There is no clear separation between inbreeding and linebreeding. Both terms are used to describe having the same ancestor on both the top and bottom of a pedigree (on both the sire and dam side), typically within the last few generations.
the mating of closely related individuals, as cousins, sire-daughter, brother-sister, or self-fertilized plants, which tends to increase the number of individuals that are homozygous for a trait and therefore increases the appearance of recessive traits.
a form of inbreeding directed toward keeping the offspring closely related to a superior ancestor.
Linebreeding is a form of inbreeding and its goal is the same, to increase the appearance of recessive traits that are manifest within a desired ancestor by increasing homozygosity in the offspring. Linebreeding is only effective because it increases homozygosity, that is the mechanism through which it works to “fix” traits. Homozygosity is directly causative to recessive allele expression. Homozygosity “fixes” recessive traits without distinction to their merits. “Good” and “bad” alleles are doubled up just the same and at random.
Just as linebreeding is only as effective as its ability to fix desired recessive traits by making them homozygous, linebreeding is only as dangerous as its ability to fix undesired recessive diseases by making them homozygous and the limiting of diversity in the MHC. Therefore, linebreeding will always have benefits and risks that are in proportion to the closeness of the breeding and the resulting level of homozygosity. If you breed closer to fix more traits you also increase the risk of expressing recessive disease. This is not to say that the benefits are equal to the risk, a close breeding might be done to “fix” some superficial physical traits that have no utility save fashion and have no impact on performance or health, but in doing so the chance of expressing recessive deleterious disease traits is also greatly increased.
Moral people would not weigh fixing of superficial traits as an equal benefit to offset the expression of a horrible disease. But again and again we observe in the world of purebred dogs people who take the risk for purely cosmetic reasons and their dogs who suffer heavily for it.
While parts of the genome are not specifically more dangerous when they are homozygous, it is certain that the Major Histocompatibility Complex (MHC), which codes for immune response, is greatly disadvantaged by being in a homozygous state: impairing immune function and increasing autoimmune disease result. Deleterious mutations are also a random and constant occurrence in all life, and all recessive disease alleles can hide within lines and populations for many generations before they are doubled up by inbreeding. This “genetic load” is an unknown quantity as we do not have tests for every disease gene, nor have we even identified them all (or most). We have only identified a small fraction of disease causing alleles. There are hundreds of millions of dogs in the world, and almost 100 million in the US alone, and each of those dogs have new mutations that are unique to them and many more mutations that were new to their parents and grandparents. There are potentially hundreds of millions of unidentified mutation alleles and yet we have DNA tests for fewer than 200 diseases and many breeds have no breed-specific DNA tests at all.
For all we do know, we are still in a profound state of ignorance. And while helpful, testing is no panacea to compensate for continued over-use of linebreeding, inbreeding, and closed stud books.
With both inbreeding and linebreeding: the greater the benefit, the greater the homozygosity, and the greater the risk. And it is a risk that we can not hope to mitigate fully with any sort of disease testing. Nor can it be mitigated with pedigree research or “knowing your lines.” You might be able to dodge one or two known issues that other breeders have been open about, but we must admit that we don’t know anything about 99% of our dogs’ genetics. We can know a few things about their size and color, a few things about the disease history of some of their ancestors, but at most this accounts for a few dozen genes. Dogs have tens of thousands of genes.
How “close” a breeding is can be measured using the Coefficient of Inbreeding, abbreviated COI. Depending on how many ancestors are in common and how far back they are and how inbred they were themselves, different ancestry patterns can create the same level of homozygosity for a trait in the offspring. For example, a half-sibling mating has the same COI and the same level of increased homozygosity as an Uncle-Neice/Aunt-Nephew breeding. Both have a COI of 12.5%. Brother-Sister breeding and Parent-Child breeding are different but both have a COI of 25%. A COI of 25% means that on average 25% of the offspring’s alleles are going to be in a homozygous state (like-pairs) based only on the pedigree information we’ve used in the calculation. This is referred to as “identical by decent.”
Whereas COI only accounts for homozygosity created by recent generations, all dog breeds have a “background” level of homozygosity which is the result of breed formation and a history of discarding genetic diversity by choice and by consequence of a limited number of founders, popular sires, only breeding a few dogs each generation, quickly purging disease carriers out of the gene pool, and the prior fixation of traits like color or hair length. This existing level of homozygosity makes further linebreeding even more problematic as far as disease expression. This homozygosity is referred to as “identical by state.”
When linebreeding more alleles double up than the ones we wish to fix. In fact many times more. There are more recessive genes that cause disease than we have tests for. We can not test for every disease. And we have no idea about new mutations. When we double up huge swaths of alleles for the sake of aesthetics or performance we create collateral damage. And this is how recessive disease becomes prevalent in lines and breeds and why dogs have rates of disease expression that are epidemic compared with other species.
As the genetic load of more than a century of closed stud books and breeding behaviors that increase homozygosity and decrease what genetic diversity remains takes its toll, more and more breeds are now finding themselves plagued by epidemic levels of inbred disease. Linebreeding as the go-to strategy to win ribbons and “improve” breeds is doing the opposite of improvement. Not only do we need to open stud books and make routine introduction of new blood a part of the culture of dog breeding, we also need to promote effective breeding strategies that still result in fixing desirable traits without compromising the immune systems and without inflicting such high levels of disease on our dogs. One such strategy is called “Assortative Mating” where breeding stock is chosen because of its likeness in the traits we desire without being closely related. Breed two fast dogs together instead of two fast siblings. Breed a dog with the desired ear-set to another dog with the desired ear-set, but not father to daughter. And if that fast dog or perfectly eared dog is from another breed, by all means include it in your breeding program.
We can have predictability without sacrificing health. Do the work to find appropriate stock outside of your own kennel instead of promoting recessive disease expression though incest.
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