It may now be profitable to take up the causes leading to the small
degree of degeneration found in Chologaster, the degenerations of the
eye in Amblyopsis, Typhlichthys and Troglichthys to a mere vestige,
together with the total disappearance of some of the accessory
structures of the eye, as the muscles.
In the outset of this consideration we must guard against the almost
universal supposition that animals depending on their eyes for food are
or have been colonizing caves, or that the blind forms are the results
of catastrophes that have happened to eyed forms depending on their
eyesight for their existence. This idea, so prevalent, vitiates nearly
everything that has been written on the degeneration of the eyes of
cave animals.
Another word of warning ought perhaps to be added. The process of
degeneration found in the Amblyopsidæ need not necessarily be expected
to be identical with the degeneration of the same organs in another
group of animals, and, however much the conditions in one group may
illuminate the conditions in another, cross-country conclusions must be
guarded against.
The degeneration of organs ontogenetically and phylogenetically has
received a variety of explanations:
1. The organ diminishes with disuse (ontogenetic degeneration--Lamarck,
Roux, Packard), and the effect of this disuse appears to some extent in
the next generation (phylogenetic degeneration--Lamarck, Roux, Packard,
Kohl).
2. Through a condition of panmixia the general average maintained
by selection is reduced to the birth mean in one generation
(ontogenetic--Romanes, Lankester, Lloyd Morgan, Weismann) to
the greatest possible degeneration in succeeding generations
(phylogenetic--Weismann), or but little below the birth average of the
first generation (Weismann’s later view, Romanes, Morgan, Lankester).
3. Through natural selection (reversed), the struggle of persons,
the organ may be caused to degenerate either (A) by the migration
of persons with highly developed eyes from the colony living in the
dark (Lankester), or (B) through economy of weight and nutriment or
liability to injury (phylogenetic purely--Darwin, Romanes).
4. Through the struggle of parts for room or for food an unused organ
in the individual may be crowded (ontogenetic--Roux). This may lead
to the development of the used organ as against the disused through a
compensation of growth (Goethe, Saint-Hilaire, Roux); this ontogenetic
result becomes phylogenetic through transmission of the acquired
character (Roux), or is in its very nature phyloblastic (Kohl).
5. Through the struggle between soma and germ to produce the maximum
of efficiency of the former with the minimum expenditure to the latter
(ontogenetic and phylogenetic--Lendenfeld).
6. Through germinal selection, the struggle of the representatives of
organs in the germ (ontogenetic and phylogenetic--Weismann).
The idea of ontogenetic degeneration is intimately bound up with the
idea of phylogenetic degeneration. Logically we ought to consider first
the causes of individual degeneration, and then the processes or causes
that led to the transmission of this. Practically it is impossible to
do so, because many of the explanations are general. Only No. 4 of
the above may be taken in the ontogenetic sense purely, though it was
certainly also meant to explain phylogenetic degeneration. In many of
the explanations of particular cases of degeneration more than one
of the above principles are invoked, though only one was meant to be
used. In most cases, however, the discussions of degeneration have
been in general terms, without direct bearing on any specific instance
of degeneration in all its details. It must be evident that such
discussions can only by accident lead to right results.
By the Lamarckian ontogenetic degeneration is considered the result
of lack of use and consequent diminished blood supply. The results of
the diminution caused by the lack of use during one generation are
transmitted in some degree to the next generation, which thus starts at
a lower level. A continuation of the same conditions leads finally to
the great reduction and ultimate disappearance of an organ.
No one, so far as I am aware, has succeeded in accounting for
the degeneration of the eye by means of this view. Packard’s[J]
explanations are evidently a mixture of Lamarckism and Darwinism.
[J] _American Naturalist_, September, 1894, vol. xxviii, p. 727.
Packard says: “When a number, few or many, of normal-seeing animals
enter a totally dark cave or stream, some may become blind sooner than
others,” some having the eye slightly modified by disuse, while others
may have in addition physical or functional defects, especially in the
optic nerves and ganglia. “The result of the union of such individuals
and adaptation to their Stygian life would be broods of young, some
with vision unimpaired, others with a tendency to blindness, while
in others there would be noticed the first steps in degeneration of
nervous power and nervous tissue.” Packard evidently had invertebrates
in mind. He clearly admits the cessation of selection or panmixia in
that those born with defects may breed with the others. He supposes
that the blind fauna may have arisen in but few or several generations,
a supposition that may be applicable to invertebrates, but certainly is
not to vertebrates. At first those becoming so modified that they can
do without the use of their eyes would greatly preponderate over those
‘congenitally blind.’ “So all the while the process of adaptation was
going on, the antennæ and other tactile organs increasing in length
and in the delicacy of structures, while the eyes were meanwhile
diminishing in strength of vision and their nervous force giving
out, after a few generations--perhaps only two or three--the number
of congenitally blind would increase, and eventually they would, in
their turn, preponderate in numbers.” Packard seems here to admit the
principle of degeneration as the result of compensation of growth, the
nervous force of the eye giving out with the increase of the tactile
and olfactory organs. It is somewhat doubtful in what sense the term
‘congenitally blind’ is used, but it probably means born blind as
the result of transmitted disuse, rather than blind as the result of
fortuitous variation. The effects of disuse are thus supposed, through
their transmission, to have given rise to generations of blind animals.
The continued degeneration is not discussed.
Romanes maintained that the beginning of degeneration was due to
cessation of selection, and continued degeneration to the reversal
of selection and final failing of the power of heredity. Selection
he supposed to be reversed because the organ no longer of use “is
absorbing nutriment, causing weight, occupying space and so on,
uselessly. Hence, even if it be not also a source of actual danger,
economy of growth will determine a reversal of selection against an
organ which is now not only useless, but deleterious.” This process
will continue until the organ becomes rudimentary and finally
disappears.
Roux[K] attempted chiefly to explain degeneration in the individual.
Degeneration is looked upon as the result of a struggle among the
parts for (_a_) room and (_b_) food. Without doubting that both these
principles are active agents in degeneration, it may be seriously
doubted whether they are effective in the degeneration of the eyes in
question. Certainly there can be no question of a struggle for room,
for the position and room formerly occupied by the eye is now filled
with fat, which can not have been operative against the eye. The
presence of this large fat mass in the former location of the eye, the
large reserve fat mass in the body, the uniformly good condition of
the fish and the low vitality, which enables them to live for months
without visible food, all argue against the possibility that the
struggle for food between parts was an active agent in the degeneration
of the eyes.
[K] Gesammelte Abhandlungen, 1895.
Kohl[L] considers that “_Der Grund und direkter oder indirekter Anlass
zum Eintreten der Entwickelungshemmung ist Lichtmangel._” The method of
operation of the lack of light he conceived to be as follows:
[L] Rudimentäre Wirbelthieraugen, 1893.
Other organs were developed to compensate for the disuse of the
eye; and as the developmental force was used in the formation of
these organs, each succeeding generation developed its eye less. The
degeneration is thus explained as the result of a struggle of parts,
although this term is nowhere used, acting through the principle of
compensation. The same objections may be offered to this explanation
of Kohl as to all his theoretical discussions--they are based on the
assumption of conditions and processes that have no existence. The
high development of ‘compensating’ organs is not primarily the result
of the loss of the eye, but the high development of the former organs
permitted the disuse and later degeneration of the latter. His whole
process is a phylogenetic one, without a preceding ontogenetic one,
though on this point he does not seem to be very clear himself, for on
one page we are told that degeneration leads to retardation, and on
another that degeneration is a consequence of retardation.
Ledenfeld[M] endeavors to apply Roux’s _Kampf der Theile_, with
reversed selection, to explain the conclusions reached by Kohl on the
processes and causes of degeneration. The struggle is represented as
taking place between the germ and soma, the former endeavoring to keep
the latter at the lowest efficient point as weapon for the germ. If a
series of individuals get into the dark the organs of vision are of no
advantage and reversed selection will bring about their degeneration.
The saving in ontogeny appears first as a retardation and then as a
cessation of development.
[M] Zoölogischer Centralblatt, 1896.
Weismann[N] more recently accepts the view of Romanes, Morgan and
Lankester on the inadequacy of panmixia to explain the whole phenomena
of degeneration, and in his ‘Germinal Selection’ rejects the idea
of reversed selection, and suggests a new explanation for what
Romanes attributed to the failure of heredity and the Lamarckians to
transmission of the effects of disuse. The struggle of the parts of
Roux has been crowded by him back to the representatives of these parts
in the germ.
[N] The Monist, 1896, pp. 250-274.
“The phenomena observed in the stunting, or degeneration, of parts
rendered useless ... show distinctly that ordinary selection, which
operates by the removal of entire persons--personal selection, as I
prefer to call it--can not be the only cause of degeneration, for
in most cases of degeneration it can not be assumed that slight
individual vacillations in the size of the organ in question have
possessed selective value. On the contrary, we see such retrogressions
effected apparently in the shape of a continuous evolutionary process
determined by internal causes, in the case of which there can be no
question whatever of selection of persons or of a survival of the
fittest--that is, of individuals with the smallest rudiments. The
gradual diminution continuing for thousands and thousands of years
and culminating in its final and absolute effacement” can only be
accomplished by germinal selection. Germinal selection as applied to
degeneration is the formal explanation of Romanes’ failure of heredity
through the struggle of parts for food. “Powerful determinants will
absorb nutriment more rapidly than weaker determinants. The latter,
accordingly, will grow more slowly and will produce weaker determinants
than the former.” If an organ is rendered useless, the size of this
organ is no longer an element in personal selection. This alone would
result in a slight degeneration. Minus variations are, however,
supposed to rest “on the weaker determinants of the germ, such as
absorb nutriment less powerfully than the rest. This will enable the
stronger determinants to deprive them even of the full quantum of food
corresponding to their weakened capacity of assimilation, and their
descendants will be weakened still more. Inasmuch, now, as no weeding
out of the weaker determinants of the hind leg [or eye] by personal
selection takes place on our hypothesis, inevitably the average
strength of this determinant must slowly but constantly diminish--that
is, the hind leg [or eye] must grow smaller and smaller until it
finally disappears altogether.... Panmixia is the indispensable
precondition of the whole process; for, owing to the fact that persons
with weak determinants are just as capable of life as those with
strong, ... solely by this means is a further weakening effected in the
following generations.”
This theory presupposes the complex structure of the germ plasm
formulated by Weismann and rejected by various persons for various
reasons. But granting Weismann the necessary structure of the germ
plasm, can germinal selection accomplish what is claimed for it? I
think not. Granting that variations occur about a mean, would not all
the effects claimed for minus variations be counteracted by positive
variations? Eye determinants, which, on account of their strength,
secure more than their fair share of food, and thereby produce eyes
that are as far above the mean as the others are below, and leave
descendent determinants that are still stronger than their ancestry
would balance the effect produced by weak-eye determinants. It is
evident that a large, really extravagant development of the eye
in such a fish as Chologaster would not effect the removal of the
individual by personal selection; still less so in Amblyopsis, which
not only lives in comparative abundance, but has lived for twenty
months in confinement without visible food, and in which the eye is
minute. It seems that all the admitted objections to degeneration by
panmixia apply with equal force to germinal selection. This, however,
would be changed were the effect of disuse admitted to affect the
determinants, and this it seems Weismann has unconsciously admitted.
So far we have considered germinal selection in the abstract only. All
its suppositions are found to be but a house of cards when the actual
conditions of degeneration are considered. We find that degeneration
is not a horizontal process affecting all the parts of an organ
alike, as Weismann presupposes, not even a process in the reverse
order of phyletic development, but the more vital, most worked parts
degenerate first with disuse and panmixia; the passive structures
remain longest. The rate of degeneration is proportional to the past
activity of the parts, and the statement that “passively functioning
parts--that is, parts which are not alterable during the individual
life by function--by the same laws also degenerate when they become
useless” finds no basis in fact, and is an example of the inexact
utterances abundant in the discussion of degeneration on which it is
entirely unsafe to build lofty theoretical structures. As one example
of the unequal degeneration we need only call attention to the scleral
cartilages and the rest of the eye of Troglichthys rosæ.
All are agreed that natural selection alone is insufficient to explain
all, if any, of the processes of degeneration. All either consciously
or not admit the principle of panmixia, and all are now agreed that
this process alone can not produce extensive degeneration. All are
agreed that the important point is degeneration beyond the point
reached by panmixia, the establishment of the degenerating process,
whatever it may be, in the germ, or, in other words, the breaking of
the power of heredity. It is in the explanation of the latter that
important differences of opinion exist.
Weismann attempts to explain the degeneration beyond the point which
panmixia can reach by a process which not only is insufficient, even
if all his premises are granted, to produce the desired result without
the help of use transmission, but has as its result a horizontal
degeneration which has no existence in fact.
Romanes supposed degeneration, beyond the point which may be reached
by panmixia, to be the result of personal selection and the failure of
the hereditary force. The former is not applicable to the species in
question, and is denied by such an ardent Darwinist as Weismann to be
applicable at all in accounting for degeneration. Moreover, the process
as explained by Romanes would result in a horizontal degeneration
which has no existence in fact. The second assumption, the failure of
hereditary force, is not distinguishable, as Morgan has pointed out,
from the effect of use transmission.
[Illustration: FIGS. 1-6.--Photographs of the upper halves of the heads
of specimens of nearly the same length under the same magnification, to
show the gradual decrease of the eye. The dotted line leads to the eye
in all cases.
FIG. 1.--_Zygonectes notatus._
FIG. 2.--_Chologaster papilliferus._
FIG. 3.--_Chologaster Agassizii._
FIG. 4.--_Amblyopsis spelæus._
FIG. 5.--_Troglichthys rosæ._
FIG. 6.--_Typhlichthys subterraneus._
]
The struggle of parts in the organism has not affected the eye through
the lack of room, since the space formerly occupied by the eye is now
filled by fat and not by an actively functioning organ. It is not
affected by the struggle for food, for stored food occupies the former
eye space. It could only be affected by the more active selection
of specific parts of food by some actively functioning organ. It
is possible that this has in fact affected the degeneration of the
eye. The theory explains degeneration in the individual, and implies
that the effect in the individual should be transmitted to the next
generation. This second part seems but the explanation of the workings
of the Lamarckian factor.
The Lamarckian view--that through disuse the organ is diminished
during the life of the individual, in part, at least, on account of
the diminution of the amount of blood going to a resting organ, and
that this effect is transmitted to succeeding generations--not only
would theoretically account for unlimited progressive degeneration,
but is the only view so far examined that does not on the face of it
present serious objections. Is this theory applicable in detail to the
conditions found in the Amblyopsidæ? Before going further, objections
may again be raised against the universal assumption that the cessation
of use and the consequent panmixia was a sudden process. This assumes
that the caves were peopled by a catastrophe. But it is absolutely
certain that the caves were not so peopled, that the cessation of use
was gradual, and the cessation of selection must also have been a
gradual process. There must have been ever-widening bounds within which
the variation of the eye would not subject the possessor to elimination.
Chologaster is in a stage of panmixia as far as the eye is concerned.
It is true the eye is still functional, but that the fish can do
without its use is evident by its general habit and by the fact that
it sometimes lives in caves. The present conditions have apparently
existed for countless generations--as long as the present habits have
existed--and yet the eye still maintains a higher degree of structure
than reverse selection, if operative, would lead us to expect, and
a lower than the birth mean of fishes depending on their eyes, the
condition that the state of panmixia alone would lead us to expect.
There is a staying quality about the eye with the degeneration, and
this can only be explained by the degree of use to which the eye is
subjected.
The results in Chologaster are due to panmixia and the limited degree
of use to which the eye is put. Chologaster Agassizii shows the rapid
diminution with total disuse.
The difference in the conditions between Chologaster and Amblyopsis,
Typhlichthys and Troglichthys, is that in the former the eyes are still
in use, except when living in caves; in the latter they have not been
in a position to be used for hundreds of generations. The transition
between conditions of possible use and absolute disuse may have been
rapid with each individual after permanently entering a cave. Panmixia,
as regards the minute eye, continued. Reversed selection, for economy,
can not have affected the eye for reasons already stated. The mere
loss of the force of heredity, unless this was caused by disuse, or
the process of germinal selection, can not have brought about the
conditions, because some parts have been affected more than others.
[Illustration: FIG. 7.--Head of a very young _Amblyopsis_ before all
the yolk is absorbed.]
Considering the parts most affected and the parts least affected, the
degree of use is the only cause capable of explaining the conditions.
Those parts most active during use are the ones reduced most--viz.,
the muscles, the retina, optic nerve and dioptric appliances, the lens
and vitreous parts. Those organs occupying a more passive position,
e. g., the scleral cartilages, have been much less affected. The lens
is one of the latest organs affected, not at all during use, possibly
because during use it would continuously be in use. It disappears most
rapidly after the beginning of absolute disuse both ontogenetically
and phylogenetically. All indications point to use and disuse as the
effective agents in molding the eye. The process, however, does not
give results with mathematical precision. In Typhlichthys subterraneus
the pigmented layer is affected differently from that of Amblyopsis.
The variable development of the eye muscles in different species would
offer another objection if we did not know of the variable condition
of these structures in different individuals. Chilton has objected
to the application of the Lamarckian factor to explain degeneration,
on account of the variable effects of degeneration in various
invertebrates. But such differences in the reaction are still less
explainable by any of the other theories.