Is the cheetah in peril? It is possible that as a direct consequence of the low
heterozygosity the cheetah produces sperm of low viability, its rate of juvenile
mortality is abnormally high, and it is particularly susceptible to disease. All these
claims have been made but no causal relationship has been established between these
putative defects and the peculiarities of the genotype. Alternatively the cheetah may
be in no danger of demographic collapse despite its low genetic variability. In
support of that is its widespread distribution, which was even wider in the recent
past, particularly in Asia. Contraction of range over the last 1000 years has been no
greater than that of the lion, another widespread species but with a standard level of
heterozygosity. For both species the contraction of range seems to be a result of exces-
sive human predation rather than of a diminished genetic fitness. As far as we know
there is no evidence from the wild suggesting that the cheetah is faced by a level of
risk beyond those hazards imparted by a rising human population (Caughley 1994).
The cheetah clearly has low genetic variance but well within the range exhibited
by mammalian species (see Fig. 17.1). The suggestion that it is in demographic peril
as a consequence of that modest genetic variance earns no support from what is known
of its ecology. There are two messages transmitted by this example. The first is special:
we need more disciplined information on the cheetah in the field to determine whether
its diminished genetic variance is associated with demographic malfunction. The
second is general: by genetic theory currently followed in conservation biology the
cheetah should be in demographic trouble, but there is no convincing evidence for
that and considerable but circumstantial evidence to the contrary. A plausible alter-
native hypothesis is that present genetic theory overestimates the amount of genetic
variation needed to sustain an adequate level of individual fitness. One should not
jump to the conclusion that a species is in danger simply because it has a low H.
There is too much evidence to the contrary.
We cannot yet lay down general rules as to the minimum genetic variance
required for adequate demographic fitness. Nor can we define a minimum viable pop-
ulation size (genetic). We need much more research on the incidence of inbreeding
depression in the field, on the population size and the period over which that size
must be maintained before inbreeding depression becomes a problem, and on the
relationship between heterozygosity and fitness.
It can happen that the size of a population appears large enough to avoid genetic
malfunction but that the population is acting genetically as if it were much smaller.
The proportion of genetic variability lost by random genetic drift may be higher than
the computed theoretical 1/(2N) per generation because that formulation is correct
only for an “ideal population.” In this sense “ideal” means that family size is dis-
tributed as a Poisson, sex ratio is 50 : 50, generations do not overlap, mating is strictly
at random, and rate of increase is zero. This introduces the notion of effective pop-
ulation sizein the genetic sense, the size of an ideal population that loses genetic
variance at the same rate as the real population. The population’s effective size (genetic)
will be less than its census size except in special and unusual circumstances.
Perhaps the greatest source of disparity between census size and effective size is
the difference between individuals in the number of offspring they contribute to the
next generation. In the ideal population their contribution has a Poisson distribu-
tion, the fundamental property of which is that the variance equals the mean. Should
the variance of offspring production between individuals exceed the mean number
CONSERVATION IN THEORY 297
17.4 Effective population size (genetic)
