The evolution of incest avoidance mechanisms
Background: Over evolutionary time, functional mechanisms are constructed
through the appearance of mutations (modifications) in the designs of
reproducers, which are then acted upon by selection (i.e., the impact of these
modifications on the reproduction of the design). If the modification increases
the number of copies of itself across generations, it will increase in frequency
until it becomes universal in the species, and the species has a useful new
component in its species-typical design.
Random, heritable modifications of all kinds are continually being injected into
populations of organisms, so to understand the evolutionary analysis of designs,
you must always ask, what would be the fate of a mutation which had property x
given the other properties of the organism and the evolutionarily long-enduring
features of the species' environment? Will it spread, be eliminated, drift
randomly, or what?
This question should be asked for any observed trait or hypothesized neural or
psychological mechanism. It will help to evaluate the plausibility of
hypotheses, and the architecture of the species under study.
Selection pressures against incestuous matings
between close, fertile relatives
For example, we can ask this question about modifications that increase or
decrease the sexual attraction between close relatives. What would be the fate
of a mutation that made, for example, mothers sexually attractive to sons, in a
world where mothers found sons attractive also? What would happen in a world
where sexually mature siblings found each other erotically compelling? What
would be the fate of an alternative modification that made individuals
uninterested in or disgusted by sex with family members?
These and other questions can be analyzed, to give expectations about the
functional organization of mechanisms relating to the behavior under question.
Genetically, unfavorable recessive mutations are always entering into the
population, every generation. These are not immediately selected out because,
being recessive, they do not express themselves unless the bearer receives the
same deleterious recessive from each parent. If the recessive is matched with a
healthy dominant, the individual bearer is fine. If the recessive is matched
with the same recessive from the other parent, the offspring expresses the
unfavorable trait, and hence may die, or be functionally impaired. So, whether
a child is injured by being homozygous for a given deleterious recessive is a
function of the probability that both parents have the same recessive gene.
The probability that both parents will have the same rare harmful recessive is
low (e.g., 1 in 1000 x 1 in 1000) unless they are related to each other. To be
related means they share genes in common from a recent common ancestor. When
close relatives mate, the probability that the resulting children will get
paired sets of deleterious recessives jumps enormously. For example, if a
lethal recessive exists in the population with a frequency of 1 in 1000, the
probability an individual who gets this gene from one parent will also get it
from the other is 1 in 1000. If, on the other hand, a father has the recessive,
there is a 1 in 4 chance that it will pass to both his son and his daughter. If
the son and daughter then mate and produce a child, the probability that they
will then both pass this gene to the child is again 1 in 4 (or a total
probability of being homozygous for this recessive of 1 in 16).
Thus, if an individual who is about to mate has a particular lethal recessive,
the probability that it will be expressed in his child, and hence kill her or
him, rises from (on the rough order of) 1 in 1000 to 1 in 16 or by a factor of
64. Humans have approximately 100,000 loci, many of which have deleterious
recessives. The probability of producing a defective individual has to be
summed across loci, so the real increase in impairment or lethality
probabilities is much higher.
The genetic load of a species is described using the measure lethal
equivalents. Most individuals have about 2 lethal equivalents, which means that
if half of their loci were made homozygous, they would be dead. Thus, in
humans, selection against incest between fertile, close genetic relatives is
intense.
In the program, you can adjust the level of lethal equivalents. The higher the
level, the more costly incest will be, and the fewer surviving descendents an
individual will leave.
Adaptations for incest avoidance:
Often, in the absence of machinery for accomplishing a function, the function
will not be accomplished. For example, being related to someone does not
automatically generate a sexual avoidance in the absence of machinery designed
to inhibit mating. For example, siblings (raised from the same parents but in
different years -- non-nestlings) in certain bird species will mate as readily
with each other as with any other comparable conspecific. They have evolved no
method of kin-recognition for siblings raised in other years. Why should this
be? When sexually mature, they disperse far enough from the nest that the
probability that they will encounter a sibling is less than 1 in 1000. The cost
of such a minor probability of an incestuous mating is not enough to drive the
evolution of neural tissue specialized for accomplishing this function.
This illuminates a general principle: the rarer an event in the evolutionary
history of a species, the less selectively important the event will be, other
things being equal. In the program you are using, you can adjust the
probability an individual will encounter a relative as a potential mate. The
lower the probability, the slower the selection for avoidance, and the more
likely drift will take over.
Secondly, natural selection inherently involves selection between two or more
alternative designs. In the absence of machinery for avoidance (or preference),
one expects a lack of discrimination in mating with respect to kinship.
So, the alternatives are: being indiscriminate, being preferential (not modeled
here), or rejecting mates who are closer than a given degree of kinship (e.g.,
siblings only; siblings and aunt/uncle/niece/nephew; cousins and closer, etc.).
So the question is, which alternatives get selected for, and which selected
against.
Humans: the Westermarck mechanism
In humans, evidence indicates that incest avoidance mechanisms exist. Since
genetic kinship is not a perceivable trait, the mechanism must be designed to
use cues that reliably predicted kinship during human evolution. In the
fusion-fission band structure of hunter-gatherers, co-residence during infancy
and early childhood was such a cue. Modern humans appear to have a mechanism
that decreases sexual attraction as a function of exposure during
(approximately) the first 6 years of life.