Hildebrand, have paid further attention to the subject, but it has
been especially studied in a most thorough manner by Hermann
Müller[215]. He looked at the subject from more than one point of
view, and showed by direct observation the species of insects which
effect cross-fertilization in various species of our native flowers:
he also studied the structure of insects in relation to that of
flowers, and attempted to establish the mutual adaptations which
exist between them. In this way he succeeded in throwing much light
upon the process of transformation in many species of flowers, and in
proving that certain insects, although unconsciously, are, as it
were, breeders of certain forms of flowers. He not only distinguished
the disagreeably smelling, generally inconspicuous flowers
(‘Ekelblumen’) produced by Diptera which live on putrid substances,
and the flowers which are produced by butterflies; but he also
distinguished the flowers bred by saw-flies, by Fossoria, and by
bees. He even believes that in certain cases (_Viola calcarata_) he
can prove that a flower which owed its original form to being bred by
bees, was afterwards adapted to cross-fertilization by butterflies,
when it had migrated into an Alpine region where the latter insects
are far more abundant than the former.
Although there must of course be much that is hypothetical in the
interpretations of the different parts of flowers offered by Hermann
Müller, the majority of these explanations are certainly correct, and
it is of the greatest interest to be able to recognise the adaptive
character of details, even when apparently unimportant, in the
structure and colours of flowers.
Sachs has offered a very convincing explanation as to the meaning of
leaf-veining, and of its significance in relation to the functions of
leaves[216]. He shows that the venation of a leaf is in every case
exactly adapted for the fulfilment of its purpose. It has, in the first
place, to conduct the nutrient fluid in both directions, and in the
second place to support the thin layers of assimilating chlorophyll
cells, and to stretch them out so as to expose as large a surface as
possible to the light; lastly, it has to toughen the leaf as a
protection against being torn. He shows in a very convincing manner
that the whole diversity of leaf venation can be understood from these
three principles. Here, again, we meet with purposeful arrangements in
a class of structures in which it was formerly thought that there was
only a chaos of accidental forms, or, as it were, the mere sport of
nature with form.
Appendix IV. On the supposed transmission of acquired characters[217].
When I previously maintained that the proofs of the transmission of
artificially produced diseases are inconclusive, I had in mind the only
experiments which, as far as I am aware, can be adduced in favour of
the transmission of acquired characters; viz. the experiments of
Brown-Séquard[218] on guinea-pigs. It is well known that he produced
artificial epilepsy in these animals by dividing certain parts of the
central and also the peripheral nervous system. The descendants of the
animals which acquired epilepsy sometimes inherited the disease of
their parents.
These experiments have been since repeated by Obersteiner[219], who has
described them in a very exact and entirely unprejudiced manner. The
fact itself cannot be doubted: it is certain that some of the
descendants of animals in which epilepsy has been artificially
produced, have also themselves suffered from epilepsy in consequence of
the disease of their parents. This fact may be accepted as proved, but
in my opinion we have no right to conclude from it that acquired
characters can be transmitted. Epilepsy is not a morphological
character; it is a disease. We could only speak of the transmission of
a morphological character, if a certain morphological change which was
the cause of epilepsy had been produced by the nervous lesion, and if a
similar change had re-appeared in the offspring, and had produced in
them also the symptoms of epilepsy. But that this really occurs is
utterly unproved; and is even highly improbable. It has only been
proved that many descendants of artificially epileptic parents are
small, weakly, and very soon die; and that others are paralysed in
various parts of the body, i. e. in one or both of the posterior or
anterior extremities; while others again exhibit trophic paralysis of
the cornea leading to inflammation and the formation of pus. In
addition to these symptoms, the descendants in very rare cases exhibit
upon the application of certain stimuli to the skin, a tendency towards
those tonic and clonic convulsions together with loss of consciousness
which constitute the features of an epileptic attack. Out of thirty-two
descendants of epileptic parents only two exhibited such symptoms, both
of them being very weakly, and dying at an early age.
These experiments, although very interesting, do not enable us to
assert that a distinct morphological change is transmitted to the
offspring after having been artificially induced in the parents. The
injury caused by the division of a nerve is not transmitted, and the
part of the brain corresponding to that which was removed from the
parent is not absent from the offspring. The symptoms of a disease
are undoubtedly transmitted, but the cause of the disease in the
offspring is the real question which requires solution. The symptoms
of epilepsy are by no means invariably transmitted; they are in fact
absent from the great majority of cases, and the very small
proportion in which they do occur, exhibit the symptoms of other
diseases in addition to those of epilepsy. The offspring are either
quite healthy (thirteen out of thirty cases) or they suffer from
disturbances of the nervous system, such as the above-mentioned motor
and trophic paralysis,—symptoms which are not characteristic of
epilepsy: however in some of the latter epilepsy is also present.
If therefore we wish to express the matter correctly we must not state
that epilepsy is transmitted to the offspring, but we must express the
facts in the following manner:—animals which have been rendered
epileptic by artificial means, transmit to some of their offspring a
tendency to suffer from various nervous diseases, viz. from motor
paralysis, to a less degree from sensory, and to a high degree from
trophic paralysis; in rare cases, when the symptoms of paralysis are
very marked, epilepsy is also transmitted.
If we now remember that a considerable number of diseases are already
known to be caused by the presence of living organisms in the body, and
that these diseases may be transmitted from one organism to another in
the form of germs, ought we not to conclude from the above-mentioned
facts, that the symptoms are due to an unknown microbe which finds its
nutritive medium in the nervous tissues, rather than to suppose that
they are due to morphological changes, such as a modification of the
histological or molecular structure of certain parts of the nervous
system? At all events, it would be more difficult to understand the
transmission of such a structural change, than the passage of a
bacillus into the sperm- or germ-cell of the parent. There is no
ascertained fact which supports the former assumption, but it is very
probable that the transmission of syphilis, small-pox and
tuberculosis[220] is to be explained by the latter method, although the
bacilli have not yet been detected in the reproductive cells.
Furthermore, this method of transmission has been rigidly proved in the
case of the muscardine disease of the silkworm. At all events we can
understand in this way how it happened that the offspring of
artificially epileptic guinea-pigs were affected with various forms of
nervous disease, a fact which would be quite unintelligible if we
assume the occurrence of a true hereditary transmission of a
morphological character, such as a pathological change in the structure
of some nervous centre.
The manner in which artificial epilepsy becomes manifest after the
operation, is also in favour of the explanation offered above. In the
first place epilepsy does not result from any one single injury to the
nervous system, but it may follow from a variety of different injuries.
Brown-Séquard produced it by removing a portion of the grey matter of
the brain, and by dividing the spinal cord, although the disease also
resulted from a transverse section through half of the latter organ, or
from the section of its anterior or posterior columns alone, or from
simply puncturing its substance. The most striking effects appeared to
follow when the spinal cord was injured in the region between the
eighth dorsal and the second lumbar vertebrae, although the results
were sometimes also produced by the injury of other parts. Epilepsy
also followed the division of the sciatic nerve, the internal
popliteal, and the posterior roots of all nerves which pass to the
legs. The disease never appears at once, but only after the lapse of
some days or weeks, and, according to Brown-Séquard, it is impossible
to conclude that the disease will not follow the operation until after
six or eight weeks have passed without an epileptic attack. Obersteiner
did not witness in any case the first symptoms of the disease for
several days after the division of the sciatic nerve. After the
operation, sensibility decreases over a certain area on the head and
neck, on the same side as the injury. If the animal be pinched in this
region (which is called the epileptic area, ‘zone epileptogène’) it
curves itself round towards the injured side, and violent scratching
movements are made with the hind leg of the same side. After the lapse
of several days or even weeks, these scratching movements which result
from pinching in the above-mentioned area, form the beginning of a
complete epileptic attack. Hence the changes immediately produced by
the division of a nerve are obviously not the direct cause of epilepsy,
but they only form the beginning of a pathological process which is
conducted in a centripetal direction from the nerve to some centre
which is apparently situated in the pons and medulla oblongata,
although, according to others[221], it is placed in the cortex of the
cerebrum. Nothnagel[222] considers that certain changes, the nature of
which is still entirely unknown, but which may be histological or
perhaps solely molecular in character, must be produced, leading to an
increased irritability of the grey matter of the centres concerned.
Nothnagel thinks it possible or even probable that in those cases in
which the division of nerves is followed by epilepsy, a neuritis
ascendens—an inflammation passing along the nerves in a central
direction—is the cause of the changes suggested by him in the epileptic
centre. All our knowledge of bacteria and of the pathological processes
induced by them, seems to indicate that such a neuritis ascendens, as
is assumed by Nothnagel, would render important support to the
hypothesis that the artificial epilepsy is due to infection. But when
we further consider that the offspring of artificially epileptic
animals may themselves become epileptic, although in most cases they
suffer from a variety of other nervous diseases (in consequence of
trophic paralysis), I hardly see how the facts can be rendered
intelligible except by supposing that in these cases of what I may call
traumatic epilepsy, we are dealing with an infectious disease caused by
microbes which find their nutritive medium in the nervous tissues, and
which bring about the transmission of the disease to the offspring by
penetrating the ovum or the spermatozoon.
Obersteiner found that the offspring were more frequently diseased when
the mother was epileptic, rather than the father. This is readily
intelligible when we remember that the ovum contains an immensely
larger amount of substance than the spermatozoon, and can therefore be
more frequently infected by microbes and can contain a greater number
of them.
Of course, I do not mean to assert that epilepsy always depends upon
infection, or upon the presence of microbes in the nervous tissues.
Westphal produced epilepsy in guinea-pigs by striking them once or
twice sharply upon the head: the epileptic attack took place
immediately and was afterwards repeated. It is obvious that the
presence of microbes can have nothing to do with such an attack, but
the shock alone must have caused morphological and functional changes
in the centres of the pons and medulla oblongata, identical with those
produced by microbes in the other cases. Nothnagel also distinctly
expresses the opinion that epilepsy ‘does not depend upon one uniform
and invariable histological change, but that the symptoms which
constitute the disease may in all probability be caused by various
anatomical alterations, provided that they take place in parts of the
pons and medulla which are morphologically and physiologically
equivalent[223].’ Just as a sensory nerve produces the sensation of
pain under various stimuli, such as pressure, inflammation, infection
with the poison of malaria, etc., so various stimuli might cause the
nervous centres concerned to develope the convulsive attack which,
together with its after-effects, we call epilepsy. In Westphal’s case,
such a stimulus would be given by a powerful mechanical shock, in
Brown-Séquard’s experiments, by the penetration of microbes.
However, quite apart from the question of the validity of this
suggestion, we can form no conception as to the means by which an
acquired morphological change in certain nerve-cells—a change which is
not anatomical, and probably not even microscopical, but purely
molecular in nature—can be possibly transferred to the germ-cells: for
this ought to take place in such a manner as to produce in their minute
molecular structure a change which, after fertilization and development
into a new individual, would lead to the reproduction of the same
epileptogenic molecular structure of the nervous elements in the grey
centres of the pons and medulla oblongata as was acquired by the
parent. How is it possible for all this to happen? What substance could
cause such a change in the resulting offspring after having been
transferred to the egg or sperm-cell? Perhaps Darwin’s gemmules may be
suggested; but each gemmule represents a cell, while here we have to do
with molecules or groups of molecules. We must therefore assume the
existence of a special gemmule for each group of molecules, and thus
the innumerable gemmules of Darwin’s theory must be imagined as
increased by many millions. But if we suppose that the theory of
pangenesis is right, and that the gemmules really circulate in the
body, accompanied by other gemmules from the diseased parts of the
brain, and that some of these latter pass into the germ-cells of the
individual,—to what strange results would the further pursuit of this
idea lead? What an incomprehensible number of gemmules must meet in a
single sperm- or germ-cell, if each of them is to contain a
representative of every molecule or group of molecules which has formed
part of the body at each period of ontogeny. And yet such is the
unavoidable consequence of the supposition that acquired molecular
states of certain groups of cells can be transmitted to the offspring.
This supposition could only be rendered intelligible by some theory of
_preformation_[224], such as Darwin’s pangenesis; for the latter theory
certainly belongs to this category. We must assume that each single
part of the body at each developmental stage is, from the first,
represented in the germ-cell as distinct particles of matter, which
will reproduce each part of the body at its appropriate stage as their
turn for development arrives.
I will only briefly indicate some of the inevitable contradictions in
which we are involved by such a theory. One and the same part of the
body must be represented in the germ- or sperm-cell by many groups of
gemmules, each group corresponding to a different stage of development;
for if each part gives off gemmules, which ultimately reproduce the
part in the offspring, it is clear that special gemmules must be given
off for each stage in the development of the part, in order to
reproduce that identical stage. And Darwin quite logically accepts this
conclusion in his provisional hypothesis of pangenesis. But the
ontogeny of each part is in reality continuous, and is not composed of
distinct and separate stages. We imagine these stages as existing in
the continuous course of ontogeny; for here, as in all departments of
nature, we make artificial divisions in order to render possible a
general conception, and to gain fixed points in the continuous changes
of form which have in reality occurred. Just as we distinguish a
sequence of species in the course of phylogeny, although only a gradual
transition, not traversed by sharp lines of demarcation, has taken
place, so also we speak of the stages of ontogeny, although we can
never point out where any stage ends and another begins. To imagine
that each single stage of a part is present in the germ, as a distinct
group of gemmules, seems to me to be a childish idea, comparable to the
belief that the skull of the young St. Laurence exists at Madrid, while
the adult skull is to be found in Rome.
We are necessarily driven to such conceptions if we assume that the
transmission of acquired characters takes place. A theory of
preformation alone affords the possibility of an explanation: an
epigenetic theory is utterly unable to render any assistance in
reaching an interpretation. According to the latter theory, the germ
does not contain any preformed gemmules, but it possesses, as a whole,
such a chemical and molecular constitution that under certain
circumstances, a second stage is produced from it. For example, the two
first segmentation spheres may be regarded as such a second stage;
these again possess such a constitution that a certain third stage, and
no other, can arise from them, forming the four first segmentation
spheres. At each of these stages the spheres produced are peculiar to a
distinct species and a distinct individual. From the third stage a
fourth arises, and so on, until the embryo is developed, and still
later the mature animal which can reproduce itself. No one of the parts
of such an animal was originally present as distinct parts in the egg
from which it was developed, however minute we may imagine these parts
to be. If now an inherited peculiarity shows itself in any organ of the
mature animal, this will be the consequence of the preceding
developmental stages, and if we were able to investigate the molecular
structure of all these stages as far back as the egg-cell, we should
trace back to the latter some minute difference of molecular
constitution which would distinguish it from any other egg-cell of the
same species, and was destined to be the cause of the subsequent
appearance of the peculiarity in the mature animal. It is only by the
aid of some such hypothesis that we can conceive the cause of
hereditary individual differences and the tendencies towards hereditary
diseases. Hereditary epilepsy would be intelligible in this way, that
is, when the disease is congenital and not due to the presence of
microbes, as is presumably the case with artificially induced epilepsy.
The question now arises as to whether we can conceive the communication
of such traumatic and therefore acquired epilepsy to the germ-cells.
This is obviously impossible under the epigenetic theory of development
described above. In what way can the germ-cells be affected by
molecular or histological changes in the pons varolii and medulla
oblongata? Even if we assume, for the sake of argument, that the
central nervous system exercises trophic influences upon the
germ-cells, and that such influences may consist of something more than
variations in nutritive conditions, and may even include the power of
altering the molecular constitution of the germ-plasm in spite of its
usual stability; even if we concede these suppositions, how is it
conceivable that the changes produced would be of the exact nature and
in the exact direction necessary in order to confer upon the germ-plasm
the molecular structure of the first ontogenetic stage of an epileptic
individual? How can the last ontogenetic stage of the ganglion cells in
the pons and medulla of such an individual, stamp upon the germ-plasm
in the germ-cells of the same animal—not indeed the peculiar structure
of the stage itself—but such a molecular constitution as will ensure
the ultimate appearance of epilepsy in the offspring? The theory of
epigenesis does not admit that the parts of the full-grown individual
are contained in the germ as preformed material particles, and
therefore this theory cannot allow that anything is added to the
germ-plasm; but in accepting the above-made supposition, we are
compelled to assume that the molecular structure of the whole of the
germ-plasm is changed to a slight extent.
Nägeli is quite right in maintaining that the solid protoplasm alone,
as opposed to the fluid part, i.e. that part of the protoplasm which
has passed into solution, can act as the bearer of hereditary
tendencies. This appears to be undoubtedly proved by the fact that the
amount of material provided by the male parent for the development of
an embryo is in almost all animals far smaller than the amount provided
by the female parent.
In Mammalia the share contributed by the father probably only forms
about one hundred-billionth part of that contributed by the mother, and
yet nevertheless the influence of the former in heredity is on an
average equal to that exerted by the latter[225]. Now, from the point
of view of epigenesis, no molecule of the brain of an epileptic animal
can reach the germ-cell except in a state of solution, and therefore no
direct increase in the germ-plasm can be referred to such molecules,
quite apart from the fact that such addition, even if possible, could
not be of any value, because the last stage of the epileptic tendency
must be represented in the nerve-cells and nerve-fibres of the diseased
brain, while the first stage ought to be represented in the germ-cell.
It may be safely asserted that according to the theory of epigenesis
the germ-cells cannot be influenced except as regards their nutrition.
Nutritive changes may be imagined to occur through the varying trophic
influence of the nervous system upon the sexual organs, but the
structure of the germ-plasm cannot be altered by mere nutritive
changes, or at all events it cannot be altered in that distinct and
definite direction which is required by the supposed transmission of
acquired epilepsy.
Thus the transmission of artificially produced epilepsy can neither be
explained upon the epigenetic theory, nor upon the theory of
preformation; it can only be rendered intelligible if we suppose that
the appearance of the disease in the offspring depends upon the
introduction and presence of living germs, viz. of microbes. The
supposed transmission of this artificially produced disease is the only
definite instance which has been hitherto brought forward in support of
the transmission of acquired characters. I believe that I have shown
that such support is deceptive, not because there is any uncertainty
about the fact of the transmission itself, but because it is a
transmission which cannot depend upon heredity, and is in all
probability due to infection.