1. Introduction
In the course of the
second half of the 19th century the method of ‘inbreeding and selection’
took hold in domestic animal breeding. From 1900 onwards it was widely
applied both for
companion animals and in agricultural animal husbandry. Especially in the
early phases of
pedigree breeding (oriented to conformation) the method yielded
advantages. With its use
breeders were able to ‘fix’ desired traits in their breeding stock, and
have these transmitted
reliably to subsequent generations.
This breeding method also has drawbacks. Its systematic application
concentrates not only
desired genes, but also the hereditary predisposition for undesired
traits. The problem is that
harmful genes are being spread while successive generations display only a
very limited part
of these in the offspring. For every harmful trait the bulk of the
unwanted genes is hidden
away in carriers. We do not notice their damaging effects until later –
many generations
down the line, by which time the harmful genes have become so widespread
that our
selection is virtually powerless. On top of that, hereditary problems
involving more complex
transmission patterns cannot be combated with this system of individual
selection at all.
In the world of
pure-bred dog breeding ‘inbreeding and selection’ is still the order of
the day.
What it basically comes down to is this: the level of inbreeding is
gradually raised (via line
breeding). The purpose is to fix the superior traits of dogs in the line.
Selection is in favour of
the desired characteristics (the most breed-typical traits), and against
undesired
characteristics (such as disorders in health and well-being). There are
two objectives here:
‘preservation’ and ‘improvement’.
Most breeders are convinced they are ‘preserving’ as long as they mate
pure-breds only. As
to ‘improving’, most breeders hold that this can be achieved by always
letting the ‘best’
animals contribute as much as possible to the next generation. They assume
that this
approach will also check the frequent occurrence of health and well-being
problems in purebred
dogs. The reality of pure-bred dog breeding, however, yields a different
picture.
Fact is that, in spite
of all our selection efforts, the percentages of animals suffering from
hereditary deviations and disorders seem to keep climbing and are
certainly not diminishing.
All our attempts to improve the quality of health and well-being in our
pure-bred dog
populations by way of selection come to next to nothing. Sometimes we can
chalk up a minor
success for one deviation, only to conclude that other deviations are
mushrooming.
Evidently, the breeding method used does not enable us to achieve genuine
improvement.
Real improvement demands a different approach. If we cannot successfully
reduce the
problems of health and well-being of our pure-bred dogs to acceptable
levels, our breeds
lose their right to exist.
For the most part the
breeding structure of our pure-bred dog populations is very complex.
Generations overlap; individual contributions to the next generation keep
changing, as do
those of lines and selected groups; every breeder has his own selection
priorities. In the real
situation of breeding practice we cannot isolate the consequences of the
various measures
of a breeding policy. A whole lot of genetic forces impacts
simultaneously. Sometimes those
forces are at cross purposes, sometimes they reinforce each other. To gain
insight into the
consequences of our breeding policy we must look at the effects of every
one of our breeding
measures separately.
We turn to a model
population to learn about the influence and effects of the genetic forces
at work. Such forces are of different kinds. Some are laws of nature. They
hold for any
population, whether we intervene or not. Other forces are triggered by us,
processes set in
motion by our breeding measures.
We can see what happens when we apply a series of measures to the model
population, and
‘translate’ the lessons learned to the reality of breeding practice. Step
by step we can
introduce complications. At the end of the exercise we arrive at
statements about conditions
that approximate the actual reality of breeding.
2. A model population
The model we use is the
so-called ‘random mating population’. This is an ideal population for
which we have formulated clear breeding rules, so that we can demonstrate
the separate
impacts of breeding measures.
We assume a ‘large’ population. In it, we use enough breeding stock, every
generation
again, to gather an a-select sample of the available genetic material to
transmit from one
generation to the next. All of these animals contribute equally to the
next generation.
Moreover, we exclude other forces that would cause changes in the genetic
composition of
the population, that is: we do not select, there are no mutations and we
allow no migration.
Finally, we exclude inbreeding, meaning that there will be no consciously
arranged parent
combinations. Mating combinations occur purely at random.
Obviously, in real life
there are no such populations, certainly not among dog breeds. This
ideal population is fictional and our conditions are strictly artificial.
The Hardy-Weinberg Equilibrium
For a population that
meets these conditions the Hardy-Weinberg Equilibrium is applicable:
there is a fixed relationship between the gene frequencies and genotype
frequencies; these
frequencies do not alter in successive generations.
Leaving details aside we can say that: if we indicate the frequency of
gene A
with
p,
and that
of a
with
q
(where
p + q = 1),
the frequencies of the genotypes
AA,
Aa
and
aa
are
p², 2pq
and
q²
respectively (where
p² + 2pq
+ q² = 1).
We can demonstrate that, as long as we stick
to the model conditions stated above, these gene and genotype frequencies
will not alter in
the succession of generations.
Thanks to the Hardy-Weinberg Equilibrium we know how often the three
genotypes
AA,
Aa,
and aa
occur in our
model population - as long as we know the gene frequencies. Table 1
presents the genotype frequencies for a number of combinations of
p
and
q.
For A
and
a
we
can take any arbitrary gene pair.
Suppose that in our
model population the frequency of the gene for black coat (A)
is 0.9, and
that hence the frequency of the gene for brown (a)
is 0.1. This means that 81% of the
animals of the population is
AA,
18% is
Aa
and 1% is
aa
(see Table
1, first row).
Since black is dominant over brown, we cannot distinguish the homozygotic
black dogs (AA)
from the black dogs carrying brown (Aa).
We notice that we have a population consisting of
99% black dogs (AA
and
Aa)
and just 1% of brown dogs (aa).
However, we know that 18%
of the blacks (one in 5 or 6) carry the gene for brown (a)
and can transmit the gene to half of
its offspring.
In actual practice this
is troublesome. In real populations we do not know the gene
frequencies, and most of the time we are dealing with gene pairs where one
gene is
completely dominant over the other. So we see no (exterior) difference (in
phenotype)
between dogs with the genotypes
AA
and
Aa.
For our example this means: the only thing we
can observe is that 1 out of 100 dogs is brown, the others are black. We
know that this is a
model population, so we also know that somewhere among all those black
dogs there are
18% of them that will transmit brown. Except, we don’t know which of our
black ones they
are.
As long as we talk about the coat colours black and brown this is not very
exciting. The coat
colours black and brown contribute little to the health and well-being of
the dog, even if the
dog’s colour may contribute to the well-being of the owner.
Suppose that in our
model population we have a form of cataract with a single-gene
recessive mode of inheritance. Let
A
stand for ‘healthy’ and
let a
refer to the
gene for
cataract. In our model population we have only two kinds of dogs: healthy
dogs (AA
and
Aa),
and dogs that suffer from cataract (aa).
Suppose also, that a survey has shown that 4% of
our dogs suffer from cataract.
Because this is a model population in which breeding is entirely according
to the stipulated
conditions, we are able to say more about the occurrence of cataract in
this population. In
Table 1 (second row) we can see that the gene frequency for cataract (a)
is 0.2. For breeding
practice this is not very interesting. We cannot see genes or gene
frequencies, and we
cannot plot a direct course on this in our breeding. On the other hand,
very important to
recognize for our breeding is that 32% of the dogs in the population carry
the harmful gene,
and every single one of these can transmit the harmful gene to half of its
offspring. That
means that one out of three ‘healthy’ dogs is carrier (Aa)
for this hereditary disorder. And that
spells a sizeable problem: all ‘healthy’ dogs are equally healthy and,
without additional
investigation (tests) we have no way of distinguishing between
AA
and
Aa
dogs. Basically
we have to assume that every healthy dog may well be a carrier.
In every real-life
breed we encounter a large number of deviations (harmful genes) each of
which occur in low to very low frequencies. Because they occur but seldom,
we believe we
have little reason to worry. These are deviations that occur so rarely
that in fact almost
nobody knows them first hand from their own breeding.
It is worthwhile to see what the Hardy-Weinberg law teaches us about the
presence of
‘carriers’ when we are faced with rare disorders (Table 2). The general
feeling is that genes
for rare disorders hardly occur in the population, and that we do not
really have to take them
into consideration.
Suppose we have a
deviation that occurs only once per 10,000 individuals. Table 2 shows
that in that case almost 200 carriers per 10,000 individuals are born.
Very concretely this
means that nearly 2% or about one in 50 dogs, carries the harmful gene.
Table 2
Gene and Genotype frequencies for populations to which the Hardy-
Weinberg Equilibrium applies
At present we know
about some four to five hundred hereditary deviations in dogs. Only a
small part of these are caused by deviating genes in a single gene pair.
Most deviations are
caused by a collaboration of a whole series of gene pairs. We can
translate our conclusions
about the occurrence of carriers to the currently known genetic diseases
in dogs. In the best researched mammal, the human being, ten times as many
hereditary disorders -- some four
or five thousand -- are identified and described. The logical assumption
is that literally every
dog carries dozens of harmful genes. What we see are (phenotypically)
healthy dogs. But
genetically (genotypically) we are dealing with dogs whose make-up
harbours many risks for
their progeny. In this respect dogs are no different from other animals,
including mankind.
Genetic disorders are simply part of life.
The incontrovertible
fact is that every individual carries the genetic predisposition for a
wide
range of deviations and disorders. We cannot prevent that. But we can
influence the degree
to which progeny is born that suffer from hereditary deviations and
disorders. This depends
on the choices we make in our breeding policy. Below we will illustrate a
number of the
choices we can make.
3. Selection against hereditary deviations and disorders
As soon as we are
confronted with a genetic problem the most logical step is to select
against it. Via our selection we exclude from breeding dogs that carry
undesired genes. In
this way we lower the frequency of those genes in the group of animals we
use as parents.
Thus, we reduce the risk that in the next generation animals are born that
suffer the same
ailment. Selection is a breeding instrument by which we can alter the
genetic composition of
populations. We will demonstrate this with examples (see Table 3).
Suppose that in our
population 4% of the dogs suffer from cataract. Once again we are
dealing with the model population described above, large, random and so
on.
From now on however we decide that we are going to select against this
disorder and we do
this by excluding dogs having cataract (affecteds,
aa-dogs).
If we keep excluding
aa-dogs
we
lower the frequency of the
a
gene every generation
again, so that every subsequent
generation gives birth to fewer cataract affecteds. Let us discuss a
number of steps in this
selection process.
When we begin our
selection (generation
0)
we have
4%
affecteds (aa
animals),
all of whom
we exclude from breeding. For the next generation (generation 1) we use
only the ‘healthy’
animals (AA
and
Aa).
This means that the gene frequencies of the generation-1 parents are
different from those of the generation-0 parents. We exclude all affecteds
of generation 0,
and so prevent a batch of
a
genes from being passed
on to the next generation.
In
generation 1
the
percentage of cataract affecteds (aa)
born is much less:
2.78%
(see
Table 3, second row). Again, we exclude affecteds from breeding. To obtain
a next
generation (generation 2) we use ‘healthy’ animals (AA
and
Aa)
only. And again, excluding
the a
genes of the
affecteds means that the gene frequencies of the parents of generation 2
are different compared with generation-1 parents.
In
generation 2
therefore
only
2.04%
affecteds are born. We keep repeating the process in
this and all following generations; every time we exclude affecteds and
breed with ‘healthy’
animals only.
Our selection programme
marches on marvellously. After two generations we already halved
our problem and in the fifth generation the percentage of cataract
affecteds born is just 1%.
After 10 generations the frequency of affecteds is brought down to 44 per
10,000 dogs (less
than 1/2 %). After 20 generations we have only 16 affects per 10,000 dogs,
after 30
generations we find 8 affecteds per 10,000, and after 40 generations we
are left with only 5
individuals suffering from cataract in 10,000 dogs (0.05%)! In short, our
programme of
selection is a resounding success, at least, in terms of reducing
well-being problems in our
dogs.
Table 3.
Progression of gene and genotype frequencies for a model population in
which cataract affecteds (aa)
are consistently excluded. The results presented are those for the first
ten
generations in our selection programme, and for generation 20, generation
30 and generation 40
We do have to add a
note here. We are talking about a selection programme covering 40
generations. If we take a generation to span two or three years, we have a
selection
programme extending over about a hundred years! For the illustration above
this means that
it takes decades before our cataract problem can be considered
‘negligible’.
There is a second
reason to be modest and reserved about the success of our breeding
programme. After 10 generations we still have over
12%
of ‘carriers’
(Aa)
in the population,
and after 40 generations (a full century) the proportion of carriers is
still over
4%.
Even if in
the course of our selection programme we see a dramatic drop in the
percentage of
affecteds we did not succeed in getting rid of the harmful gene. It
remains very much present
in all those invisible and hence unidentifiable carriers.
We are forced to
conclude that we will in fact never do away with the harmful gene. It will
continue to lurk in the population’s carriers. This confirms our earlier
proposition to the effect
that genetic disorders are part and parcel of life.
4. Over-use of breeding stock
Against the background
of the above we run into another problem. The tendency in modern
breeding is to make much use of dogs (especially males) that score well in
terms of
conformation or performance. These are dogs that display outstanding
breed-typical
qualities, and meet the health requirements as stipulated for the breed.
These dogs, it is
believed, are they that will provide essential contributions to further
development
(improvement) of the breed. The idea is that their ‘superior genetic
make-up’ should be
spread throughout the population with almost no restriction.
The problem that these
dogs have in common with any other dog (or any other mammal) is
that they are carriers for a large number of genetic deviations and
disorders. Mind you, as far
as we can see they are entirely healthy. Nevertheless, like any other
individual, they bring
with them the usual genetic load. For every characteristic of which they
are ‘carrier’ they will
pass on the harmful gene to half of their children. These are dogs that,
just like any other dog
in the population, can cause a breed-specific problem if we make
disproportionate use of
them. A few examples will show us how it works.
For the sake of clarity
we will again limit ourselves to one pair of genes. Let’s go back to our
selection programme against cataract. We introduced selection in our model
population, and
so managed a drastic reduction of the percentage of cataract affecteds. An
important
condition in our model is that for every successive generation again we
rely on a large
number of breeding animals, all of them contributing to the next
generation to the same
degree.
Suppose now that we
discover a male dog that, we are truly convinced, possesses so many
superior traits that we really think this male should have more progeny
than a run-of-the-mill
dog in the population. After some deliberation we decide that this
extremely beautiful or top performing male should sire 10% of litters in
the next generation. After all, this is a rare,
‘once-in-a-lifetime’ dog, and we are prepared to relax just once the
strict breeding discipline
we agreed on when we began breeding in our model population.
Suppose, next, that we
are unlucky. It so happens that our superior sire turns out to be
carrier for the cataract gene (Aa).
This is not really far-fetched. We have seen that even after
a hundred years of selective breeding one in 25 dogs is still carrier.
What is the effect of our
decision regarding this male in our agreed-upon selection programme
against cataract?
The lower, gradually
decreasing curve shows the result of our selection program when we
strictly maintain our agreed-upon policy, i.e., exclusion of affecteds and
proportional use of
all breeding animals.
In addition, we pictured four situations where we trace what happens if we
assign 10% of our
litters of the 10th, the 20th, the 30th or the 40th generation to a
carrier male (Aa).
This Aa
sire
will pass gene
a
on to half of its
children and so increase the occurrence of affecteds (and
carriers) in the population.
Each of the four
examples represents one violation of our breeding agreements for the model
population, other than that we stick to the rules and continue our
selection programme.
At first glance at the
figure already shows that the impact of over-use is significantly greater
than the influence exerted by our selection against affecteds. Whereas our
selection is a
laborious attempt over many generations to improve the situation step by
step, over-use
(even on a scale as modest as described) turns out to have large
consequences.
The results as sketched
in Figure 1 actually picture exactly what we wanted to happen,
namely, that the genes of this male would impact on the population. Except
that we hoped to
restrict this to all those good genes that male carried. It was, we said,
a male with
outstanding traits, and we made extra room for him in our breeding
precisely because we
wanted to spread his excellent qualities throughout the breed, not
realizing that the very
same thing would happen with the ‘bad’ genetic predispositions that any
dog is sure to carry
along with the good.
Table 4 summarises what
Figure 1 shows us. Over-use of the one male has consequences
for the genetic composition of the population. Due to the use of an
Aa
male in the 10th
generation the percentage of affecteds rises by more than
40%;
our selection programme
experiences a setback of about
3 generations
and thus we
lose the equivalent of more than
7 years
of selection
activity.
We can express in the
same way the influence of the Aa male at other moments of time in
the selection programme. In the 20th, 30th and 40th generation, we see
rises in the percentage
of affecteds of more than 100%, almost 200% and almost 300% respectively.
This means
that our selection programme suffers a corresponding setback of 9, 16 and
24 generations.
Expressed in years of selection lost, we are talking about 22, 40 and 60
years respectively. It
is hard to show more clearly that over-use of breeding animals is an
instrument many times
more incisive in breeding than selection can be.
In the above example we
assumed that we had ‘bad luck'. The one time that we felt called
upon to bend our breeding rules for the model population it transpired
that the chosen
superior male ‘happened’ to be a carrier (Aa).
According to the laws of chance the dog was
far more likely to be free of cataract (AA).
For this one harmful gene the reasoning was sound: in the population we
had ‘only’ four,
seven or twelve per cent carriers, and in our example the fates surely
visited us. On the other
hand, every dog carries some dozens of harmful genes and even if the male
had been free
of the genetic disposition for cataract he was still carrier for a large
number of other harmful
genes.
Critics are likely to
argue that our dog populations are inbred to the point that a large part
of
the original genetic diversity is lost. That means that not only many of
the ‘good’ genes are
gone, but a large part of the bad and harmful genes have disappeared as
well. This is true.
The process of diminishing genetic diversity due to inbreeding does not
distinguish between
desired and undesired genes. Reality however teaches us that in all our
breeds we are still
left with so many undesired genes that getting rid of some of them leaves
us with no extra
room for breeding. What actually happens is the opposite. Due to
progressive loss of genetic
diversity the population slowly loses vitality. This leads to more rather
than fewer hereditary
problems in the breeds: increasingly we are faced with groups of
deviations and disorders,
with complex modes of inheritance, that formerly occurred rather rarely.
Over-use of
breeding animals, including “top-sires”, is one of the main causes of
genetic loss.
Let us turn again to
the mutually opposing forces of selection and over-use. In Figure 1 we
have seen what this might mean for a hereditary deviation that hardly ever
occurs. Say we
have a very rare disorder in our breed. It occurs only in 5 out of 10,000
dogs and, for 10% of
the litters of the next generation, we decide to use a male that, as it
turns out, carries this
rare gene.
This is the situation we encounter in the 39th and 40th generation in
Figure 1. If we really were
to let this dog sire 10% of the 40th-generation litters we would cause a
rise in the percentage
of affecteds that would saddle us with sixty more years of consistent
selection to restore the
old situation.
Compared to the reality
of present-day dog breeding the chosen example is extremely mild.
The truth is that, especially in numerically small breeds, a significantly
higher over-use of
males is applied than the 10% chosen here. To this we must add that, since
these are dogs
of which everybody has high expectations, large numbers of their progeny
tend to be used
for breeding as well. Consequently, the percentage of affecteds will often
climb far more than
Figure 1 has it and in the generations to follow the rate keeps going up.
In many breeds we
have seen examples of this. ‘Suddenly’ a hereditary deviation that hardly
troubled us
explodes into a ‘breed-specific’ problem.
There is a second
reason why we can call the example very mild. We spoke of a ‘once-in-alifetime’
sire, a dog of exceptional quality such as we are not likely to meet again
in a
hundred years. But in dog breeding over-use is the rule rather than the
exception. ‘Once-ina-
lifetime’ sires are emerging every year. The whole of the breeding
exercise is oriented to
using too small a number of usually close kin to produce the next
generation, most of which
(especially males) supply a disproportionately large contribution to the
breed. A fair
representation of genetic material is in no way transferred from one
generation to the next.
On the contrary, over-use has become the basis for breeding pure-bred
dogs.
To let the model
approximate a little more the actual practice of dog breeding, let us see
what impact repeated over-use has in relation to our selection programmes.
In Figure 2 we
compare the progression of the frequency of dogs suffering from some
genetic deviation
(affecteds,
aa)
in three situations. Once again we start from our model population (Table
3) in
which we select against affected dogs and assign 10% of the litters to an
Aa
sire in
every 3rd,
5th or 10th generation.
Figure 2 shows that an
‘equilibrium’ is attained between the reduction of the percentage of
affecteds thanks to selection, and the increase of that percentage due to
repeated over-use
of Aa
males.
Whereas our selection programme in the long run held promise to effectuate
a
‘negligibly low’ level of affecteds in the population (see Figure 1), we
must now learn to live
with on average one-half or three-quarters of one percent affecteds in the
population. We
arrive at a ‘chronic lowest level of affecteds’ against which our
selection programme is powerless. As long as we continue to breed in this
way we have turned this disorder into a
breed characteristic.
Selection is an
important instrument in breeding. But with our selection we are waging a
lost
battle against the impact that over-use has on the genetic composition of
the population.
There are plenty of examples of this in the actual practice of breeding.
In spite of all selection
efforts breeders are often unable to really reduce the level of deviations
in their breed.
The breeding method as
applied in fact draws us into a kind of vortex. The percentage of
affecteds (aa)
keeps increasing because every generation again we breed with too few
animals. On top of this the percentage of carriers (Aa)
keeps increasing too, to the measure
we diverge from the breeding rules of the model population more often and
in more ways
(see Figure 3).
Figure 3.:
Progression of the frequency of Aa with the use of an Aa male
for 10% of the litters every 3rd, 5th and 10th generation
When we discussed the
model population (Tables 1 and 2) we noted that for all disorders the
‘visible part’ (affected individuals) is only the tip of the iceberg. Most
of the harmful genes are
hidden in the carriers, invisible and very hard to find. A higher
percentage of affecteds means
a higher percentage of carriers, and hence per successive generation it is
more and more
likely that an over-used dog happens to be a carrier.
In the selection
programme (Table 3) we saw the percentage of carriers between the 20th
and the 40th generation diminishing from 7.68 to 4.35 per cent. But in the
examples chosen in
Figure 3 we have to accept an average percentage of carriers of 10 per
cent to more than 15
per cent.
This means that the
risk we run of using a carrier is also two to three times greater.
And so the vortex sucks
us down, inexorably, unless we take measures to redirect the
breeding management of our dog breed populations. We cannot go on with our
‘repair
policy’, persistently introducing still more expensive selection
programmes to keep health
and well-being problems within bounds. It has not helped us to
systematically reduce the
problems to an acceptable level. Moreover, on the level of prevention we
neglect to do
almost everything that we could do to forestall problems. Even if we want
to believe that in
technical and business-economic terms the current breeding method is still
acceptable, it is
certain that from the point of view of animal well-being our present
breeding method has long
ceased to be justifiable.
5. Expansion of scale in breeding
When, a hundred years
ago, breeding pure-bred dogs took hold, we were dealing with a
small-scale breeding structure. Breeders applied ‘inbreeding and
selection’ and built their
own inbred line. ‘Over-use’ was the order of the day, but it was small
scale and mostly
restricted within the lines of individual breeders. As soon as problems
emerged in their line
that could not be overcome via selection, the breeders would turn to a
fellow breeder to
introduce ‘new blood’.
Translated into terms of breeding: as soon as the level of inbreeding
became too high, so
that little room was left for selection, breeders restored part of the
genetic diversity by
crossing in more or less unrelated animals. They sacrificed some of their
line’s homogeneity,
repaired part of the selection room and were then able to continue their
‘inbreeding and
selection’ again.
In the early days, when
breeding was still modest in scale, this breeding method was
satisfactory. Every time a breeder ‘ran stuck’ with his own line he could
find another breeder
from whom to obtain breeding stock that was sufficiently unrelated to his
own line. This went
awry after World War II, when society became increasingly mobile. It
became a whole lot
easier to move around and to come into contact with distant breeders.
Breeders acquired the
‘new breeding stock’ they needed far away from home. But this also meant
that increasingly
breeders made use of the same (champion) lines and that slowly but surely
the mutual
kinship between the distinct lines grew. In most breeds we see that this
process has
accelerated over the last decades and that breeds are gradually turning
into one large single
inbred line. The breeder whose line experiences problems pays the price.
In search of
breeding stock unrelated to his own, to restore some genetic diversity, he
has nowhere left to
turn to.
Of course, the first to
pay the price are the dogs. When the breeder runs into problems there
is no solution for his line (for his dogs) to keep health and well-being
problems in hand. Overuse
of breeding animals and lines produces dogs that possess the same genetic
predisposition, deriving from the same shared ancestors. As we saw above,
the effects of
this on the genetic composition of the population can no longer be
controlled through
selection. And so it is that genetic problems become breed-specific
traits.
In
recent health surveys it became painfully clear that most of our dog
breeds are struggling
with an unnaturally high level of genetic deviations and disorders. In
other animal species we
express the frequency of genetic disorders almost exclusively in per mil
(or even fractions of
per mil). In pure-bred dogs we are forced to express disorder frequencies
in terms of
percentages and multiple percentages.
How this came about we
can understand very clearly from the history of pedigree dog
breeding. We understand, but need not accept. Our joint responsibility for
our breeds dictates
that we must find solutions.
Throughout the past
century population management and breeding policy for almost all
breeds was established as the sum total of individual breeder decisions.
Because there was
no policy for the breed as a whole it happened that breeders made choices
that for their own
line were often quite defensible and correct, but proved harmful for the
breed. Here lies the
root of the current health and well-being problems in our pure-bred
populations.
6. A new breeding policy
Above, we tried to
demonstrate in a number of steps the consequences of our breeding
decisions. We did this with the help of a model population in which the
effects of our breeding
decisions were visualised. In this way we could get around the complexity
of ‘real life’ and
see what genetic forces actually come into play when we take specific
breeding decisions.
We first focussed on
‘preservation’, the basic objective of every breed club. In the model
population (random mating) we preserve the gene pool and hence the
characteristics of the
population (the breed). Preservation is assured because every generation
again we transfer
a sufficiently large sample of the genetic material to the next
generation. Moreover, we ruled
out all forces that could alter the genetic composition of the population.
This model
population therefore remains constant; it does not ‘improve’ nor does it
‘deteriorate’. The
traits occurring in the population will resurface with the same frequency
in each new
generation. Actually, this is not very satisfactory; in every real-life
population there are
aspects that we might want to improve on. Maybe we’d like to make our dogs
still more
‘breed typical’ and certainly we would prefer to breed without any genetic
health and wellbeing
problems at all. Especially this second wish is, in light of current
social developments,
the more relevant and pressing.
The breeding instrument
to alter a population (a breed) is selection. Selection is the way to
deal with shortcomings occurring frequently, but the closer we come to our
goal the less
effective selection will be. In the course of the selection process the
relation between the part
that can be controlled (the affecteds) and the part that cannot (the
carriers) becomes in fact
more unfavourable in each successive generation. Selection will never
enable us to get
completely rid of a genetic problem. At best we can bring down the
occurrence of disorders
to a biologically attainable and morally acceptable level.
Traditionally, breeders
applied inbreeding (line breeding). Initially inbreeding was a breeding
instrument applied small-scale, and the breeds could be characterised as a
pluriform collection
of inbred lines (one look at a dog told you what kennel he came from). In
our efforts to achieve
our breeding goals more quickly (our ‘improvement drive’) we have in the
past years turned
more and more often to fewer and fewer breeding animals. We were not
satisfied with good
representatives of the breed, we wanted the best. Because everyone wanted
the best, and
because everyone agreed on which animals were the ‘best’, we ran into the
phenomenon of
‘over-use’. We turned a lot of breeds into a single inbred line where all
animals have a
shared ancestry. All this exacted its toll from the original genetic
diversity in the breeds;
‘preservation’ was squeezed.
Breeders overlooked
that in tandem with the spread of desired genes the unwanted genes
were being spread apace. The given to the effect that literally every
animal is carrier for
dozens of harmful genes was neglected. Breeders believed that they could
stay on top of the
problems by selecting against undesired traits. Selection however will not
reverse the effects
of over-use and concomitantly rising inbreeding levels throughout the
population. The above
has demonstrated this.
Our breeding has now
come to the point that we have to make choices. If we carry on with
our current breeding policy continued existence of a large number of
breeds is at risk: we will
simply be unable to contain the rampage of genetic problems. It is at
population (total breed)
level that we must arrive at agreed-upon rules intended to halt the
development of past
decades and next to turn these around. Very concretely this means:
1. We must attune the
use (the contribution to the next generation) of breeding
animals to the size of the population. No single dog should have an impact
on the
genetic composition of subsequent generations such that ‘genetic
disasters’ can
arise.
2. If we do this we can
once again make effective use of the old method of ‘individual
selection’, and take the first steps towards genuine improvement of the
health and
well-being condition of the breeds.
3. We will have to
provide breeders with instruments that allow them to give steering
to the level of inbreeding in their lines. The use of inbreeding can be
advantageous in breeding, but it must remain an instrument rather than
turn into
an irreversible and unavoidable force.
4. Over and above the
individual selection that has been applied since 1900 we
must make modern methods of selection available for dog breeding (breeding
value estimates, genetic risk assessments).
In short this means
that, we must first make sure that we do not add to our problems (1), that
we next use currently available methods to work on improvement (2), that
we must make
haste to provide breeders with modern instruments to guide breeding with
and to combat
problems in our dogs (3 and 4). It is only then that we can justifiably
talk about responsible
genetic management of our pure-bred dog populations.
Source:Centennial Conference of the Dutch Kennel Club, 2 July 2002, Amsterdam, The Netherlands.