and is counteracted by the administration of thyroid extract. Excess of the secretion produces a state of restlessness and excitement associated with an abnormally rapid rate of metabolism and protrusion of the eye-balls (Graves' disease). The physiological text-books, however, say nothing of precocity of development in children as a result of hyperthyroidism. This, however, is undoubtedly what occurs in the case of tadpoles. The legs would naturally develop at some time or other, after a prolonged period of larval life. Feeding with thyroid causes them to develop at once. I have repeated Gudernatsch's experiment with the following results:—
This year I had a considerable number of tadpoles of the common English frog, which were hatched between March 26 and March 29. On April 12, when they had all passed the stage of external gills and developed internal gills and opercula, I divided them into two lots, one in a shallow pie-dish, the other in a glass cylinder. To one lot I gave a portion of rabbit's thyroid, to the other a piece of rabbit's liver. They fed eagerly on both. Afterwards I obtained at intervals of a week or so the thyroid of a sheep. I have seen no precise details of Gudernatsch's method of feeding tadpoles, but my own method was simply to put a piece of thyroid into the water containing the tadpoles and leave it there for several days, then to take it out and put in another piece, changing the water when it seemed to be getting foul.
April 22. Noticed that the non-thyroid tadpoles were larger than those fed on thyroid. Changed the former into the pie-dish and the latter into the glass jar, to make sure that the difference in size was not due to larger space.
May 3. Only eighteen of the non-thyroid tadpoles surviving, owing to the water having become foul, but these are three times as large as those fed on thyroid. In the latter no trace of hind-legs was visible, but the abdominal region was much emaciated and contracted, while the head region was broader.
May 4. Noticed minute white buds of hind-legs in the thyroid-fed tadpoles.