Hormones and Heredity
J. T. Cunningham

Part 2 out of 4

dominant. Hermaphrodite animals, as has been pointed out by Correns and
Wilson, cannot be brought under this scheme at all. In the earthworms, for
instance, we have, in every individual developed from a zygote, ova and
spermatozoa developing in different gonads in different parts of the body.
The differentiation here, therefore, must occur in some cell-division
preceding the reduction divisions. Every zygote must have the same
composition, and yet give rise to two sexes in the same individual.

Further light on the sex problem, as in many other problems in biology,
can only be obtained by more knowledge of the physical and chemical
processes which take place in the chromosomes and in the relations of
these structures to the rest of the cell. The recent advances in cytology,
remarkable as they are, consist almost entirely of observations of
microscopic structure. They may be said to reveal the statics of the cell
rather than its dynamics. Cytology is in fact a branch of anatomy, and in
the anatomy of the cell we have made some progress, but our knowledge of
the physiology of the cell is still infinitesimal. The nucleus, and
especially the chromosomes, are supposed in some unknown way to influence
or govern the metabolism of the cytoplasm. From this point of view the
hypothesis mentioned above that the sex-difference in the gametes is not
qualitative but quantitative is probably nearer to the truth. Geddes and
Thomson and others have maintained that the sex-difference is one of
metabolism, the ovum being more anabolic, the sperm more katabolic. A
double quantity of special chromatin may be the cause of the greater
anabolism of the ovum. In that case the difficulty indicated in a previous
part of this chapter, that the ovum after reduction resembles the sperm in
having only one X chromosome, may be explained by the fact that the growth
of the ovum and its accumulation of yolk substances has been already
accomplished under the influence of the two chromosomes before reduction.
Other difficulties previously discussed also appear to be diminished if we
adopt this point of view. We need not regard maleness and femaleness as
unit characters in heredity of the same kind as Mendelian characters of
the soma. Instead of saying that the zygote composed of ovum and
spermatozoon is incapable of giving rise in the male to ova, or in the
female to sperms, we should hold that the gametocytes ultimately give rise
to ova or to sperms according to the metabolic processes set up and
maintained in them through their successive cell-divisions under the
influence of the double or single X chromosome. There still remains the
difficulty of explaining why the male gametocytes after reduction develop
into similar sperms, with their heads and long flagella, although half of
them possess one X chromosome each and the other half none. We can only
suppose that the final development of the sperms is the result of the
presence of the single X chromosome in the successive generations of male
gametocytes before the reduction divisions.

The Mendelian theory of sex-heredity assumed that in the reduction
divisions the two sex-characters, maleness and femaleness, were segregated
in the same way as a pair of somatic allelomorphs, but the words maleness
and femaleness expressed no real conceptions. The view above suggested
merely attempts to bring our real knowledge of the difference between ovum
and sperm into relation with our real knowledge of the sex-chromosomes and
their behaviour in reduction and fertilisation.


Influence Of Hormones On Development Of Somatic Sex-Characters

We have next to consider what are commonly called secondary sexual
characters. These are characters or organs more or less completely limited
to one sex. When we distinguish in the higher animals the generative
organs or gonads on the one hand from the body or soma on the other, we
see that all differences between the sexes, except the gonads, are
somatic, and we may call them somatic sexual characters. The question at
once arises whether the soma itself is sexual, that is to say, whether on
the assumption that the sex of the zygote is already determined before it
begins to develop, the somatic cells as well as the gametocytes are
individually and collectively either male or female. In previous
discussions of the subject I have urged that the only meaning of sex was
the difference between the megagamete or ovum, and the microgamete or
sperm. But if the zygote, although compounded of ovum and sperm, is
predestined to give rise in the gametes descended from it, either to
sperms only or to ova only, it may be suggested that all the somatic cells
descended from the zygote are likewise either male or female, although
they do not give rise to gametes. It is evident, however, that the somatic
cells, organs, and characters do not differ necessarily or universally in
the two sexes. On the one hand, we have extraordinary and very conspicuous
peculiarities in the male, entirely absent in the female, such as the
antlers of stags, and the vivid plumage of the gold pheasant; on the other
we have the sexes externally alike and only distinguished by their sexual
organs, as in mouse, rabbit, hare, and many other Rodents, most Equidae,
kingfisher, crows and rooks, many parrots, many Reptiles, Amphibia,
Fishes, and invertebrate animals. In the majority of fishes, in which
fertilisation is external and no care is taken of the eggs or young, there
are no somatic sexual differences. Moreover, somatic sexual characters
where they do occur have no common characteristics either in structure or
position in the body. It may be said that any part of the soma may in
different cases present a sex-limited development. In the stag the male
peculiarity is an enormous development of bone on the head, in the peacock
it is the enlargement of the feathers of the tail. In some birds there are
spurs on the legs, in others spurs on the wings. It is no explanation,
therefore, to say that these various organs and characters are the
expression of sex in the somatic cells.

As I pointed out in my _Sexual Dimorphism_ (1900), the common
characteristic of somatic sexual characters is their adaptive relation to
some function in the sexual habits of the species in which they occur.
There is no universal characteristic of sex except the difference between
the gametes and the reproductive organs (gonads) in which they are
produced. All other differences, therefore, including genital ducts and
copulatory or intromittent organs, are somatic. When we examine these
somatic differences we find that they can be classified according to their
relation to fertilisation and reproduction, including the care or
protection of the offspring. The precise classification is of no great
importance, but we may distinguish the following kinds to show the
chief functions to which the characters or organs are adapted.

1. GENITAL DUCTS AND INTROMITTENT ORGANS.--According to the theory of the
coelom which we owe to Goodrich, in all the coelomata the coelom is
primarily the generative cavity, on the walls of which the gametocytes are
situated, and the coelomic ducts are the original genital ducts. In
Vertebrates we find two such ducts in both sexes in the embryo, originally
formed apparently by the splitting of a single duct. In the male one of
these ducts becomes connected with the testis while the other degenerates:
the one which degenerates in the male forms the oviduct in the female,
while the one which is functional in the male degenerates in the female.

Intromittent organs are formed in all sorts of different ways in different
animals. In Elasmobranchs (sharks and skates) they are enlarged portions
of the pelvic fins, and therefore paired. In Lizards they are pouches of
the skin at the sides of the cloacal opening. In Mammals the single penis
is developed from the ventral wall of the cloaca. In Crustacea certain
appendages are used for this function. There are a great many animals,
from jelly-fishes to fishes and frogs, in which fertilisation is external,
and there are no intromittent organs at all.

thumb-pads of the frog, and a modification of the foot in a water-beetle.
Certain organs on the head and pelvic fins of the Chimaeroid fishes are
believed to be used for this purpose.

3. WEAPONS.--Organs which are employed in combats between males for the
exclusive possession of the females. For example, antlers of stags, horns
of other Ruminants, tusks of elephants, spurs of cocks and Phasiamidae
generally, horns and outgrowths in males of Reptiles and many Beetles,
probably used for this purpose.

4. ALLUREMENTS.--Organs or characters used to attract or excite the
female. These might be called the organs of courtship, such as the
peacock's tail, the plumes of the birds-of-paradise, and the brilliant
plumage of humming birds and many others. The song of birds is another
example, and sound is produced in many Fishes for a similar purpose.

5. ORGANS FOR THE BENEFIT OF THE OFFSPRING: for example, the extraordinary
pouches in which the eggs are developed in certain Frogs. In the South
American species, _Rhinoderma darwinii_, the enlarged vocal sacs are used
for this purpose. Pouches with the same function are developed in many
animals, for instance in Pipe-fishes and Marsupials. Abdominal appendages
are enlarged in female Crustacea for the attachment of the eggs, the
abdomen also being larger and broader.

The argument in favour of the Lamarckian explanation of the evolution of
these adaptive characters is the same as in the case of adaptations common
to both sexes, namely that in every case the function of the organs and
characters involves special irritations or stimulations by external
physical agents. Mechanical irritation, especially of the interrupted
kind, repeated blows or friction causes hypertrophy of the epidermis and
of superficial bone. I have stated this argument and the evidence for it
in some detail in my volume on _Sexual Dimorphism_. It is one of the most
striking facts in support of this argument that the hypertrophied plumage
which constitutes the somatic sexual character of the male in so many
birds is habitually erected by muscular action for the purpose of display
in the sexual excitement of courtship. I doubt if there is a single
instance in which the male bird takes up a position to present his
ornamental plumage to the sight of the female without a special erection
and movement of the feathers themselves. Such a stimulation must affect
the living epidermic cells of the feather papilla. Even supposing that the
feather is not growing at the time, it is probable, if not certain, that
the stimulation will affect the papilla at the base of the feather
follicle, so as to cause increased growth of the succeeding feather. But
we have no reason to believe that erection in display occurs only when the
growth of the feathers is completed, still less that it did so always at
the beginning of the evolution.

The antlers of stags are the best case in favour of the Lamarckian view of
the evolution of somatic sexual characters. The shedding of the skin
('velvet') followed by the death of the bone, and its ultimate separation
from the skull, are so closely similar to the pathological processes
occurring in the injury of superficial bones, that it is impossible to
believe that the resemblance is only apparent and deceptive. In an
individual man or mammal, if the periosteum of a bone is destroyed or
removed the bone dies, and is then either absorbed, or separated from the
living bone adjoining, by absorption of the connecting part. In the stag
both skin and periosteum are removed from the antler: probably they would
die and shrivel of their own accord by hereditary development, but as a
matter of fact the stag voluntarily removes them by rubbing the antler
against tree trunks, etc. When the bone is dead the living cells at its
base dissolve and absorb it, and when the base is dissolved the antler
must fall off.

The adaptive relation is not the only common characteristic of these
somatic sexual characters. Another most important fact is not only that
they are fully developed in one sex, absent or rudimentary in the other,
but that their development is connected with the functional maturity and
activity of the gonads. There is usually an early immature period of life
in which the male and female are similar, and then at the time of puberty
the somatic sexual characters of either sex, generally most marked in the
male, develop. In some cases, where the activity of the gonads is limited
to a particular season of the year, the sexual characters or organs are
developed at this season, and then disappear again, so that there is a
periodic development corresponding to the periodic activity of the testes
or ovaries. Stags have a limited breeding or 'rutting' season in autumn
(in north temperate regions), and the antlers also are shed and developed
annually. In this case we cannot assert that the development of the antler
takes place during the active state of the testes. The antlers are fully
developed and the velvet is shed at the commencement of the rutting
season, and development of the antlers takes place between the beginning
of the year and the month of August or September. In ducks and other birds
there is a brilliant male-breeding plumage in the breeding season which
disappears when breeding is over, so that the male becomes very similar to
the female. In the North American fresh-water crayfishes of the genus
Cambarus there are two forms of males, one of which has testes in
functional activity, while in the other these organs are small and
quiescent: the one form changes into the other when the testes pass from
the one condition to the other.

It has long been known that the development of male sex-characters is
profoundly affected by the operation of castration. The removal of the
testes is most easily carried out in Mammals, in consequence of the
external position of the organs in these animals, and the operation has
been practised on domesticated animals as well as on man himself from very
ancient times. The effect is the more or less complete suppression of the
male insignia, in man, for example, the beard fails to develop, the voice
does not undergo the usual change to lower pitch which takes place at
puberty, and the eunuch therefore has much resemblance to the boy or
woman. Many careful experimental researches have been made on the subject
in recent years. The consideration of the subject involves two questions:
(1) What are the exact effects of the removal of the gonads in male and
female? (2) By what means are these effects brought about, what is the
physiological explanation of the influence of the gonads on the soma?

I have quoted the evidence concerning the effects of castration on stags
in my _Sexual Dimorphism_ and in my paper on the 'Heredity of Secondary
Sexual Characters.' [Footnote: _Archiv fuer Entwicklungesmechanik_, 1908.]
When castration is performed soon after birth a minute, simple spike
antler is developed, only two to four inches in length: it remains covered
with skin, is never shed, and develops no branches. When the operation is
performed on a mature stag with antlers, the latter are shed soon after
the operation, whether they have lost their velvet or not. In the
following season new antlers develop, but these never lose their velvet or
skin and are never shed.


The removal of the testes from young cocks has been commonly practised in
many countries, _e.g._ France, capons, as such birds are called, being
fatter and more tender for the table than entire birds. The actual effect,
however, on the secondary sexual characters has not in former times been
very definitely described. The usual descriptions represent the castrated
birds as having rather fuller plumage than the entire birds; but the comb
and wattles are much smaller than in the latter, more similar to those of
a hen. It is stated that the capon will rear chickens, though he does not
incubate, and that they are used in this way in France.

The most precise of the statements on the subject by the earlier
naturalists is that of William Yarrell [Footnote: _Proc. Linn. Soc.,
1857.] (1857), who writes as follows:--

'The capon ceases to crow, the comb and gills do not attain the size of
those parts in the perfect male, the spurs appear but remain short and
blunt, and the hackle feathers of the neck and saddle instead of being
long and narrow are short and broadly webbed. The capon will take to a
clutch of chickens, attend them in their search for food, and brood them
under his wings when they are tired.'

It would naturally be expected, on the analogy of the case of stags, that
when a young cock was completely castrated all the male secondary
characters would be suppressed, namely, the greater size of the comb and
wattles in comparison with the hen, the long neck hackles, and saddle
hackles, long tail feathers, especially the sickle-feathers, and the
spurs. As a matter of fact, the castrated specimen usually shows only the
first of these effects to any conspicuous degree. The comb and wattles of
the capon are similar to those of the hen, but he still has the plumage
and the spurs of the entire cock. Many investigators have made experiments
in relation to this subject, and most of them have found that complete
castration is difficult, and that portions of the testes left in the bird
during the operation become grafted in some other position either on the
parietal peritoneum, or on that covering the intestines, and produce
spermatozoa, which, of course hare no outlet. In such cases the secondary
male characters may fee more or less completely developed. Thus Shattock
and Seligmann (1904) state that ligature of the vas deferens made no
difference to the male characters, and that after castration detached
fragments were often left in different positions as grafts, when the
secondary characters developed. In one particular case only a minute
nodule of testicular tissue showing normal spermatogenesis was found on
post mortem examination attached to the intestine. In this bird there was
no male development of comb or wattles, a full development of neck
hackles, a certain development of saddle hackles, a few straggling badly
curved feathers in the tail and short blunt spurs on the legs. Lode
[Footnote: _Wiener klin. Wochenschr._, 1895.] (1895) found that testes
could easily be transplanted into subcutaneous tissue and elsewhere, and
that the male characters then developed normally. Hanau [Footnote: _Arch.
f. ges. Physiologie_, 1896.] (1896) obtained the same result.

The question, however, to what degree the male characters of the cock are
suppressed after complete castration is not so definitely answered in the
literature of the subject. Shattock and Seligmann in their 1904 paper make
no definite statement on the subject. Rieger (1900), Selheim (1901), and
Foges [Footnote: _Pfuegers Archiv_, 1902.] (1902) state that the true capon
is characterised by shrivelling of the comb, wattles, _and spurs_; poor
development of the neck and tail feathers; hoarse voice and excessive
deposit of fat. Shattock and Seligmann, on the other hand, have placed in
the College of Surgeons Museum the head of a Plymouth Rock which was
castrated in 1901. It was hatched in the spring of that year. In December
1901 the comb and wattles were very small, the spurs fairly well
developed, and the tail had a somewhat masculine appearance. In September
1902, when the bird was killed, the comb and wattles were still poorly
developed, the neck hackles fairly well so; saddle hackles rather well
developed; the tail contained rather loosely-grouped long sickle feathers;
the spurs stout. The description states that dissection showed no trace of
either testicle, and I am informed by Mr. Shattock that there were no
grafts. The description ends with the conclusion that the growth of the
spurs, and to a certain extent that of the long, curved sickle feathers,
is not prevented by castration. With regard to the spurs this result does
not agree with that of the German investigators, but it must be remembered
that the latter speak only of the reduction of the spurs, not entire
absence. It is important in discussing the effects of castration in cocks
to bear in mind the actual course of development of the secondary sexual
characters. When the chicks are first hatched they are in the down:
rudimentary combs are present, wattles can scarcely be distinguished, and
there is no external difference between the sexes. The ordinary plumage
begins to develop immediately after hatching, the primaries of the wings
being the first to appear. The feathers are completely developed in about
five weeks, and still there is no difference between the sexes. The first
sexual difference is the greater size of the combs in the males, and this
is quite distinct at the age of six weeks. At nine to ten weeks in
black-red fowls, in which the cocks have black breasts and red backs with
yellow hackles, the black feathers on the breast and red on the back are
gradually developing, both sexes previously having been a dull speckled
brown, closely similar to the adult hens. The spurs are the last of the
male characters to develop, these at the age of four months being still
mere nodules, scarcely, if at all, larger than the rudiments visible in
adult hens. This is the age at which castration is usually performed, as
at an earlier age the birds are too small to operate on successfully. It
follows, therefore, that the spurs develop after castration, and it would
seem that their development does not depend upon the presence of the
sexual organs. It is a question, however, whether castration in the cock
is ever quite complete. In the original wild species and in the majority
of domesticated breeds the spurs are confined to the male sex, and are
typical secondary sex-characters, as much so as the antlers of stags or
the beard of man, yet the above discussion shows that there is some doubt
whether their development is prevented as much as in other cases by the
absence of the sexual organs. Even if it should be proved that in supposed
cases of complete castration, such as that of Shattock and Seligmann, some
testicular tissue remained at the site of the testes, it would still be
true that the development of the comb and wattles is more affected by the
removal of the sexual organs than that of the spurs or tail feathers.

My own experiments in castrating cocks were as follows: On August 20,
1910, I operated on a White Leghorn cock about five months old. One testis
was removed, with a small part of the end broken off, but the other, after
it was detached, was lost among the intestines. On the same day I operated
on another about thirteen weeks old, a speckled mongrel. In this case both
testes were extracted but one was slightly broken at one end, although I
was not sure that any of it was left in the body. An entire White Leghorn
of the same age as the first was kept as a control. On August 27 the two
castrated birds had recovered and were active. Their combs had diminished
in size and lost colour considerably, that of the White Leghorn was
scarcely more than half as large as that of the control. Such a rapid
diminution can scarcely he due to absorption of tissue, but shows that the
size of the normal cock's comb is largely due to distension with blood,
which ceases when the sexual organs are removed. In the following January,
the second cock, supposed to be completely castrated, was seen to make a
sexual gesture like a cock, though not a complete action like an entire
animal: this showed that the sexual instinct was not completely
suppressed. In February this same bird was seen to attempt to tread a hen,
while the white one, supposed to be less perfectly emasculated, had never
shown such male instinct.

The White Leghorn cock was killed and dissected on May 13, 1911, nine
months after castration. I found an oval body of dark, dull brown colour
loose among the intestines: this was evidently the left testis which was
separated from its natural attachment and lost in the abdomen at the time
of the operation. I examined the natural sites of the testes: on the right
side there was a small testis of considerable size, about half an inch in
diameter. When a portion of this was teased up and examined under the
microscope moving spermatozoa were seen, but they were not in swarms as in
a normal testis, but scattered among numerous cells. On the left side was
a much smaller testis, in the tissue of which I with difficulty detected a
few slowly moving spermatozoa. The vasa deferentia were seen as white
convoluted threads on the peritoneum, but contained no spermatozoa.

On July 29, 1911, a little more than eleven months after the operation,
I examined and killed the second of these castrated cocks, the speckled
mongrel-bred bird. I measured the comb and wattles while it was alive, in
case there might be reduction in the size of these appendages when the
bird was killed. The comb was 1-1/3 inches high by 2-3/8 inches in length.
The spurs were 1 inch long, curved and pointed. Saddle hackles short,
hanging only a little below the end of the wing. Neck hackles well
developed, similar to those of an entire cock. Longest tail feather 15-5/8
inches, blue-black in colour.

I had no entire cock of same breed, but measured the entire White Leghorn
for comparison. Comb 1-3/4 inches high by 3-3/4 inches in length. (It is
to be remembered that the comb and wattles are especially large in
Leghorns.) Wattle 1-1/4 inches in vertical length. Spur 1 inch long,
stouter and less pointed than in the capon. Longest tail feather 12 inches

When killed the capon was found to be very fat: there were masses of fat
around the intestines and under the peritoneum, which made it impossible
to make out details such as ureter and vas deferens properly. I found a
white nodule about half an inch in diameter attached to mesentery. The
liquid pressed from this was swarming with spermatozoa in active motion.
Two other masses about the same size or a little larger were found on the
sites of the original testes. These also were full of mobile spermatozoa,
and must have grown from portions of the testes left behind at castration.

In ducks the sexual characters of the male differ from those in the fowl,
especially in the fact that they almost completely disappear after the
breeding season and reappear in the following season. In the interval the
drake passes into a condition of plumage in which he resembles the female;
and this condition is known as 'eclipse.' The male plumage, therefore, in
the drake has a history somewhat similar to that of the antlers in deer.
Two investigations of the effects of castration on ducks and drakes have
been recorded. H. D. Goodale [Footnote: 'Castration of Drakes.' _Biol.
Bulletin_, Wood's Hole, Mass., vol. xx., 1910] removed the generative
organs from both drakes and ducks of the Rouen breed, which is strongly
dimorphic in plumage. One drake was castrated in the early spring of 1909
when a little less than a year old. This bird did not assume the summer
plumage in 1909, that is, did not pass into eclipse. It was in the nuptial
plumage when castrated. This breeding or nuptial plumage is well known: it
includes a white neck-ring, brilliant green feathers on the head, much
claret on the breast, brilliant metallic blue on the wing, and two or more
upward curled feathers on the tail. The drake mentioned above was
accidentally killed in the spring of 1910. Another drake was castrated on
August 8, 1909: only the left testis was removed, the other being
ligatured. At this time the bird would be in eclipse plumage. It appears
from the description that it assumed the nuptial plumage in the winter of
1909, and did not pass into eclipse again in the summer of 1910. Thus in
drakes the effect of castration is that the secondary sexual character
remains permanently instead of being lost and renewed annually. Goodale,
however, does not describe the moults in detail. In the natural condition
the drake must moult twice in the year, once when he sheds the nuptial
plumage, and again when he drops the summer dress. Goodale insists, from
some idea about secondary sexual characters which is not very obvious,
that the eclipse or summer plumage is not the same as that of the female.
He states that the male in summer plumage merely mimics the female but
does not become entirely like her. In certain parts of the body there are
no modifications toward the female type. In others, i.e. head, breast, and
keel region, the feathers of the male become quite like those of the
female. 'It can hardly be maintained that this is an example of assumption
by the male of the female's plumage, especially as the presence of the
testis is necessary for its appearance.' The idea here seems to be that
since the eclipse plumage is only assumed when the testis is present,
therefore it must be a male character.

Out of five females on which the operation was performed only two lived
more than a few days afterwards. One of these (a) was castrated in the
spring of 1909 when a little less than a year old, the other (b) on August
13 when twelve weeks old. In October 1909 they showed no marked
modifications. In July 1910 it was noticed that they had the male curled
feathers in the tail, and (a) had breast feathers similar to those of the
male in summer plumage, (b) was rather more strongly modified: she had a
very narrow white neck-ring, and breast feathers distinctly of male type.
The next moult began in September, and in November was well advanced. On
the whole (a) had made little advance towards the male type, but (b)
closely resembled the male in nuptial plumage. It had brilliant green
feathers on the head, a white neck-ring, much claret colour on the breast,
and some feathers indistinguishable from those of the male, and also the
male sex feathers on the tail. Goodale concludes that the female owes her
normal colour to the ovaries or something associated with them which
suppresses the male characters and ensures the development of her own
type. He considers it is quite as conceivable that selection should
operate to pick out inconspicuously coloured females as that selection of
brilliantly coloured males should bring about an addition to the female
type. But as pointed out above, selection cannot explain the dimorphism in
either case.

It may be mentioned here that owing to the fact that the single (left)
ovary in birds is very closely attached to the peritoneum immediately
covering the great post-caval vein, it is generally impossible to remove
the whole of the ovary without cutting or tearing the wall of the vein and
so causing fatal hemorrhage. The above results observed by Goodale are
therefore all the more remarkable, and it may be assumed that he removed
at any rate nearly all the ovary.

The research of Seligmann and Shattock [Footnote: Relation between
Seasonal Assumption of the Eclipse Plumage in the Mallard _(Anas boscas_)
and the Functions of the Testicle.' _Proc. Zool. Soc._ 1914.] begins with
a comparison between the stages of the development of the nuptial plumage
and the stages of spermatogenesis. In the young pheasant the male plumage
is fully developed in the autumn of its first year, but no pairing occurs
and no sexual instinct is exhibited till the following spring. The wild
duck pairs in autumn or early winter, after the assumption of the nuptial
plumage, but copulation does not occur till spring is advanced. The
investigation here considered was made upon specimens of semi-domesticated
_Anas boscas_, such as are kept in London parks and supplied from game
farms. The testes attain their maximum size during the breeding season--
end of March or beginning of April. At this time each organ is almost as
large as a pigeon's egg, is very soft, and the liquid exuding from it when
cut is swarming with spermatozoa. The bird is of course in full nuptial
plumage. By the end of May, although the plumage is unchanged, the testes
have diminished to the size of a haricot bean, and spermatogenesis has
ceased. They diminish still further during June, July, and August, and
acquire a yellow or brownish colour, while microscopically there is no
sign of activity in the spermatic cells. The change from nuptial plumage
to eclipse takes place between the beginning of June and the middle of
July. The reappearance of the nuptial plumage takes place in the month of
September, and while this process takes place there is no sign of change
or renewed activity in the testes. During October and November, when the
brilliant plumage is fully developed, the testes increase slowly in size
but remain yellow and firm and exude no liquid on incision.
Spermatogenesis does not commence until the end of November or beginning
of December. The testes increase greatly in size in January and February,
and again reach their maximum size by the end of March. It is shown,
therefore, that the loss of the nuptial plumage takes place in June when
spermatogenesis has ceased and the testes are diminishing in size, but the
redevelopment of this plumage takes place in September without any renewed
activity of the testis and long before the beginning of spermatogenesis.
The case of the antlers in the stag is probably very similar.

The important statement is made with regard to castration (under
anaesthetics, of course) that it was found impossible to extirpate the
testes completely. When the bird was killed some months after the
operation, a greater or lesser amount of regenerated testicular tissue was
found either on the original site of the organs or engrafted upon
neighbouring organs. This experience, it will be noted, agrees with my own
in the case of fowls. There were, however, reasons for believing that the
results observed within the first six or eight months after the operation
are not much different from those which would follow complete castration.

Castration carried out when the drake was in nuptial plumage produced the
same effect which was observed by Goodale, namely, delay, and imperfection
in the assumption of the eclipse condition, but the observations of
Seligmann and Shattock are more precise and detailed. One example
described was castrated in full winter plumage in December 1906. On July
11, when normally it would have been in eclipse, the nuptial plumage was
unmodified except for a diffuse light-brown coloration on the abdomen,
which is stated to be due not to any growth of new feathers but to
pigmentary modification in the old. By September 1 this bird was almost in
eclipse but not quite; curl feathers in the tail had disappeared, the
breast was almost in full eclipse, the white ring was slightly indicated
at the sides of the neck, the top of the head and the nape had still a
good deal of gloss. After this the nuptial plumage developed again, and on
November 12 the bird was in full nuptial plumage, with good curl feathers
in the tail. The only trace of the eclipse was the presence of a few brown
feathers on the flanks. This bird was killed July 30, 1908, when the bird
was in eclipse, but not perfectly so, as there were vermiculated feathers
mixed with eclipse feathers on the breast, abdomen, and flanks. Dissection
showed on the right side a series of loosely attached nodular grafts of
testicular tissue, in total volume about the size of a haricot bean: on
the left side two small nodules, together about the size of a pea, and two
other grafts at the root of the liver and on the mesentery. Several other
cases are described, and the general result was that the eclipse was
delayed and never quite complete, while although the nuptial plumage was
almost fully developed in the following winter, it retained some eclipse
feathers, and was also delayed and developed slowly.

Several drakes were castrated in July when in the eclipse condition, and
although the authors state, in their general conclusions, that this does
not produce any constant appreciable effect upon the next passage of the
bird into winter plumage, they describe one bird so treated which on
November 18 retained many eclipse feathers: the general appearance of the
chestnut area of the breast was eclipse.

It must be remembered that not only was the castration in these cases
incomplete, but also that it was performed on mature birds. Birds differ
from Mammals, firstly, in the difficulty of carrying out complete
castration, and secondly, in the fact that the occurrence of puberty is
not so definite, and that immature birds are so small and delicate that it
is almost impossible to operate upon them successfully.


That male somatic sexual characters are latent in the female is shown by
the frequent appearance of such characters in old age, or in individual
cases. The development of hair on the face of women in old age, or after
the child-bearing period, is a well-known fact. Rorig, [Footnote: 'Ueber
Geweihbildung und Geweihentwicklung.' _Arch. Ent.-Mech._ x. and xi.] who
carefully studied the antlers of stags, states that old sterile females,
and those with diseased ovaries, develop antlers to some degree. Cases of
crowing hens, and female birds assuming male plumage have long been known,
but the exact relation of the somatic changes to the condition of the
ovaries in these cases is worthy of consideration in view of the results
obtained by Goodale after removal of the ovaries from ducks. Shattock and
Seligmann [Footnote: 'True Hermaphroditism in Domestic Fowl, etc.' _Trans.
Path. Soc._, Lond., 57. 1, 1906.] record the case of a gold pheasant hen
which assumed the full male plumage after the first moult: it had never
laid eggs or shown any sexual instincts. The only male character which was
wanting was that of the spurs. The ovary was represented by a smooth,
slightly elevated deep black eminence 1 cm. in length and 1-5 mm. in
breadth at its upper end. These authors also mention three ducks in male
plumage in which the ovary was similarly atrophied but not pigmented. They
regard the condition of the ovary as insufficient to explain the
development of the male characters, and suggest that such birds are really
hermaphrodite, a male element being possibly concealed in a neighbouring
organ such as the adrenal or kidney. This hypothesis is not supported by
observation of testicular tissue in any such case, but by the condition
found in a hermaphrodite specimen of the common fowl described in the
paper. This bird presented the fully developed comb and wattles and the
spurs of the cock, but the tail was quite devoid of curved or sickle
feathers, and resembled that of the hen. Internally there were two
oviducts, that of the left side normally developed, that of the right
diminutive and less than half the full length. The gonad of the left side
had the tubular structure of a testis, but showed no signs of active
spermatogenesis, but in its lower part contained two ova. The organ of the
right side was somewhat smaller, it had the same tubular structure, and in
one small part the tubules were larger, showed division of nuclei (mitotic
figures), and one of them showed active spermatogenesis.

In discussing Heredity and Sex in 1909, [Footnote: _Mendel's Principles of
Heredity_. Camb. Univ. Press, 1909.] Bateson referred to the effects of
castration as evidence that in different types sex may be differently
constituted. Castration, he urged, in the male vertebrate on the whole
leads merely to the non-appearance of male features, not to the assumption
of female characters, while injury or disease of the ovaries may lead to
the assumption of male characters by the female. This was supposed to
support the view that the male is homozygous in sex, the female
heterozygous in Vertebrates: that is to say, the female sex-character and
the female secondary sex-characters are entirely wanting in the male. This
argument assumes that the secondary characters are essentially of sexual
nature without inquiring how they came to be connected with sex, and it
ignores the fact that the influence of castration on such characters is a
phenomenon entirely beyond the scope of Mendelian principles altogether.
The fact that castration does affect, in many cases very profoundly,
somatic characters confined to one sex, proves that Mendelian conceptions,
however true up to a certain point, are by no means the whole truth about
heredity and development. For it is the essence of Mendelism as of
Weismannism that not only sex but all other congenital characters are
determined in the fertilised ovum or zygote. The meaning of a recessive
character in Mendelian terminology is one that is hidden by a dominant
character, and both of them are due to factors in the gametes,
particularly in the chromosomes of the gametes which come together in
fertilisation. For example, in fowls rose comb is dominant over single. A
dominant is something present which is absent in the recessive: the rose
comb is due to a factor which is absent from the single. The two segregate
in the gametes of the hybrid or heterozygote, and if a recessive gamete is
fertilised by another recessive gamete the single comb reappears. But
castration shows that the antlers of stags and other such characters are
not determined in the zygote when the sex is determined, but owe their
development, partly at least, to the influence of another part of the
body, namely, the testes during the subsequent life of the individual.
According to Mendelism the structure and development of each part of the
soma is due to the constitution of the chromosomes of the nuclei in that
part. The effects of castration show that the development of certain
characters is greatly influenced in some way by the presence of the testes
in a distant part of the body. The Mendelians used to say it was
impossible to believe in the heredity of somatic modifications due to
external conditions, because it was impossible to conceive of any means by
which such modifications could affect the constitution of the chromosomes
in the gametes within the modified body. It would have been just as
logical to deny the proved effects of castration, because it was
impossible to conceive of any means by which the testes could affect the
development of a distant part of the body.

But this is not all. The supposed fact that female secondary characters in
Vertebrates are absent in the male is completely disproved for Mammals by
the presence of rudimentary mammary glands in the male. It is true that
secondary sex-characters are usually positive in the male, while those of
the female are apparently negative, but in the case of the mammary glands
the opposite is the case. There is no room for doubt that the mammary
glands are an essentially female somatic sex-character, not only in their
function but in the relation between the periodicity of that function and
those of the ovaries and uterus, and it is equally certain from their
presence in rudimentary condition in the male that they are not absent
from the male constitution.


The existence and the influence of hormones or internal secretions may be
said to have been first proved in the case of the testes, for Professor A.
A. Berthold [Footnote: 'Transplantation der Hoden,' _Archiv. f Anat. u.
Phys._, 1849.] of Goettingen in 1849 was the first to make the experiment
of removing the testicles from cocks and grafting them in another part of
the body, and finding that the animals remained male in regard to voice,
reproductive instinct, fighting spirit, and growth of comb and wattles. He
also drew the conclusion that the results were due to the effect of the
testicle upon the blood, and through the blood upon the organism. Little
attention was paid to Berthold's experiment at the time. The credit of
having been the first to formulate the doctrine of internal secretion is
generally given to Claude Bernard. He discovered the glycogenic function
of the liver, and proved that in addition to secreting bile, that organ
stores up glycogen from the sugar absorbed in the stomach and intestines,
and gives it out again as sugar to the blood. In 1855 he maintained that
every organ of the body by a process of internal secretion gives up
products to the blood. He did not, however, discover the action of such
products on other parts or functions of the body. Brown-Sequard, in his
address before the Medical Faculty of Paris in 1869, was the first to
suggest that glands, with or without ducts, supplied special substances to
the blood which were useful or necessary to the normal health, and in 1889
at a meeting of the Societe de Biologie he described the experiment he had
made upon himself by the injection of testicular extract. This was the
commencement of organotherapy. Since that time investigation of the more
important organs of internal secretion--namely, the gonads, thyroid,
thymus, suprarenals, pituitary, and pineal bodies--has been carried on
both by clinical observation and experiment by a great number of
physiologists with very striking results, and new hormones have been
discovered in the walls of the intestine and other organs.

Here, however, we are more especially concerned with the gonads and other
reproductive organs. A great deal of evidence has now been obtained that
the influence of the testes and ovaries on secondary sexual characters is
due to a hormone formed in the gonads and passing in the blood in the
course of the circulation to the organs and tissues which constitute those
characters. The fact that transplanted portions of testes in birds (cocks
and drakes) are sufficient to maintain the secondary characters in the
same condition as in normal individuals shows that the nexus between the
primary and somatic organs is of a liquid chemical nature and not
anatomical, through the nervous system for example. Many physiologists in
recent years have maintained that the testicular hormone is not derived
from the male germ-cells or spermatocytes, but from certain cells between
the spermatic tubuli which are known as interstitial cells, or
collectively as the interstitial gland.

The views of Ancel and Bouin, [Footnote: _C. R. Soc. Biol., iv._]
published in 1903, may be described in large part as theory. They state
that the interstitial cells appear in the male embryo before the
gametocytes present distinctive sex-characters. They conclude that the
interstitial cells supply a nutritive material (hormone?), which has an
effect on the sexual orientation of the primitive generative cells. In
addition to this function, the interstitial cells by their hormone also
give the sexual character to the soma. When castration is carried out at
birth the male somatic characters do not entirely disappear, because the
hormone of the interstitial cells has acted during intrauterine life. The
functional independence between the interstitial cells and the seminal
tubules is shown by the fact that if the vasa deferentia are closed the
seminal gland (_i.e._ tubules) degenerates while the interstitial cells do
not. In the embryo the interstitial gland is large, in the adult
proportionately small.

There is complete disagreement between the results of Ancel and Bouin on
the one hand, and those of Shattock and Seligmann on the other, with
regard to the effects of ligature of the vasa deferentia. The latter
authors, as mentioned above, found that after ligature not only the
somatic characters but the testis itself developed normally. The
experiments were performed on Herdwick sheep and domestic fowls. They
state that on examination the testes were found to be normally developed,
and spermatogenesis was in progress. The experiments of Ancel and Bouin
were carried out on rabbits seven to eight weeks old, and consisted in
removing one testis, and ligaturing the vas deferens of the other. About
six months after the operation the testis left _in situ_ was smaller, the
seminal tubules contained few spermatogonia, though Sertoli's cells (cells
on the walls of the tubules to which the true spermatic cells are
attached) were unchanged; while the interstitial cells were enormously
developed, by compensatory hypertrophy in consequence of the removal of
the other testis. At the same time the male instincts and the other
generative organs were unchanged. In a few cases, however, Ancel and Bouin
observed atrophy of the interstitial cells as well as the spermatic cells.
They believe this is due to the nerves supplying the testis being included
in the ligature. This is rather a surprising conclusion in view of the
fact that testicular grafts show active spermatogenesis. It is difficult
to understand why nerve connection should be necessary for the
interstitial cells and not for the spermatic, and, moreover, if the
interstitial cells are really the source of the hormone on which the
somatic characters depend, they must be acting in the grafts in which the
nerve connections have been all severed.

The facts concerning cryptorchidism, that is to say, failure of the
descent of the testes in Mammals, seem to show that the hormone of the
testis is not derived from semen or spermatogenesis, for in the testes
which have remained in the abdomen there is no spermatogenesis, while the
interstitial cells are present, and the animals in some cases exhibit
normal or even excessive sexual instinct, and all the male characteristics
are well marked. It may be remarked, however, in criticism of this
conclusion that the descent of the testes being itself a somatic sexual
character of the male, its failure when the interstitial cells are normal
and the spermatic cells defective, would rather tend to prove that the
defect of the latter is itself the cause of cryptorchidism.

Many investigators have found that the Roentgen rays destroy the spermatic
cells of the testis in Mammals, leaving the cells of Sertoli, the
interstitial tissue, nerves, and vessels uninjured. Tandler and Gross
[Footnote: _Wiener klinische Wochenschrift_, 1907.] found that the antlers
of roebuck were not affected after the testes had been submitted to the
action of the rays, showing that the interstitial cells were sufficient to
maintain the normal condition of the antlers. Simmonds, [Footnote:
_Fortschr. a. d. G. d. Roentgenstr._, xiv., 1909-10.] however, found that
isolated seminal tubules remained, and regeneration took place, and
concludes that both spermatic cells and interstitial cells take part in
producing the testis hormone. The conclusions of two other investigators
have an important bearing on this question--namely, that of Miss Boring
[Footnote: _Biol. Bull._, xxiii. 1912.] that there is no interstitial
tissue in the bird's testis, and that of Miss Lane-Claypon, [Footnote:
_Proc. Roy. Soc._, 1905] that the interstitial cells of the ovary arise
from the germinal epithelium, and are perfectly equipotential with those
which form the ova and Graafian follicles. It seems possible, although no
such suggestion has been made, that the interstitial cells might either
normally or exceptionally give rise to ova and spermatocytes. The
observations of Seligmann and Shattock on the relation of spermatogenesis
to the development of nuptial plumage in drakes probably receive their
explanation from the above facts. Spermatogenesis is not the only source
of the testicular hormone: changes in the secretory activity of the
interstitial cells or spermatocytes are sufficient to account for periodic
development of somatic sex-characters, and the same reasoning applies to
the antlers of stags.


The milk glands in Mammals constitute one of the most remarkable of
secondary sexual characters. Except in their functional relations to the
primary organs, the ovaries, and to the uterus, there is nothing sexual
about them. They are parts of the skin, being nothing more or less than
enormous enlargements of dermal glands, either sebaceous or sudoriparous.
Uterine and mammary functions are generally regarded as essentially female
characteristics, and are included in the popular idea of the sex of woman.
Scientifically, of course, they are not at all necessary or universal
features of the female sex, but are peculiar to the mammalian class of
Vertebrates in which they have been evolved. Milk glands, then, are
somatic sex-characters common to a whole class, instead of being
restricted to a family like the antlers in Cervidae. There is not the
slightest trace or rudiment of them in other classes of Vertebrates, such
as Birds or Reptiles. They are not actually sexual in their nature, since
their function is to supply food for the young, not to play a part in the
relations of the sexes. What is sexual about them is--firstly, that they
are normally fully developed only in the female, rudimentary in the male;
secondly, that their periodical development and functional activity
depends on the changes which take place in the ovary and uterus. Many
investigators have endeavoured to discover the nature of the nexus between
the latter organs and the milk glands.

That this nexus is of the nature of a hormone is generally agreed, and may
be regarded as having been proved in 1874 when Goltz and Ewald [Footnote:
_Pfluegers Archiv,_ ix., 1874.] removed the whole of the lumbo-sacral
portion of the spinal cord of a bitch and found that the mammae in the
animal developed and enlarged in the usual way during pregnancy and
secreted milk normally after parturition. Ribbert [Footnote: _Fortschritte
der Medicin,_ Bd. 7.] in 1898 transplanted a milk gland of a guinea-pig to
the neighbourhood of the ear, and found that its development and function
during pregnancy and at parturition were unaffected. The effective
stimulus, therefore, is not conveyed through the nervous system, but must
be a chemical stimulus passing through the vascular system.

Physiologists, however, are not equally in agreement concerning the source
of the hormone which regulates lactation. Starling and Miss Lane-Claypon
concluded from their experiments on rabbits that the hormone originated in
the foetuses themselves within the pregnant uterus. In virgin rabbits it
is difficult to find the milk glands at all. When found the nipple is
minute and sections through it show the gland to consist of only a few
ducts a few millimetres in length. Five days after impregnation the gland
is about 2 cm. in diameter. Nine days after impregnation the glands have
grown so much that the whole inner surface of the skin of the abdomen is
covered with a thin layer of gland tissue. In six cases by injecting
subcutaneously extracts of foetus tissue Starling and Lane-Claypon
obtained a certain amount of growth of the milk glands. The hormone in the
case of the pregnant rabbit is of course acting continuously for the whole
period of pregnancy, while the artificial injection took place only once
in twenty-four hours, and the amount of hormone it contained may have been
absorbed in a very short time. The amount of growth obtained
experimentally in five weeks was less than that occurring in pregnancy in
nine days. Extracts of uterus, placenta, or ovary produced no growth,
although the ovaries used were taken from rabbits in the middle of
pregnancy. In one experiment ovaries from a pregnant rabbit were implanted
into the peritoneum of a non-pregnant rabbit, but on post-mortem
examination of the latter eleven days later the implanted ovaries were
found to be necrosed and no proliferation of milk gland had taken place.

The conclusions of Starling and Lane-Claypon were confirmed by Foa,
[Footnote: _Archivo d. Fisiologia_, v., 1909.] and by Biedl and
Koenigstein, [Footnote: _Zeitschrift f. exp. Path. und Therap_., 1910.] Foa
states that extracts of foetuses of cows produced swelling of the mammae
in a virgin rabbit.

O'Donoghue, however, concludes from a study of the Marsupial _Dasyurus_
that the stimulus which upon the milk glands proceeds from the corpora
lutea in the ovary. In this animal changes in the pouch occur in
pregnancy, which are doubtless also due to hormone stimulation, but which
we will not consider here. The most important evidence in O'Donoghue's
paper [Footnote: _Quart. Journ. Mic. Sci_., lvii., 1911-12.] is that
development of the milk glands takes place after ovulation not succeeded by
pregnancy; that is to say, when corpora lutea are formed but no fertilised
ova or foetus are present in the uterus. In one case eighteen days after
heat, the milk gland was in a condition resembling that found in the
stages twenty-four and thirty-six hours after parturition. In another
specimen, twenty-one days after heat, the milk glands were still more
advanced, with distended alveoli and enlarged ducts. The alveoli contained
a secretion which was almost certainly milk, O'Donoghue states that the
entire series of growth changes in these animals up to twenty-one days
after heat in identical with that which occurs in normally pregnant

O'Donoghue's conclusion is in agreement with that of Basch,[Footnote:
_Monatesschr. f. Kinderh. V._, No. ix., Dec. 1909.] who states that
implantation of the, ovaries from a pregnant bitch under the skin of the
back of a one-year-old bitch that was not pregnant was followed by
proliferation of the mammary glands of the latter. After six weeks the
glands were considerably enlarged, and after eight weeks they were caused
to secrete milk by the injection of extract of the placenta. It has to be
remembered, however, that the milk glands undergo considerable growth,
especially in the human species, at puberty and at every menstruation, or
at oestrus in animals, which correspond to menstruation. In these cases
there is no question of any influence of the foetus, and experiment has
shown that if the ovaries are removed before puberty, the milk glands nor
the uterus undergo the normal development and menstruation does not occur.
According to Marshall to Jolly [Footnote: _Quart. Journ. Exp. Phys._, i.
and ii., 1906.] the symptoms of oestrus in castrated bitches were found to
result from the implantation of ovaries from other individuals in the
condition of oestrus.

Before considering further the question of the corpora lutea as organs of
internal secretion, we may briefly refer to the origin and structure of
these bodies and of other parts of the mammalian ovary. The mature
follicle containing the ovum differs from that of other Vertebrates in the
fact that it is not completely filled by the ovum and the follicular cells
surrounding it, but there is a cell-free space of large size into which
the ovum covered by follicular cells projects. In the wall of the follicle
two layers are distinguished, the theca externa, which is more fibrous,
and the theca interna, which is more cellular. In the connective tissue
stroma of the ovary between the follicles are scattered, or in some cases
aggregated, epithelioid cells known as the interstitial cells, and it is
stated that the cells of the theca interna are exactly similar to the
interstitial cells. According to Limon [Footnote: _Arch. d'Anat. micr._,
v., 1902.] and Wallart [Footnote: _Arch. f. Gynock_, vi. 271.] the
interstitial cells are actually derived from those of the theca interna of
the follicles. Numbers of ova die without reaching maturity, the
follicular cells degenerate, and the follicle becomes filled with the
cells of the theca interna, which have a resemblance to those of the true
corpus luteum. These degenerate follicles have been termed spurious
corpora lutea, or atretic vesicles. The interstitial cells are the remains
of these atretic vesicles. The true corpora lutea arise from follicles in
which the ova have become mature and from which they have escaped through
the surface of the ovary. As a result of the escape of the ovum and the
contents of the cell-free space, the follicle contracts and the follicular
(so-called granulosa) cells secrete a yellow substance, lutein, and
enlarge. Buds from the theca interna invade the follicle and form the
connective tissue of the corpus luteum.

Somewhat similar processes take place in the ovaries of Teleostean fishes,
as I know from my own observations, but no corpora lutea are formed in
these, although the degenerating follicles in course of absorption
correspond to corpora lutea. The spawning of Fishes, usually annual,
corresponds to ovulation in Mammals, and in the ovary after spawning the
numerous collapsed follicles containing the follicular cells may be seen
in all stages of absorption. [Footnote: Cunningham, 'Ovaries of
Teleosteans.' _Quart. Journ. Mic. Sci._, vol. xl. pt. 1., 1897.] At other
times of the year sections of the ovary show here and there ova which
after developing to a certain stage die and undergo absorption with their

In the higher Mammals (Eutheria) the corpora lutea show a special relation
in their development to the occurrence of pregnancy, that is to say, they
have a different history when ovulation is followed by pregnancy to that
which they have when the ova, from the escape of which they arise, are not
fertilised. When fertilisation occurs the corpus luteum increases in size
during the first part of the period of gestation (four months, or nearly a
half of the whole period in the human species). It then remains without
much change till parturition, after which it shrinks and is absorbed. When
pregnancy does not occur the corpus luteum is formed, but begins to
diminish within ten or twelve days in the human species and is then
gradually absorbed. According to O'Donoghue, in the Marsupial _Dasyurus_
there seems to be no difference either in the development of the milk
glands or of the corpora lutea between the pregnant and the non-pregnant
animal. Sandes [Footnote: _Proc. Lin. Soc._, New South Wales, 1903.]
showed that in the same species the corpora lutea persisted not only
during the whole of pregnancy, which Professor J. P. Hill [Footnote:
_Anat. Anz._, xviii., 1900.] estimates at a little over eight days, but
during the greater part of the period of lactation, which according to the
same authority is about four months. In the specimens of _Dasyurus_
described by O'Donoghue, in which the milk glands developed after
ovulation without ensuing pregnancy, normally developed corpora lutea were
present in the ovary. Of the five females which he mentions, the first
three, one with unfertilised ova in the uteri, two five and six days after
heat, could not have been pregnant, but the other two killed eighteen and
twenty-one days after heat might, since pregnancy lasts only eight days,
have been pregnant, the young having died at parturition or before. To
make certain on this point it would have been necessary to examine the
ovaries and milk glands of females which had been kept separate from a
male the whole time. There is no doubt, however, about the development of
the milk glands in the first three specimens, which were certainly not

It is difficult to reconcile entirely the evidence described by O'Donoghue
from _Dasyurus_, with that obtained from higher Mammals, although on the
whole there is reason to conclude that the corpora lutea have an important
influence on the development of the milk glands. According to Lane-Claypon
and Starling, if the ovaries and uteri are removed from a pregnant rabbit
before the fourteenth day the development of the mammary gland ceases,
retrogression takes place, and no milk appears in the gland. If, on the
other hand, the operation be performed after the fourteenth day, milk
appears within two days after the operation. It is to be concluded from
this that the cause of _secretion_ of milk is the withdrawal of a stimulus
proceeding from ovary or uterus. But O'Donoghue believes that milk is
secreted in _Dasyurus_ when no pregnancy has occurred. Ancel and Bouin
[Footnote: _C. R. Soc. de Biol._, t. lxvii., 1909.] have shown that the
growth of the mammary glands was produced in rabbits by the artificial
rupture of egg follicles and consequent production of corpora lutea: the
growth of the glands continued up to the fourteenth day, after which
regression set in. This shows that the development of the milk glands in
rabbits is due to the corpora lutea. On the other hand, Lane-Claypon and
Starling state that in rabbits the corpora lutea diminish after the first
half of pregnancy, while the growth of the milk glands is many times
greater during the second half than during the first half of the period,
and during the second half the ovaries may be removed entirely without
interfering with the course of pregnancy or the normal development of the
milk glands. It is evident, therefore, that in rabbits, whatever influence
the corpora lutea may have in the first half of pregnancy, they have none
in the second half, and that at this period the essential hormone proceeds
from the developing foetus or foetal placenta. Again, if it is the
withdrawal of a hormone stimulus which changes the milk gland from growth
to secretion, it cannot be the corpora lutea which are exclusively
concerned even in _Dasyurus_, for they persist during lactation, while
secretion begins shortly after parturition.

Gustav Born suggested, and Fraenkel tested the suggestion experimentally,
that the corpus luteum of pregnancy is a gland of internal secretion whose
function is to cause the attachment of the ovum in the uterus and the
normal development of uterus and placenta. Fraenkel found that removal of
both ovaries in rabbits between the first and sixth days after
fertilisation prevented pregnancy, and that the same result followed if
the corpora lutea were merely destroyed _in situ_ by galvano-cautery.
Either process carried out between the eighth and twentieth days of
pregnancy causes abortion.

Lane-Claypon and Starling also found that removal of both ovaries in the
rabbit before the fifteenth day was apt to cause abortion, but at a later
stage the same operation could be performed without interfering with the
course of pregnancy. According to these authors numberless instances prove
that in women double ovariotomy does not necessarily interfere with the
course of pregnancy or the development of the milk glands. Parturition may
take place and be followed by normal lactation. This shows that a hormone
from the corpora lutea is not necessary either to the uterus or the milk
glands, at any rate in the last third of pregnancy, though of course this
does not prove that such a hormone is not necessary for the earlier stages
both of pregnancy and growth of the milk glands.

The results of Steinach, if confirmed, would prove conclusively that the
ovaries and testes produce hormones which determine the development of all
the sexual characters, not merely physical but psychical. He adopts the
view that the interstitial cells or gland are the source of the active
hormone. He claims by transplantation of the gonads in young rats and
guinea-pigs to have feminised males and masculised females. The females
are smaller, and hare finer, softer hair than the males. The testes were
removed and ovaries implanted in young males. The animals so treated grew
less than the merely castrated specimens, and therefore when full-grown
resembled females in size. In the young state both sexes have fine, soft
hair, the feminised males had the same character, like the normal females.
They also developed teats and milk glands like the females, and were
sought and treated as females by the normal males. When the implanted
ovaries are able to resist the influence of their new surroundings, the
female interstitial gland, which Steinach calls the puberty gland,
develops so much that an intensification of the female character takes
place: the animals are smaller than normal females, the milk glands
develop and secrete milk, which can be easily pressed out, and if young
are given to them they suckle them and show all the maternal instincts.

Why the ovary in normal circumstances only when in the gravid condition
calls forth this perfection of femaleness is to be shown in a later
publication. By acting with Roentgen rays on the region where the ovaries
lie, Steinach and his colleague Holzknecht brought about all the symptoms
of pregnancy, development of teats and milk glands, secretion of milk, and
great growth of the uterus in all its layers.

Masculising of females was much more difficult than feminising of males
because the testicular tissue was less resistent, and could not be grafted
so easily. When it succeeded, however, degeneration of the seminal tubules
took place, with increase of the interstitial or Leydig's cells. The
vaginal opening in rats disappeared, partly or completely. The sexual
instincts became male, the animals recognised a female in heat from one
that was not, and attempted to copulate.

Steinach considers that he has proved from results that sex is not fixed
or predetermined but dependent on the puberty gland. By sex here he
obviously means the instincts and somatic characters, for sex in the first
instance, as we have already pointed out, means the difference between
ovary and testis, between ova and spermatozoa. It is difficult to accept
all Steinach's results without confirmation, especially those which show
that the feminised male is more female than the normal female. Such a
conclusion inevitably suggests that the investigator is proving too much.

The subject of the influence of hormones from the gonads is mentioned, but
not fully discussed, in a volume by Dr. Jacques Loeb, entitles _The
Organism as a Whole_. [Footnote: Putnam's Sons, 1916.] Loeb entirely omits
the problem of the _origin_ of somatic sex-characters, and fails to
perceive that the fact that such characters are dependent to a marked
degree on hormones derived from the gonads, together with their relation
to definite habits and functions connected with the behaviour of the sexes
to each other, is proof are these characters are not gametogenic, but were
originally due to external stimulation of particular parts of the soma.


Origin Of Somatic Sex-Characters In Evolution

In his _Mendel's Principles of Heredity_, 1909, Bateson does not discuss
the nature of somatic sex-characters in general, but appears to regard
them as essential sex-features, as male or female respectively. As
mentioned above, he argues from the fact that injury or disease of the
ovaries may lead to the development of male characters in the female, that
the female is heterozygous for sex, and from the supposed fact that
castration of the male leads merely to the non-appearance of male somatic
characters, that the female sex-factor is wanting in the male. He does not
distinguish somatic sex-characters from primary sex-factors, and discusses
certain cases of heredity limited by sex as though they were examples of
the same kind of phenomenon as somatic sex-characters in general. One of
these cases is the crossing by Professor T. B. Wood of a breed of sheep
horned in both sexes with another hornless in both sexes. In the _F1_
generation the males were horned, the females hornless. Here, with regard
to the horned character, both sexes were of the same genetic composition,
_i.e._ heterozygous, or if we represent the possession of horns by _H_,
and their absence by _h_, both sexes were _Hh_. Thus _Hh[male]_ was horned
and _Hh[female]_ was hornless, or, as Bateson expresses it, the horned
character was dominant in males, recessive in females. Bateson offers no
explanation of this, but it obviously suggests that some trace of the
original dimorphism of the sheep in this character was retained in both
horned and hornless breeds. We may suppose that the factor for horns had
disappeared entirely from the hornless sheep by a mutation, but in the
horned breed another mutation had been a weakening of the influence of the
sexual hormones on the development of the character, which, as in all such
cases, is really inherited in both sexes. In the _F1_, when the horned
character in the female is only inherited from one side, the hereditary
tendency is not enough to overcome the influence of the absence of the
testis hormone and presence of the ovarian hormone, and so the horns do
not develop. The Mendelian merely sees a relation of the character to sex,
but overlooks entirely the question of the dimorphism in the original
species from which the domesticated breeds are descended. Similarly, with
regard to cattle where it has been found that hornlessness is dominant or
nearly so in both sexes, no reference is made to the opposite fact that
wild cattle have horns in both sexes and are not dimorphic in this

Bateson proceeds to consider colour-blindness as though its heredity were
of similar kind. He refers to it as a male character latent in the female,
remarks that we should expect that disease or removal of the ovaries might
lead to the occasional appearance of colour-blindness in females. He also
discusses the case of _Abraxas grossulariata_ and its variety
_lacticolor_, and other cases of sex-linked heredity, apparently with the
idea that all such cases are similar to those of sexual dimorphism. _A.
lacticolor_ occurs in nature only in the female sex, and when bred with
_grossulariata_ [male] produces [male]'s and [female]'s all
_grossulariata_, these of course being heterozygous. When the _F1
grossulariata_ [male] was bred with the wild _lacticolor_ [female] it
produced both forms in both sexes, and thus _lacticolor_ [male] was
obtained for the first time. When this _lacticolor_ [male] was bred with
_F1 grossulariata_[female] it produced all the [male]'s _grossulariata_
and all the [female]'s _lacticolor_. Bateson's explanation is that the
female, according to the Mendelian theory of sex, is heterozygous in sex,
the male homozygous and recessive, and that _lacticolor_ is linked with
the female sex-character, _grossulariata_ being repelled by that
character. Thus we have, the _lacticolor_ character being recessive,

lact. male, LL male male x F, gross. female, GL female male
Gametes L male + L male x G male + L female
| |
GL male male LL male female
gross. male lact. female

It will be seen that although in the progeny of this mating all the
_grossulariata_ were males and all the _lacticolor_ females, yet this case
is by no means similar to that of sexual dimorphism in which the
characters are normally always confined to the same sex. For the
_lacticolor_ character in the parent was in the male, while in the
offspring it was in the female. We cannot say here that in the theoretical
factors which are supposed to represent what happens, the _lacticolor_
character is coupled with the female sex-factor, for we find it with the
male sex-character in the _lacticolor_ [male]. It is so coupled only in
the heterozygous _grossulariata_ [female], and at the same time the
_grossulariata_ character is repelled.

According to Doncaster [Footnote: _Determination of Sex_, Camb. Univ.
Press, 1914.] sex-limited, or as it is now proposed to call it sex-linked,
transmission in this case means that the female _grossulariata_ transmits
the character to all her male offspring and to none of the female, while a
heterozygous male _grossulariata_ mated with _lacticolor_ female transmits
the character equally to both sexes: that is to say, the heredity is
completely sex-limited in the female but not at all in the male. This is
evidence that the female produces two kinds of eggs, one male producing
and the other female producing.

With regard to the ordinary form of colour-blindness, Bateson's first
explanation was that it was like the horns in the cross-bred sheep,
dominant in males, recessive in females. About 4 per cent. of males in
European countries are colour-blind, but less than 1/2 per cent. of
females. Affected males may transmit the defect to their sons but not to
their daughters: but daughters of affected persons transmit the defect
frequently to their sons. Bateson gives [Footnote: _Mendel's Principles of
Heredity_, 1909.] a scheme of the transmission, but corrects this in a
note stating that colour-blindness does not descend from father to son,
unless the defect was introduced by the normal sighted mother also, _i.e._
was carried by her as a recessive. The fact that unaffected males do not
transmit the defect shows, according to Bateson, that it is due to the
addition of a factor to the normal, not to omission of a factor.

According to later researches as quoted by Doncaster, colour-blindness is
due to the loss of some factor which is present in the normal individual.
The normal male is heterozygous for this normal factor. If we denote the
presence of the normal factor by _N_ and its absence or recessive by _n_,
then the male is _Nn_, while the female is homozygous or _NN_. But in
addition to this it is the male in this case which is heterozygous
for sex, and _n_ goes to the male-producing sperms, _N_ to the
female-producing. Thus in the mating of normal man with normal woman the
transmission is as follows:--

Nn (male) x NN (female)
Gametes n (male) + N (female) x N + N

n (male) + N N (female) + N
| |
Nn (male) NN (female)

That is all offspring normal, but the males again heterozygous.

An affected male has the constitution _nn_, and if he marries a normal
woman the descent is as follows:--

nn (male) x NN (female)
Gametes n (male) + n (female) x N + N

n (male) + N N (female) + N
| |
nN (male) nN (female)

When a normal male is mated with a heterozygous _nN_ female we get

nN (male) x nN (female)
Gametes n (male) + N (female) x n + N
| | | |
nn (male) nN (male) nN (female) NN (female)

that is, half the sons are normal and half colour-blind, while half the
females are homozygous and normal, and the other half heterozygous and

T. H. Morgan [Footnote: _A Critique of the Theory of Evolution._] has
observed a number of cases of sex-linked inheritance in the mutations
which occurred in his cultures of _Drosophila_. The eye of the wild
original fly is red, one of the mutants has a white eye, _i.e._ the red
colour and its factor are absent. When a white-eyed male is mated to a
red-eyed female all the offspring have red eyes. If these are bred _inter
se_, there are, as in ordinary Mendelian cases, three red-eyed to one
white-eyed in the _F2_ generation, but white eyes occur only in the males,
in other wards half the males are white-eyed. On the other hand, when a
white-eyed _female_ is mated to a red-eyed male all the daughters have red
eyes, and all the sons white eyes. This has been termed crisscross
inheritance. If these are bred together the result in _F2_ is equal
numbers of red-eyed and white-eyed females, and equal numbers of red-eyed
and white-eyed males. The ration of dominant to recessive is 2 to 2
instead of the usual Mendelian ration of 3 to 1.

According to Morgan the interpretation is as follows: In the nucleus
of the female gametocytes there are two _X_ chromosomes related to sex,
in those of the male there is one _X_ chromosome and one _Y_ chromosome
of slightly different shape. The factor for red eye occurs in the
sex-chromosomes, that is to say, according to this theory, the
sex-chromosome does not merely determine sex but carries other factors
as well, and this fact is the explanation of sex-linked inheritance. The
factor for red eye then is present in both _X_ chromosomes of the wild
female, absent from both _X_ and _Y_ chromosomes of the white-eyed male.
The gametes of the female each carry one _X_ red chromosome, of those of
the male half carry an _X_ white chromosome, and half the _Y_ white
chromosome. The fertilised female ova therefore carry an _X_ red
chromosome + an _X_ white chromosome, the male producing ova one _X_ red
chromosome and one _Y_ white chromosome. They are all therefore red-eyed,
but heterozygous--that is, the red eye is due to one red-eye factor, not
two. When the _F1_ are bred together, half the female gametes carry one
_X_ red chromosome, the other half one _X_ white chromosome; half the male
gametes carry one _X_ red chromosome, the other half one _Y_ white
chromosome. The fertilisations are therefore one _X_ red _X_ red, one _X_
red _X_ white, one _X_ red _Y_ white, and one _X_ white _Y_ white. These
last are the white-eyed males. The two different crosses are represented
diagrammatically below, the dark rod representing the _X_ red chromosome,
the clear rod the _X_ white chromosome, and the bent clear rod the _Y_
white chromosome.

According to Morgan, the heredity of colour-blindness in man is to be
explained exactly in the same way as that of white eye in _Drosophila_.
A colour-blind man married to a normal (homozygous) woman transmits the
peculiarity to half his grandsons and to none of his grand-daughters.
Colour-blind women are rare, but in the few cases known where such women
have married normal husbands the defect has appeared only in the sons, as
in the second of the diagrams below.

Parents Red-eyed male White-eyed female

F1 Red-eyed male Red-eyed female

F2 Red-eyed male Red-eyed male Red-eyed female White-eyed female
Homozygous. Heterozygous. Heterozygous. Homozygous.

White-eyed male Red-eyed female

F1 Red-eyed male White-eyed female

F2 White-eyed male Red-eyed male White-eyed female Red-eyed female
Homozygous. Heterozygous. Homozygous. Heterozygous.

It must be explained that according to this theory the normal male is
always heterozygous, because the _Y_ chromosome never carries any other
factor except that for sex; it is thus of no more importance than the
absence of an _X_ chromosome which occurs in those cases where the male
has one sex-chromosome and the female two. According to the researches of
von Winiwarter [Footnote: 'Spermatogenese humaine,' _Arch. de Biol._,
xxvii., 1912.] on spermatogenesis in man, the latter is actually the case
in the human species. This investigator found that there were 48
chromosomes in the female cell, 47 in the male; after the reduction
divisions the unfertilised ova had 24 chromosomes, half the spermatids 24
and half 23, so that sex is determined in man by the spermatozoon.

Morgan believes that the heredity of haemophilia (the constitutional
defect which prevents the spontaneous cessation of bleeding) follows the
same scheme, and also at least some forms of stationary night-blindness--
that is, the inability to see in twilight.

We may mention a few other in animals, referring the reader for a fuller
account to the works cited. One example in the barred character of the
feathers in the breed of fowls called Plymouth Rock. In this the female is
heterozygous for sex as in _Abraxas grossulariata_, and the barred
character is sex-linked. When a barred hen is crossed with an unbarred
cock all the male offspring are barred, all the females plain. On the
other hand, if a barred cock is crossed with an unbarred hen, the barred
character appears in all the offspring, both and females. The female thus
transmits the character only to her sons. If we represent the barred
character by _B_, and its absence by _b_, we can represent the heredity as


B female b male X b male b male

Bb male bb female

Barred male. Unbarred female.
Heterozygous. Homozygous.

B male B male X b female b male

B male b female b male b male

Barred female. Barred male.
Heterozygous. Heterozygous.]

This case is thus exactly similar to that of _Abraxas grossulariata_ and
_A. lacticolor_. The barred character like _grossulariata_ is dominant,
the unbarred recessive, and to explain the results it is necessary to
assume that the female is not only heterozygous for the barred character,
but also for sex, with the female sex-factor dominant. The recessive
character in this case is linked to the female sex chromosome, or,
as Bateson described it, the dominant character is repelled by the
sex-factor. We may make a diagram of the kind given by Morgan if we use
a rod of different shape for the female-producing sex-chromosome, and use
the black rod for the dominant character:--

BARRED female x unbarred male
BX uY uX uX
| \/ |
| /\ |
BX uX uY uX
BARRED male unbarred female
Heterozygous Homozygous

BARRED male x unbarred female
| \/ |
| /\ |
BARRED male BARRED female
Heterozygous Heterozygous

Another case is that of tortoise-shell, _i.e._ black and yellow cats. The
tortoise-shell with very rare exceptions is female, the corresponding male
being yellow, without any black colour. Doncaster found that a yellow male
mated to a black female produced black male offspring and tortoise-shell
females. When a black male is mated to a yellow female, the female kittens
are tortoise-shell as before, but the males yellow. The Mendelian
hypothesis which explains these results is that the male is always
heterozygous, or has only one colour factor whether yellow or black, and
transmits these colours only to his daughters, while the female has two
colour factors, either _BB_, _YY_, or _BY_. Thus the crosses are:--

YELLOW male x BLACK female
YO male BB female
| \/ |
| /\ |
YB female BO male
Tortoise-shell female BLACK male

BLACK male x YELLOW female
BO male YY female
| \/ |
| /\ |
BY female YO male
Tortoise-shell female YELLOW male

The sex 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.


It is obvious from the above facts that however interesting and important
sex-linked heredity may be, it is not the same thing as the heredity of
secondary sexual characters, and does not in the least explain sexual
dimorphism. In the first place, the term sex-linked does not mean
occurring always exclusively in one sex, but the direct contrary--
transmitted by one sex to the opposite sex--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
sexual 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 sex-linked characters, of which examples have been given above,
have originated in this way, and that their relation to sex 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 sex-chromosome.
Morgan, however, also states that a case of true sexual 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
assertion 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 Sex_ [Footnote: Camb.
Univ. 1914, p. 99.] in which he remarks: 'It follows that the secondary
sexual 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 sexes is a question already
mentioned, but it is obvious that in each individual the somatic sexual
characters proper to its species are present potentially in its
constitution 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 sex-characters and hormones produced by the
reproductive organs exists, the characters are inherited by both sexes. In
one sex they are fully developed, in the other rudimentary or wanting. But
the sex, 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 sexual 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 sexual life of the individual, the internal relation in the
fact that their development is affected by the sexual 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 assumed too much importance in recent biological research. No
increase in the number of facts or experimental results of a particular
class 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 butting 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 quantity 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

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 sexual character does not
develop until the time of puberty, 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
constitutes 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
interstitial 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

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 sexual characters,
while at the same time explaining the adaptive relation of these
characters or organs to the sexual 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 sexual dimorphism, and to
supersede Darwin's complicated theory of sexual selection. The possibility
of a Lamarckian explanation he does not even mention. He would doubtless
assume 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 sexual instincts, themselves dependent on
the testicular hormone, which develop sexual jealousy and rivalry, and the
Ruminants fight by butting 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 horny 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 Japanese Tosa-fowls,
[Footnote: 'Observations and Experiments on Japanese Long-tailed Fowls,'
_Proc. Zool. Soc._, 1903.] which is a modification of a secondary sexual
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 Japan, that the Japanese 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 cocks, 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 horny tubular sheath extending up the
base of the feather for about one inch. When growth ceases this sheath is
shed. In cock 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 cock 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 cock 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 cock 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 cocks A and B, I commenced early in March 1903
to pull and stroke the feathers of the left side only in cock 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 Japanese,
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 sexual characters exist which cannot be said to have a
use or function. For example, the comb and wattles of _Gallus_ are
sexually dimorphic, being in the original species larger in the cock 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 cocks 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.


Mammalian Sexual Characters
Evidence Opposed To The Hormone Theory

Perhaps the most remarkable of all somatic sexual characters are those
which are almost universal in the whole class of Mammalia, the mammary
glands in the female, the scrotum 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
invagination 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
invagination, 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 sexual characters
there is no difference between the male and female in the heredity of the
organs. The zygote therefore, whether the sex 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 sex-chromosomes, and must be present in
every zygote. All the cells of the body, assuming that somatic segregation
does not occur, must possess the same chromosomes as the zygote from which
it developed, and whether the sex 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 bitches, 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 assimilative, 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 assumed 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 association 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 constitute 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 passed 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, passed through
the follicle cells, and it is probable that these cells were not entirely
passive, 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 pronounced 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


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