The average individual taken from a population with a low genetic load will generally, when grown in the same conditions, have more surviving offspring than the average individual from a population with a high genetic load.
[3] High genetic load may put a population in danger of extinction.
[5] The Haldane-Muller theorem of mutation–selection balance says that the load depends only on the deleterious mutation rate and not on the selection coefficient.
A slightly deleterious mutation may not stay in mutation–selection balance but may instead become fixed by genetic drift when its selection coefficient is less than one divided by the effective population size.
[7] In asexual populations, the stochastic accumulation of mutation load is called Muller's ratchet, and occurs in the absence of beneficial mutations, when after the most-fit genotype has been lost, it cannot be regained by genetic recombination.
[8] Sexually reproducing species are expected to have lower genetic loads.
[11][12] The accumulation of deleterious mutations in humans has been of concern to many geneticists, including Hermann Joseph Muller,[13] James F. Crow,[10] Alexey Kondrashov,[14] W. D. Hamilton,[15] and Michael Lynch.
The difference between the theoretical maximum (which may not actually be present) and the average is known as the "lag load".
[17] Motoo Kimura's original argument for the neutral theory of molecular evolution was that if most differences between species were adaptive, this would exceed the speed limit to adaptation set by the substitutional load.
[19] More recent "travelling wave" models of rapid adaptation derive a term called the "lead" that is equivalent to the substitutional load, and find that it is a critical determinant of the rate of adaptive evolution.
[22] In a species that habitually inbreeds, e.g. through self-fertilization, a proportion of recessive deleterious alleles can be purged.
Segregation load occurs in the presence of overdominance, i.e. when heterozygotes are more fit than either homozygote.
In such a case, the heterozygous genotype gets broken down by Mendelian segregation, resulting in the production of homozygous offspring.
Recombination load arises through unfavorable combinations across multiple loci that appear when favorable linkage disequilibria are broken down.
[27] Evidence was reviewed indicating that meiosis reduces recombination load, thus providing a selective advantage of sexual reproduction.
[28] Migration load is hypothesized to occur when maladapted non-native organisms enter a new environment.
[29] On one hand, beneficial genes from migrants can increase the fitness of local populations.
[30] On the other hand, migration may reduce the fitness of local populations by introducing maladaptive alleles.
[31][32] Most studies have only found evidence for this theory in the form of selection against immigrant populations, however, one study found evidence for increased mutational burden in recipient populations, as well.