Hormones and Heredity Part 6

YELLOW male x BLACK female YO male BB female | / | | / | YB female BO male Tortoise-sh.e.l.l female BLACK male

BLACK male x YELLOW female BO male YY female | / | | / | BY female YO male Tortoise-sh.e.l.l female YELLOW male

The s.e.x must be determined therefore by the spermatozoa, as in the case of colour-blindness, etc., in man, and the colour factor must always be in the female-producing sperm.

s.e.xUAL DIMORPHISM

It is obvious from the above facts that however interesting and important s.e.x-linked heredity may be, it is not the same thing as the heredity of secondary s.e.xual characters, and does not in the least explain s.e.xual dimorphism. In the first place, the term s.e.x-linked does not mean occurring always exclusively in one s.e.x, but the direct contrary-- transmitted by one s.e.x to the opposite s.e.x--and in the second place there is no suggestion that the development of the character is dependent in any way on the presence or function of the gonad. The problem I am proposing to consider is what light the facts throw on the origin of the secondary s.e.xual characters in evolution. In endeavouring to answer this question there are only two alternatives: either the characters are blastogenic-- that is, they arise from some change in the gametocytes occurring somewhere in the succession of cell-divisions of these cells--or they arise in the soma and are impressed on the gametocytes by the influence of the soma within which these gametocytes are contained--that is to say, they are somatogenic. That characters do originate by the first of these processes may be considered to be proved by recent researches, and such characters are called mutations. There can be little doubt that the so- called s.e.x-linked characters, of which examples have been given above, have originated in this way, and that their relation to s.e.x is part of the mutation. According to T. H. Morgan, it is simply due to the fact that the determinants for such characters are situated in the s.e.x-chromosome.

Morgan, however, also states that a case of true s.e.xual dimorphism arose as a mutation in his cultures of _Drosphilia_. The character was eosin colour in the eye instead of the red colour of the eye in the original fly. In the female this was dark eosin colour, in the male yellowish eosin. But this case differs from the characters particularly under consideration here in two points: (1) there is no suggestion that it was adaptive, (2) or that it was influenced by hormones from the gonads.

No character whose development is dependent in greater or less degree on the stimulation of some substance derived from the gonads can have originated as a mutation, because the term mutation means a new character which develops in the soma as a result of the loss or gain of some factor or determinant in the chromosomes. To say that certain mutations consist of new factors which only the development of characters in the soma when the part of the soma concerned is stimulated by a hormone, is a mere a.s.sertion unsupported at present by any evidence. As an example of the way in which Mendelians misunderstand the problem to be considered, I may refer to Doncaster's book, _The Determination of s.e.x_ [Footnote: Camb.

Univ. 1914, p. 99.] in which he remarks: 'It follows that the secondary s.e.xual characters cannot arise simply from the action of hormones; they must be due to differences in the tissues of the body, and the activity of the ovary or testis must be regarded rather as a stimulus to their development than as their source of origin.' This seems to imply a serious misunderstanding of the idea of the action of the hormones from the gonads and of hormones in general. No one would suggest that the hormones from the testis should be regarded as in any sense the origin of the antlers of a stag. If so, why should not antlers equally develop in the stallion or in the buck rabbit, or indeed in man? How far Doncaster is right in holding that the soma is different in the two s.e.xes is a question already mentioned, but it is obvious that in each individual the somatic s.e.xual characters proper to its species are present potentially in its const.i.tution by heredity--in other words, as factors or determinants in the chromosomes of the zygote from which it was developed; but the normal development of such characters in the individual soma is either entirely dependent on the stimulus of the hormone of the gonad or is profoundly influenced by the presence or absence of that stimulus. The evidence, as we have seen, proves that, at any rate in the large number of cases where this relation between somatic s.e.x-characters and hormones produced by the reproductive organs exists, the characters are inherited by both s.e.xes. In one s.e.x they are fully developed, in the other rudimentary or wanting. But the s.e.x, usually the female, in which they are rudimentary or wanting is capable of transmitting them to offspring, and also is capable of developing them more or less completely when the ovaries are removed, atrophied or diseased. If we state these facts in the terms of our present conceptions of chromosomes and determinants or factors, we must say that the factors for these characters are present in the chromosomes of both male and female gametes. The question then is, how did these factors arise? If they were mutations not caused by any influence from the exterior, what is the reason why these particular characters which alone have an adaptive relation to the s.e.xual or reproductive habits of the animal are also the only characters which are influenced by the hormones of the reproductive organs? The idea of mutations implies neither an external relation nor an internal relation in the organ or character; but these characters have both, the external relation in the function they perform in the s.e.xual life of the individual, the internal relation in the fact that their development is affected by the s.e.xual hormones. There is no more striking example of the inadequacy of the current conceptions of Mendelism and mutation to cover the of bionomics and evolution.

The truth is that facts and experiments within a somewhat narrow field have a.s.sumed too much importance in recent biological research. No increase in the number of facts or experimental results of a particular cla.s.s will compensate for the want of sound reasoning and a comprehensive grasp of the phenomena to be explained. The coexistence of the external and the internal relation in the characters we are considering suggests that one is the cause of the other, and as it is obvious that the relation for instance of a stag's antlers to a testicular hormone could not very well be the cause of the use of the antlers in fighting, the reasonable suggestion is that the latter is the cause of the former. We have already seen that the development and shedding of the antler are processes of essentially the same kind physiologically, or pathologically, as these which can be and are occasionally produced in the individual soma by mechanical stimulus and injury to the periosteum. The fact that a hormone from the testis affects the development of the antler, as well as our knowledge of hormones in general, suggests a special theory of the heredity of somatic modifications due to external stimuli. Physiologists are apt to look for a particular gland to produce every internal secretion. But the fact that the wall of the intestine produces secretion, which carried by the blood causes the pancreas to secrete, shows that a particular gland is not necessary. There is nothing improbable in supposing that a tissue stimulated to excessive growth by external irritation would give off special substances to the blood. We know that living tissues give off products, and that these are not merely pure CO2 and H2O, but complicated compounds. The theory proposed by me in 1908 was that we have within the gonads numerous gametocytes whose chromosomes contain factors corresponding to the different parts of the soma, and that factors or determinants might be stimulated by products circulating in the blood and derived from the parts of the soma corresponding to them. There is no reason to suppose that an exostosis formed on the frontal bone as a result of repeated mechanical stimulation due to the b.u.t.ting of stags would give off a special hormone which was never formed in the body before, but it would probably in its increased growth give off an increased quant.i.ty of intermediate waste products of the same kind as the tissues from which it arose gave off before. These products would act as a hormone on the gametocytes, stimulating the factors which in the next generation would control the development of the frontal bone and adjacent tissues.

The difficulty of this theory is one which has occurred to biologists who have previously made suggestions of a connexion between hormones and heredity--namely, how hormones or waste products from one part of the body could differ from these from the same tissue in another part of the body.

If there were no special relation, hypertrophy of bone on one part of the body such as the head, would merely stimulate the factor for the whole skeleton in the gametocytes, and the result would merely be an increased development of the whole skeleton. On the other hand, we have the evident fact that a number of chromosomes formed apparently of the same substance, by a series of equal chromosome divisions determine all the various special parts of the complicated body. This is not more difficult to understand than that every part of the body should give off special substances which would have a special effect on the corresponding parts of the chromosomes. We know that skin glands in different parts of the body produce special odours, although all formed of the same tissue and all derived from the epidermis. It seems not impossible that bones of different parts of the body give off different hormones. If the factors in the gametes were thus stimulated they would, when they developed in a new individual, product a slightly increased development of the part which was hypertrophied in the parent soma. No matter how slight the degree of hereditary effect, if the stimulation was repeated in every generation, as in the case of such characters as we are considering it undoubtedly was, the hereditary effect would constantly increase until it was far greater than the direct effect of the stimulation. We may express the process mathematically in this way. Suppose the amount of hypertrophy in such a case as the antlers to be _x,_ and that some fraction of this is inherited. Then in the second generation the same amount of stimulation together with the inherited effect would produce a result equal to _x+x/n_. The latter fraction being already hereditary, a new fraction _x/n_ would be added to the heredity in each generation, so that after _m_ generations the amount of hereditary development would be _x+mx/n_. If _n_ were 1000, then after 1000 generations the inherited effect would be equal to _x_. This, it is true, would not be a very rapid increase. But it is possible that the fraction _x/n_ would increase, for the heredity might very well consist not only in a growth independent of stimulation, but in an increasing response to stimulation, so that _x_ itself might be increasing, and the fraction _x/n_ would become larger in each generation.

The death and loss of the skin over the antler, originally duo to the laceration of the skin in fighting, has also become hereditary, and it is certainly difficult to conceive the action of hormones in this part of the process. All we can suggest is that the hormone from the rapidly growing antler, including the covering skin, is acting on the corresponding factor in the gametocytes for a certain part of every year, and then, when the skin is stripped off, the hormone disappears. The factor then may be said to be stimulated for a time and then the stimulus suddenly ceases. The bone also begins to die when the skin and periosteum is stripped off, and the hormone from this also ceases to be produced.

The annual shedding and recrescence of the antler, however, is only to be understood in connexion with the effect of the testicular hormone.

According to my theory there are two hormone actions, the centripetal from the hypertrophied tissue to the corresponding factor in the gametocytes, and the centrifugal from the testis to the tissue of the antler or other organ concerned. The reason why the somatic s.e.xual character does not develop until the time of p.u.b.erty, and develops again each breeding season in such cases as antlers, is that the original hypertrophy due to external stimulation occurred only when the testicular hormone was circulating in the blood. The factor in the gametocytes then in each generation acted upon by both hormones, and we must suppose that in some way the result was produced that the hereditary development of the antler in the soma only took place when the testicular hormone was present. It is to be remembered that we are unable at present to form a clear conception of the process of development, to understand how the simple fertilised ovum is able by cell-division and differentiation to develop into a complicated organism with organs and characters predetermined in the single cell which const.i.tutes the ovum. If we accept the idea that characters are represented by particular parts of the chromosomes, according to Morgan's scheme, our theory of development is the modern form of the theory of preformation. When in the course of development the cells of the head from which the antlers arise are formed, each of these cells must be supposed to contain the same chromosomes as the original ovum from which the cells have descended by repeated cell-division. The factors in these chromosomes corresponding to the forehead have been stimulated while in the parent animal by hormones from the outgrowth of tissue produced by external mechanical stimulation, while at the same time they were permeated by the testicular hormone produced either by the gametocytes themselves or by interst.i.tial cells of the testis. When the head begins to form in the process of individual development, the factors, according to my theory, have a tendency to form the special growth of tissue of which the incipient antler consists, but part of the stimulus is wanting, and is not completed until the testicular hormone is produced and diffused into the circulation--that is to say, when the testes are becoming mature and functional.

I do not claim that this theory in complete--it is impossible to understand the process completely in the present state of knowledge--but I maintain that it is the only theory which affords any explanation of the remarkable facts concerning the influence of the hormones from the reproductive organs on the development of secondary s.e.xual characters, while at the same time explaining the adaptive relation of these characters or organs to the s.e.xual habits of the various species. On the mutation hypothesis, adaptation is purely accidental. T. H. Morgan considers that the appearance of two slightly different shades of eye colour in male and female in a culture of a fruit-fly in a bottle is sufficient to settle the whole problem of s.e.xual dimorphism, and to supersede Darwin's complicated theory of s.e.xual selection. The possibility of a Lamarckian explanation he does not even mention. He would doubtless a.s.sume that the antlers of stags arose as a mutation, without explaining how they came to be affected by the testicular hormone, and that when they arose the stags found them convenient as fighting weapons. But the complicated adaptive relations are not to be disposed of by the simple word mutation. The males have s.e.xual instincts, themselves dependent on the testicular hormone, which develop s.e.xual jealousy and rivalry, and the Ruminants fight by b.u.t.ting with their heads because they have no incisor teeth in the upper jaw, or tusks, which are used in fighting in other species. Doubtless, mutations have occurred in antlers as in other characters; in fact all hereditary characters are subject to mutation.

This in the most probable explanation, not only of the occasional occurrence of hornless individual stags, but of the differences between the antlers of different species, for there is no reason to believe that the special character of the antler in each species is adapted to a special mode of fighting in each species.

The different structure of the horns of the Bovine and Ovine Ruminants is, in my view, the result of a different mode of fighting. If we suppose that the fighting was slower and less fierce in the Bovidae, so that the skin over the exostosis was subject to friction but not lacerated, the result would be a thickening of the h.o.r.n.y layer of the epidermis as we find it, and the fact that the skin and periosteum are not destroyed explains why the horns are not shed but permanent.

There is a tendency among Mendelians and mutationists to overestimate the importance of experiments in comparison with reasoning, either inductive or deductive. Bateson, however, has admitted that Mendelian experiments and observations on mutation have not solved the problem of adaptation. It seems to be demanded, nevertheless, that characters must be produced experimentally and then inherited before the hereditary influence of external stimuli can be accepted. Kammerer's experiments in this direction have been sceptically criticised, and it must be granted that the evidence he has published is not sufficient to produce complete conviction. But experiments of this kind are from the nature of the case difficult if not impossible. There is, however, another method--namely, to take a character which is certainly to some extent hereditary, and then to ascertain by experiment if it is 'acquired.' If it be proved that a hereditary character was originally somatogenic, it follows that somatogenic characters in time become hereditary. This is the reasoning I have used in reference to my experiments on the production of pigment on the lower sides of Flat-fishes, and I obtained similar evidence with regard to the excessive growth of the tail feathers in the j.a.panese Tosa-fowls, [Footnote: 'Observations and Experiments on j.a.panese Long-tailed Fowls,'

_Proc. Zool. Soc._, 1903.] which is a modification of a secondary s.e.xual character. In these fowls the feathers of the tail in the hens are only slightly lengthened.

I learned from Mr. John Sparks, who himself brought specimens of the breed from j.a.pan, that the j.a.panese not only keep the birds separately on high perches in special cages, but pull the tail feathers gently every morning in order to cause them to grow longer. One question which I had to investigate on my specimens, hatched from eggs obtained from Mr. Sparks, was the relation of the growth of the feathers to the moult which occurs in ordinary birds. My experiment consisted in keeping two c.o.c.ks, A and B, the first of which was left to itself, while in the second the feathers were gently pulled by stroking between the finger and thumb from the base outwards. The feathers in the tail were seven pairs of rectrices, two rows of tail coverts, anterior and posterior, four or five pairs in each row, a number of transition feathers: all these were steel-blue, almost black; in front of them on the saddle were a number of reddish yellow, very slender saddle hackles.

In September 1901, when the birds ware just over three months old, the adult feathers of the tail were all growing. The growing condition can be distinguished by the presence of a h.o.r.n.y tubular sheath extending up the base of the feather for about one inch. When growth ceases this sheath is shed. In c.o.c.k A growth continued till the end of the following March, when the longest feathers, the central rectrices, 2 feet 4-1/2 inches long. One of the feathers--namely, one of the anterior tail coverts--was accidentally pulled out on 11th February 1902, when it was 15-1/4 inches long and had nearly ceased to grow and formed its quill, and it immediately began to grow again and continued to grow till the following September, when it was accidentally broken off at the base: it was then 18 inches (44.5 cm.) long.

The effect of stroking in c.o.c.k B was to pull out from time to time one of the growing feathers. Of the original feathers, one, the left central posterior covert, continued to grow till 13th July 1902, when it was 2 feet 9-1/2 inches long without the part contained in the follicle. All the feathers pulled out immediately commenced to grow again, except the last two pulled out 27th May and 13th July, which did not grow again till the following moulting season, in September.

The first right central rectrix in c.o.c.k B was accidentally pulled out on 13th April 1902, when it was 2 feet 9-7/8 inches long. Its successor began to grow immediately, and in course of time pieces of it were broken off accidentally without injury to the base in the socket, which continued to grow until 16th June 1905, when it torn out of its socket. The total length of the feather with the pieces previously broken off, which were measured and preserved, was 11 feet 5-1/2 inches. It therefore continued to grow without interruption for three years and two months at an average rate of 3.6 inches per month.

In c.o.c.k A only four of the short outer rectrices were moulted in the beginning of September 1902: the longer feathers--namely, central rectrices and tail coverts--which ceased to grow naturally in the spring of 1902, were not moulted till the beginning of October. This shows the great importance of pulling out the feathers as soon as they show signs of ceasing to grow, in order to obtain the abnormally long feathers. The central rectrices continued to grow till the beginning of September 1903, when that of the left side was 3 feet 6 inches long, that of the right about an inch shorter. The coverts had ceased to grow of their own accord some time before this, and the central ones of the posterior row were about 3 feet long.

As it seemed possible that there was some natural congenital difference in growth of feathers between c.o.c.ks A and B, I commenced early in March 1903 to pull and stroke the feathers of the left side only in c.o.c.k A, leaving those of the right side untouched. On 30th July on the left side the central rectrix and the first and second posterior coverts were still growing, on the right side the central rectrix was also growing, but the first and second posterior coverts had ceased growth and formed their quills. The first posterior covert on the left or pulled side was 3 inches longer than that of the right. The second posterior covert on the left side was still longer. The first and second posterior coverts of left side did not cease growth till 26th August. On 2nd September the left central rectrix was almost at the end of its growth, the right had ceased to grow a little before. The left was about an inch longer than the right. Thus both in length in duration of growth the feathers of the pulled side were longer than those of the right, and this was the result of treatment continued only six months, and commenced some months after the feathers had begun to grow. I have no doubt, however, that the pulling out of the feather as soon as it shows signs of forming quill, so that its successor at once grows again, is even more important in producing the great length of feather than the stroking of the feather itself.

In this case, then there is no doubt (_a_) that the long-tailed birds are artificially treated with the utmost care and ingenuity by the j.a.panese, who produced them; (_b_) that the mechanical stimulus in my experiments did cause the feathers to grow for a longer period and attain greater length; (_c_) that the tendency to longer growth is, even when no treatment is applied, distinctly inherited. It is a legitimate and logical conclusion that the inherited tendency is the result of the artificial treatment. No other breed of fowls shows such excessive growth of tail feathers. It may be admitted that individuals differ considerably in their congenital tendency to greater growth, _i.e._ greater length of the tail feathers, but according to my views this is not contradictory to the main conclusion, for every hereditary character shows individual variation.

It may be pointed out here that on the Lamarckian theory the conception of adaptations is not teleological: they do not exist for a certain purpose, but are the result of external stimulations arising from the actions and habits of the organism. The latter conception is the more general, for cases of somatic s.e.xual characters exist which cannot be said to have a use or function. For example, the comb and wattles of _Gallus_ are s.e.xually dimorphic, being in the original species larger in the c.o.c.k than in the hen. There is no convincing evidence that these appendages are either for use or ornament. They are, in fact, a disadvantage to the bird, being used by his adversary to take hold of when he strikes. The first thing that happens when c.o.c.ks fight is the bleeding and laceration of the comb, as they peck at each other's heads. This laceration of the skin is, in my view, the primary cause of the evolution of these structures, leading to hypertrophy. But in this, as in other cases, the hereditary result is regular, constant, and symmetrical, while the immediate effect on the individual is doubtless irregular.

CHAPTER V

Mammalian s.e.xual Characters Evidence Opposed To The Hormone Theory

Perhaps the most remarkable of all somatic s.e.xual characters are those which are almost universal in the whole cla.s.s of Mammalia, the mammary glands in the female, the s.c.r.o.t.u.m in the male. We have considered the evidence concerning the relation of the development and functional action of the milk glands to hormones arising in the ovary or uterus, now we have to consider the origin of the glands and of their peculiar physiology in evolution. The obvious explanation from the Lamarckian point of view, and in my opinion the true one, is that they owed their origin at the beginning to the same stimulation which is applied to them now in every female mammal that bears young. There is, as we have seen, a difficulty in explaining how the occurrence of parturition causes the secretion of milk to begin, but it is certain that the secretion soon stops if the milk is not drawn from the glands by the sucking action of the offspring, or the artificial imitation of that action. A cow that is not milked or milked incompletely ceases to give milk. When the stimulus ceases, lactation ceases. The pressure of the secretion in the alveoli causes the cells to cease to secrete, much in the same way that pressure in the ureters injures the secretory action of the renal epithelium. In the earliest Mammals we may suppose that the young were born in a well-developed condition, for at first the supply of milk would not have been enough to sustain them for a long time as their only food. We must also suppose that the mother began to cherish the young, keeping them in contact with her abdomen. Then being hungry they began to suck at her hair or fur. The actual development of the milk glands in Marsupials has been described by Bresslau [Footnote: Stuttgart, 1901.] and by O'Donoghue. [Footnote: _Q.J.M.S._, lvii., 1911-12.] The rudiment of the teat is a depression or inv.a.g.i.n.ation of the epidermis from the bottom of which six stout hairs arise. The follicles of these hairs extend down into the derma, and from the upper end of the follicle, _i.e._ near the aperture of the inv.a.g.i.n.ation, a long cellular outgrowth extends down into the derma, branches at its end, and becomes hollow. These branches are the tubules of the future milk gland. Another outgrowth from the follicle forms a sebaceous gland. Later on the hairs and the sebaceous glands entirely disappear, and the milk gland alone is left with its tubules and ducts opening into the cavity of the teat. This is clear evidence that the milk gland was evolved in connexion with hairs, and was an enlargement of glands opening into the hair follicle, but it is difficult to understand why a sebaceous gland is developed and afterwards disappears. This would seem to indicate that the milk gland was not a hypertrophied sebaceous gland, but a distinct outgrowth, which however had nothing to do with sweat glands.

That the intra-uterine gestation, or its cessation, were not originally necessary to determine the functional periodicity of the milk glands is proved by their presence in the Monotremes, which are oviparous. It is evident from the conditions in these mammals that both hair and milk glands were evolved before the placenta.

It may also be pointed out here that, according to the evidence of Steinach, in the milk glands at least among somatic s.e.xual characters there is no difference between the male and female in the heredity of the organs. The zygote therefore, whether the s.e.x of it is determined as male or female, has the same factor for the development of milk glands. On the chromosome theory as formulated by Morgan this factor must be in the somatic chromosomes and not in the s.e.x-chromosomes, and must be present in every zygote. All the cells of the body, a.s.suming that somatic segregation does not occur, must possess the same chromosomes as the zygote from which it developed, and whether the s.e.x chromosomes are _XX_ or _XY_ or _X_, there must be at any rate one chromosome bearing the factor for milk glands. The functional development of these depends normally, according to the evidence hitherto discovered, on the presence or absence of hormones from the ovary or from the uterus.

If we attribute, as in my opinion we must, the primary origin of the milk glands in evolution to the mechanical stimulus of sucking, we may attempt to reconstruct the stages of the evolution of the present relation of the glands to the other organs and processes of reproduction. In the earliest stage represented by the Monotremata or Prototheria, there was no intra-uterine development. We must suppose that in the beginning the sucking stimulus caused both growth and secretion, for at first there was nothing but sebaceous or sweat glands, and although a mutation might be supposed to have produced larger glands, no mutation could explain the influence of hormones on the growth and function of such glands. Then heredity of the effect of stimulus took place to some slight degree, and this would occur, according to my theory, only in the presence of the hormone from the ovary in the same condition as that in which the modification was first caused. This would be of course after ovulation, and after hatching of the eggs. In the next stage, if we adopt the modern view that Marsupials are descended from Placental Mammals, the eggs would be retained for increasing periods in the uteri, and would be born in a well-developed condition, since lactation would demand active sucking effort on the part of the young. The early Placentalia would inherit from the Monotreme-like ancestors the development of the milk glands after ovulation, although no sucking was taking place while the young were inside the uterus. It seems probable that the relation between parturition and actual milk secretion originated with the sucking stimulus of the young after birth.

There is good evidence that the secretion of milk may continue almost indefinitely under the stimulus of sucking or milking. Neither menstruation nor gestation put an end to it. Cows may continue to give milk until the next parturition, and if castrated during lactation will continue to yield milk for years. Women also may continue to produce milk as long as the child is allowed to suck, and this has been in some cases two or three years or even more. Moreover, lactation may be induced by the repeated act of sucking without any gestation. This has happened in mares, virgin b.i.t.c.hes, mules, virgin women, and in one woman lactation continued uninterruptedly for forty-seven years, to her eighty-first year, long after the ovary had ceased to be functional. Lactation has also been induced in male animals, _e.g._ in a bull, a male goat, male sheep, and in men. [Footnote: Knott, 'Abnormal Lactation,' _American Medicine_, vol. ii (new series), 1907.] We may conclude, therefore, that the secretion of milk normally begins by heredity after parturition, and this, in accordance with what we have learned about hormones in connexion with the reproductive system, is probably the consequence of the withdrawal of the hormone absorbed from the foetus. I do not think it is necessary to suppose, as do Lane-Claypon and Starling, that the hormone physiologically inhibits the dissimilative process and augments the a.s.similative, and that the withdrawal of the hormone at parturition therefore causes the dissimilative process, _i.e._ secretion of milk. My conclusion is that the process of secretion set up by the mechanical stimulus of sucking is inherited as it was acquired, so that it only begins to take place in the individual in the absence of the hormone from the foetus, which was absent when the process was acquired. The growth of the gland during gestation would then be due to the postponement of the process of secretion in consequence of the presence of the foetal hormone, and in this way this hormone has become in the course of evolution at once the stimulus to growth and the cause of the inhibition of secretion.

This interpretation does not, however, agree with the case of _Dasyurus_.

If the foetal hormone is absorbed from the pouch, as I have suggested, in order to explain the persistence of the corpora lutea during lactation, then the secretion of milk after parturition ought not to take place. But in this case the sucking stimulus has been applied to the glands after a very short gestation, while the hormone from the foetus is being absorbed in the pouch, and therefore the hereditary correlation between secretion and absence of foetal hormone may be a.s.sumed to have been lost in the course of evolution.

We have next to consider the question of the evolution of the corpora lutea. If these bodies are formed only in Mammals which have uterine gestation, and not in Prototheria, they cannot be the only essential source of the hormone which stimulates the development of the milk glands, since the latter develop in Prototheria. Again it is difficult, it might be said impossible, to believe that an accidental mutation gave rise to corpora lutea the secretion of which caused uterine gestation and ultimately the formation of the placenta. It seems more probable that the retention of the originally yolked ova within the oviduct, however this retention arose, was the essential cause of the formation of the placenta and all the changes which the uterus undergoes in gestation. The absorption of nutriment from the walls of the uterus, and the chemical and mechanical stimulation of those walls, might well be the cause of the diversion of nutrition from the ovary, leading gradually to the decline of the process of secretion of yolk in the ova.

The conceptions and the mode of reasoning of the physiologist are very different from those of the evolutionist. The former concludes from certain experiments that a given organ of internal secretion has a certain function. The corpora lutea, for example, according to one theory are ductless glands, the function of whose secretion is to establish ova in the uterus and promote their development. Another function suggested for the secretion of the corpora lutea is to prevent further ovulation during pregnancy. The evolutionist, on the other hand, asks what was the origin of this corpora lutea, why should the ruptured ovarian follicles after the escape of the ova in Mammals undergo a progressive development and persist during the greater part of the whole of pregnancy? It seems obvious that the corpora lutea in evolution were a consequence of intra-uterine gestation, for they occur only in a.s.sociation with this condition, and it is impossible to suppose that a mutation could arise accidentally by which the ruptured follicles should produce a secretion which would cause the fertilised ova to develop within the oviducts. The developing ovum within the uterus may, however, reasonably be supposed to give off something which is absorbed into the maternal blood, and this something would be of the same nature as that which was given off by the ovum while still within the ovarian follicle. The presence of this hormone might cause the follicular cells to behave as though the ovum was still present in the follicle, so that they would persist and not die and be absorbed. But this leaves the question, what is lutein and why is it secreted? Lutein is a colouring matter sometimes found in blood-clots, and probably derived from haemoglobin. In the corpus luteum the lutein is contained in the cells, not in a blood-clot.

Chemical investigation shows that the lutein of the corpus luteum is almost if not quite identical with the colouring matter of the yolk in birds and reptiles. Escher [Footnote: _Ztschr. f. Physiol. Chem._, 83 (1912).] found that the lutein of the corpus luteum had the formula C{40}H{56} and was apparently identical with the carotin of the carrot, while the lutein of egg-yolk was C{40}H{56}O{2} and more soluble in alcohol, less soluble in petroleum ether, than that of the corpus luteum.

The difference, if it exists, is very slight, and it is evident that one compound could easily be converted into the other. Moreover, the hypertrophied follicular cells which const.i.tute the corpus luteum secrete fat which is seen in them in globules. The similarity of their contents therefore to yolk is very remarkable, and it may be suggested that the hormones absorbed from the ovum or embryo in the uterus acts upon the follicular cells in such a way as to cause them to secrete substances which in the ancestor were pa.s.sed on to the ovum and formed the yolk. It may be urged that this idea is contradictory to the previous suggestion that the absorption of nourishment by the intra-uterine embryo was the cause of the gradual decline of the process of yolk-secretion by the ova in the ovary, but it is not really so. Originally in the reptilian ancestor, or in the Monotreme, the ovum in the follicle secreted yellow-coloured yolk. The materials for this, at any rate, pa.s.sed through the follicle cells, and it is probable that these cells were not entirely pa.s.sive, but actively secretory in the process. Substances diffusing from the ovum would be present in the follicle cells during this process, and probably act as a stimulus. The same substances diffusing from the ovum during its development in the uterus would continue to stimulate the follicle cells, and thus explain not merely their persistence, but their secretory activity. The ovum being no longer present in the ovary, the secretions would remain in the follicular cells, and the corpus luteum would be explained.

If this theory is sound, it would follow that corpora lutea are not formed in cases where the ova are not retained in the oviduct during their development. The essential process in the development of these structures is the hypertrophy and, in some cases at least, multiplication of the follicular cells in the ruptured follicle. I have already mentioned that this process does not occur in Teleosteans whose ovaries were studied by me. These were species of Teleosteans in which fertilisation is external.

Marshall, in his _Physiology of Reproduction_, [Footnote: London, 1910, p.

151.] quotes a number of authors who have published observations on the changes occurring in the ruptured follicle in the lower Vertebrata, and also in the Monotremes. According to Sandes, [Footnote: 'The Corpus Luteum of Dasyurus,' _Proc. Lin. Soc._, New South Wales, 1903.] in the latter there is a p.r.o.nounced hypertrophy of the follicular epithelium after ovulation, but no ingrowth of connective tissue or blood-vessels from the follicular wall. Marshall himself examined sections of the corpus luteum of _Ornithorhynchus_ and saw much hypertrophied and apparently fully developed luteal cells, but no trace of any ingrowth from the wall of the follicle. This fact would appear to be quite inconsistent with the theory above proposed, but it must be remembered that the ovum of Monotremes is known to remain for a short period in the oviduct, or in other words to pa.s.s through it very slowly, and to absorb fluid from its walls, as shown by the considerable increase in size which the ovarian ovum undergoes before it is laid. It would be interesting to know how long the rudimentary corpus luteum persists in _Ornithorhynchus_: the period, according to my views, should be very short. It is remarkable that in the results quoted by Marshall a well-developed corpus luteum was found and exclusively found in the lower Vertebrates which are viviparous. For example, among fishes in the Elasmobranchs _Myliobatis_ and _Spinax_; in Teleosteans, in _Zoarces_; in Reptiles, in _Anguis_ and _Seps_. Buhler on the other hand, confirmed my own negative result with regard to oviparous Teleosteans, and also found no hypertrophy of the follicle in Cyclostomes which are also oviparous. In the viviparous forms mentioned there is yolk in the ovum which is retained in oviduct or ovary, but additional nutriment is also absorbed from the uterine or ovarian walls. In these cases there is no placenta and generally no adhesion of ovum or embryo to walls of oviduct or ovary. These facts alone would be sufficient to disprove the theory that the corpora lutea are organs producing a secretion whose function is to cause the attachment of the embryo to the uterine mucosa. It is also, in my opinion, unreasonable to suppose that the rudimentary corpora lutea of lower viviparous Vertebrates arose as a mutation the result of which was to cause internal development of the ovum. Habits might easily bring about retention of the fertilised ova for gradually increasing periods, [Footnote: According to Geddes and Thomson (_Evolution of s.e.x_, 1889), the common gra.s.s-snake has been induced under artificial conditions to bring forth its young alive.] and the correlation between the retained developing ova and the hypertrophy of the ruptured follicles is comprehensible on my theory of the influence of substances absorbed by the walls of oviduct or ovary from the developing ovum.

The case of _Dasyurus_, however, seems inconsistent with this argument, for, as previously mentioned, Sandes found that in this Marsupial the corpora lutea persisted during the greater part of the period of lactation, which continues for four months after parturition. During the whole of this time there are no embryos in the uteri, and therefore it might be urged absorption of hormones from the embryos cannot be the cause of the persistence of corpora lutea in pregnancy. But it seems to me that a complete answer to this objection is supplied by the peculiar relations of the embryos to the pouch in _Dasyurus_ and other Marsupials. The skin of the pouch while the embryos are in it is very soft, congested, and glandular; at the same time the embryos when transferred to the pouch at parturition are very small, immature, and have a soft delicate skin. The relation of embryos to pouch in _Dasyurus_, therefore, is closely similar to that of embryos to uterus after the first few days of pregnancy in the Eutheria. It is true there is no placenta, but the mouths of the embryos are in very close contact with the teats, and both the skin of the embryos and that of the pouch are soft and moist. If any special substances are given off by the embryos in the uterus in ordinary gestation, the same substances would continue to be given off by the embryos in the marsupial pouch, and these must be absorbed by the skin of the pouch. In this way it seems to me we have a logical explanation of the fact that the corpora lutea in the Marsupial are not absorbed at parturition as in Eutheria. As Sandes says the 'greater part of the period of lactation,' it would appear that absorption of the corpora lutea takes place when the young _Dasyurus_ have grown to some size, become covered with hair, and are able to leave the teats or even the pouch at will. Under these conditions it is obvious that diffusion of chemical substances from the young through the walls of the pouch would come to an end. It would be interesting in this connexion to know more of the relation of egg and embryo to the pouch and to the corpora lutea in _Echidna_. In _Ornithorhynchus_ the eggs are hatched in a nest and there is no pouch.

On this view that the corpora lutea are the result, not the cause, of intra-uterine gestation, it would no longer be possible to maintain the theory that the corpus luteum in the human species is the cause by its internal secretion of the phenomenon of menstruation. This was the theory of Born and Frankel. [Footnote: See Biedl, _Internal Secretory Organs_ (Eng. trans.), 1912, p. 404.] Biedl's conclusion is that the periodic development and disintegration of the uterine mucous membrane in the menstrual cycle is due to the hormone of the interst.i.tial cells of the ovary. Leopold and Ravana found that ovulation as a rule coincides with menstruation, but may take place at any time. Here, again, the problem must be considered from the point of view of evolution. It can scarcely be doubted that the thickening and growth of the mucous membrane in the menstrual cycle is of the same nature as that which takes place in pregnancy. When the ovum or ova are not fertilised the development comes to an end after a certain time, differing in different species of Mammals, and the membrane sloughs, returns to its original, state, and then begins the same process of development again.

Menstruation, then, must be interpreted as an abortive parturition, both in woman and lower Mammals, though in the latter it is not usually accompanied by hemorrhage, and is called pro-oestrus. The question then to be considered is, what determines parturition and menstruation? The presence of the fertilised ovum must have been the original cause of the hypertrophy of the uterine mucous membrane, and in its congenital or hereditary development the chemical substances diffusing from the ova in the uterus or even in the Fallopian tube may well be the stimulus starting the hypertrophy. But what determines the end of the pregnancy? Is it merely the increasing distension of the uterus by the developing foetus?

This could scarcely be the case in the Marsupials in which the foetus when born is quite minute. Nor can we attribute parturition to renewed ovulation, for this occurs in _Dasyurus_ only once a year. All we can suggest at present is that a certain periodic development takes place by heredity in presence of the hormones exuded by the fertilised ovum and the embryo developed from it. When the ovum or ova, not being fertilised, die the period of development is (usually) shortened and pro-oestrus or menstruation occurs. In the dog, however, the period of the oestrus cycle is about the as that of gestation--namely, six months.

The so-called descent of the t.e.s.t.i.c.l.es occurs exclusively in Mammals, in which with a few important exceptions it is universal. This is a very remarkable case of the change of position of an organ in the course of development. The original position of the testis on either side is quite similar to that of the same organ in birds or reptiles. The genital ridge runs along the inner edge of the mesonephros, with which the testicular tubules become connected. The testis, with the mesonephros, forming the epididymis, closely attached to it, projects into the coelom, and without losing its connexion with the peritoneum changes its position gradually during development, pa.s.sing backwards and downwards until it comes to lie over the wall of the abdomen just in front of the pubic symphysis of the pelvic girdle. There the abdominal wall on either side of the middle line becomes thin and distended to form a pouch, the scrotal sac, into which the testis pa.s.ses, still remaining attached to the peritoneum which lines the pouch, while the distal end of the vas deferens retains its original connexion with the urethra. The movement of the testis can thus be accurately described as a transposition or dislocation.

Various causes have been suggested for the formation of the s.c.r.o.t.u.m, but no one has ever been able to suggest a use for it. It has always been quite impossible to bring it within the scope of the theory of natural selection. The evolution of it can only be explained either on the theory of mutation or some Lamarckian hypothesis. The process of dislocation of the testis does not conform to the conception of mutation, nor agree with other cases of that phenomenon. A mutation is a change of structure affecting more or less the whole soma, but showing itself especially in some particular organ or structure. But I know of no mutation occurring under observation which consisted, not in a change of structure or function, but merely in a change of position of an organ from one part of the body to another, and moreover a change which takes place by a continuous process in the course of development. If the testes were developed from the beginning in a different part of the abdomen, there might be some reason in calling the change a mutation. Moreover, if it is a mutation, why has it never occurred in any other cla.s.s of Vertebrates except Mammals?

In 1903 Dr. W. Woodland published [Footnote: _Proc. Zool. Soc._, 1903, Part 1.] a Lamarckian theory of this mammalian feature, the probability of which it seems to me has been increased rather than decreased by the progress of research concerning heredity and evolution since that date.

Dr. Woodland correlated the dislocation of the testes with the special mechanical features of the mode of locomotion in Mammalia. His words are: 'The theory here advocated is to the effect that the descent of the testes in the Mammalia has been produced by the action of mechanical strains causing rupture of the mesorchial attachments, such strains being due to the inertia of the organs reacting to the impulsiveness involved in the activity of the animals composing the group.' The 'impulsiveness' is the galloping or leaping movement which is characteristic of most Mammals when moving at their utmost speed, as seen, for example, in horses, deer, antelopes, dogs, wolves, and other Ungulata and Carnivora. It is obvious that when the body is descending to the ground after being hurled upwards and forwards, the abdominal organs have acquired a rapid movement downwards and forwards; when the body reaches the ground its movement is stopped suddenly, while the abdominal organs continue to move. The testes therefore are violently jerked downwards away from their attachments and at the same time forward. The check to the forward movement, however, is momentary, while the body is immediately thrown again upwards and forwards, which by the law of inertia means that the testes are thrown still more downwards and backwards. There is no reason to suppose, as Dr.

Woodland suggests, that any rupture of the mesorchium was the usual result of these strains, but a constant pull or tension was caused in the direction in which the testes actually move during development. On this theory we have to consider (1) how such strains could cause a shifting of the peritoneal attachment, (2) why the testes should be supposed to be particularly affected more than other abdominal organs. The answer to the first question is that the strains would cause a growth of the connecting membrane (mesorchium) at the posterior end, accompanied by an absorption of it at the anterior end. The answer to the second question is that the testes are at once the most compact and heaviest organs in the abdomen, and at the same time the most loosely attached. The latter statement does not apply to the mesonephros or epididymis which has moved with the testis, but the latter cannot function without the former, and it may be supposed that the close attachment of the epididymis to the testis had come about in the early Mammalia before the change of position was evolved.

It is evident that the violent shocks of the galloping or leaping movement do not occur in Birds, Reptiles, or Amphibia. Ostriches run very fast and do not fly, but their progression is a stride with each foot alternately, not a gallop. The Anura among the Amphibia are saltatory, but their leaps are usually single, or repeated only a few times, not sustained gallops.

The exceptions among the Mammalia still more tend to prove the close correspondence between the 'impulsive' mode of progression and the dislocation of the male gonads. In the Monotremata there is no s.c.r.o.t.u.m, the testes are in a position similar to that which obtains in Reptiles, and they are the only Mammals in which these organs are anterior to the kidneys. In locomotion they are sluggish, there is no running or galloping among them. _Ornithorhynchus_ is aquatic in its habits, and _Echidna_ is nocturnal and moves very slowly. In Marsupials the s.c.r.o.t.u.m is in front of the p.e.n.i.s, but really in the same position as in other Mammals--that is, in front of the ventral part of the pelvic girdle. It is the p.e.n.i.s which is different, as the skin around the organ has not united in a ventral suture below it, while the organ itself has not grown forward adnate to the abdominal skin as in most other Mammals. The s.c.r.o.t.u.m is always anterior to the origin of the p.e.n.i.s, although in the Eutheria apparently behind that organ. The larger Marsupials like the kangaroos are eminently saltatory, and the others are active in locomotion. The aquatic Mammals Sirenia and Cetacea have no s.c.r.o.t.u.m, the testes being abdominal. It is unnecessary to inquire whether this is the original position, or whether they are descended from ancestors which had a s.c.r.o.t.u.m: in either case the position of the testes corresponds to the absence of what Dr. Woodland calls impulsiveness in progression. The Fissipedia offer an instructive example, for while the Otariidae have the hind feet turned forward and can move on land somewhat like ordinary Mammals, the Phocidae cannot move their hind legs independently or turn them forward, and can only drag themselves about on land for short distances. In the former the testes are situated in a well-defined s.c.r.o.t.u.m, in the latter these organs are abdominal. The Phocidae are probably descended from Mammals of the terrestrial type with a s.c.r.o.t.u.m, which has disappeared in the course of evolution. Perhaps the most curious exception is that of the elephants, in which the testes are abdominal. Here, in consequence of their structure and ma.s.sive shape, locomotion in usually a walk, and though they run occasionally the gait is a trot, not a sustained gallop, and leaping is out of the question. Sloths which hang from branches upside down have abdominal testes, but even here they are in a posterior position, between, the r.e.c.t.u.m and the bladder, so there has apparently been a degree of dislocation, probably inherited from ancestors with more terrestrial habits.

The fact that the ovaries do not occupy normally a position similar to that of the testes is in accordance with the theory, for they are very much smaller than the testes; and yet they have undergone some change of position, for they are posterior to the kidneys.