Is inbreeding really efficient at producing homozygosity?

Is inbreeding really efficient at producing homozygosity?

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Inbreeding results in homozygosity.

I've come across this concept many times and there's a question that comes to my mind every time I read it.

Let us suppose the character we are trying to establish is dominant trait controlled by a biallelic gene and the two individuals (animals) we have selected to inbreed both have the genotypes Aa.

Aa x Aa = AA/ Aa/ aa in the ratio 1:2:1

So the possibility of having a homozygous dominant is 25% while that of heterozygous is 50%. As the breeder has no access to technologies and find out the genotype of the F1 individuals there's a possibility that he would choose two F1 individuals with Aa genotype once again (which has the highest possibility of occurrence). And the same is repeated , production of F2 offsprings with 50% possibility of heterozygous individuals.


So getting a homozygous dominant individual is very less likely to happen.

My question, is inbreeding really efficient at producing homozygosity?

And the same is repeated , production of F2 offsprings with 50% possibility of heterozygous individuals.

That's not correct.

Let's start with a population with 100% of heterozygotes:

100% Aa

And, just to create a highly exaggerated model, let's suppose that these individuals perform the most drastic case of inbreeding: self-fertilization. Inbreed occurs when an individual perform sexual reproduction with a closely related organism, and no one is more closely related to someone than himself!

After the first "inbreeding" generation, we'll have:

25% AA 50% Aa 25% aa

So, 50% of heterozygotes.

If this population inbreeds again, we'll have at the second generation:

37.5% AA 25% Aa 37.5% aa

So, 75% of homozygotes versus 25% of heterozygotes.

In the third generation:

43.75% AA 12.5% Aa 43.5% aa

And in the fourth generation:

46.875% AA 6.25% Aa 46.875% aa

Thus, in only 4 generations, we have 93.75% of homozygotes versus 6.25% of heterozygotes. Mathematically, the heterozygotes never disappear. Biologically, however, if a population shows self-fertilization, heterozygotes disappear in few generations.

Now, let's get out of this overly exaggerated example with self-fertilization and back to your question, where the organisms perform cross-fertilization:

The problem with your reasoning is that (correct me if I'm wrong) you're starting with a couple (Aa) and supposing that all their descendants will mate randomly. Of course, the allele frequencies will remain the same. But that's not inbreeding. By definition, inbreed is a non-random mating system. For a real inbreed to occur, the mating individuals should be more closely related than those drawn by chance from the population.

In conclusion, given enough time, inbreeding (and genetic drift as well) has the effect of eradicating heterozygotes from the population.

Still bluffing it re co-efficients of inbreeding?

It was at Crufts 2008, five months before Pedigree Dogs Exposed broadcast, that the KC's then-genetics advisor Jeff Sampson told me: "We will never give breeders COIs (co-efficients of inbreeding). They wouldn't know what to do with them."

Three years on, in May 2011, the Kennel Club launched Mate Select - giving breeders, owners and researchers access to inbreeding data (and health info) on individual dogs and breeds for the first time. The KC has claimed several times that, at best, PDE sped up reform and didn't instigate it. But of course it had had plenty of opportunity to tell me about Mate Select if it had really been in development pre-PDE and it didn't.

(One day, I'll blog what they sent me regarding the breeds on the then high-profile list pre-PDE too. absolutely pitiful.)

Now, Mate Select has its flaws but there's no doubt that it's a fantastically useful tool - as is its sister utility MyKC, which gives access to more detailed breeding data. Both are free, too - all kudos to the Kennel Club for that and the other data it is now making available.

So. for those of you still struggling with COI is, here are two guides.

The first is this very simple explanation written by me a while back - how hosted on Carol Fowler's website:

And here's a comprehensive guide from Carol Beuchat at the Institute for Canine Biology:


That is good news, but it's still just shuffling deck chairs on the Titanic. Until kennel clubs change their paradigm and open all registries, they are dooming their dogs to inbreeding depression.

BTW - The photograph above is such a clear illustration of inbreeding. If that doesn't help proponents of pure-breeding realize that many of their breeds are really just canine versions of those human genetic disorders, I don't know what we can do to get through to them.

I've long been a fan of PDE and your efforts, Jemima, but the inflammatory picture at the head of the post is rather in poor taste.

1. There's no indication as to the source. To me, they look like unrelated individuals with various genetic and perhaps birth defects. There is no evidence that they are related and that their conditions are a result of inbreeding. Also, it's unseemly to poke fun at people at people with genetic disorders or disabilities, even obliquely like you've done here.

2. It hurts your mission by making you look like you're mudslinging. I understand completely what you're driving at with the image, but it's not making the point you think it's making.

3. You're missing an opportunity to provide an image or images of dogs who DO suffer both inwardly and outwardly as a result of inbreeding.

Just something to consider. There is more than enough legitimate science and research behind your mission and there are plenty of pictures out there of dogs gone awry. You don't need gruesome or shocking images of people (like the fellow in the somewhat recent Boston Terrier post) to bring your point across.

Anon 7:19, in essence I agree with your comments. HOWEVER, breeders do not seem to understand the "conditions" they breed into dogs hurt or are damaging to the well being of that animal and future generations. English Setters for eg. now plagued with awful itchy skin, painful for the dog, stressful for their usually pet owners not to say expensive, but the breeders pass it off as a minor problem. It isn't. Throw a breeder into a bed of stinging nettles naked and then come back with what their response is, they won't be happy. SO - in order to get breeders to relate to the horrible afflictions that they are deliberately breeding into dogs a photograph of the sort shown above should make them think. Think "how would they cope with poor hips, skin condition, digestive problems, sore eyes, etc etc" assuming that they are intelligent of course, and have compassion they may come to understand. By relating a word to an illness should make them realise that that word is causing pain, discomfort, and life comprising afflictions. The photograph shows a classic state of what will happen if there is too much inbreeding in a bloodline in my opinion. Too many breeders have no actual understanding of what they are doing they just don't feel the pain of what they are producing in their dogs and until they do the dogs will continue to suffer.

Cocoa (Theobroma cacao L.)


Inbreeding forms a part of the breeding activities not only to breed parents with some degree of homozygosity for the production of hybrids but also breed materials homozygous for such desirable traits as disease resistance. Self-incompatibility makes inbreeding difficult or impossible. In cocoa, certain incompatible trees are encountered in a population, and in these plants selfing is possible. The selfing needs to be continued up to six to seven generations to attain homozygosity, and thereafter these plants can be utilized for crossing to exploit hybrid vigor. An inbreeding program has been in progress in the Kerala Agricultural University ( Mallika et al., 2002a ) since 1987.

How to handle the burden of deleterious mutations

With the increasingly pressing matter of populations being threatened by fragmentation and isolation, and with progressively more efficient sequencing technologies and analytical tools at hand, conservation genetics is starting to turn the spotlight on the topic of genetic load. It has become clear that population survival is not only about population sizes and estimates of genetic diversity. Some populations thrive despite extremely low genome-wide diversity, while others go extinct despite seemingly much better prospects.

The buzzword that keeps coming up in recent publications, is purging. Purging is defined as the “increased purifying selection facilitated by inbreeding as it increases the homozygosity of partially recessive deleterious variants” (Hedrick and Garcia-Dorado 2016). In other words, in small populations, where the inbreeding usually increases homozygosity, more of the really nasty stuff [aka highly deleterious mutations] is revealed in homozygous state, which makes it easier for purifying selection to act upon.

The problem is that studies examining bottlenecked natural populations are not conclusive on how much mutational load accumulates in small populations and how much is purged by selection. Remember that in small populations, selection is assumed to be overshadowed by the effects of genetic drift, therefore it is not clear how much power it has for eliminating deleterious mutations.

While some studies found empirical evidence of accumulation of genetic load in a population with low effective population size, for instance in the woolly mammoth (Rogers and Slatkin 2017) and the crested ibis (Feng et al. 2019), others showed that purging of highly deleterious mutations does take place in populations of extremely bottlenecked species, for example in the Channel Island foxes (Robinson et al. 2018) and mountain gorillas (Xue et al. 2015).

The new study by Christine Grossen and colleagues (Grossen et al. 2020) looked at the problem in a beautiful model system of the once near-extinct Alpine ibex. Back at the beginning of the 19 th century, there were less than 100 individuals left in a single population in Gran Paradiso, Italy. After recolonizations, the Alpine ibex is now at a census size of 50,000 individuals. Interestingly, the successful recolonized populations were used to found other populations, and thus, the extant populations experienced two to four bottlenecks, which are also well documented in the records.

Grossen et al. analysed 60 high-coverage genomes of seven species, the domestic goat and six wild goat species. The wild species cover a range of population sizes (from 200,000 in the Siberian ibex to 2,500 in the Nubian ibex), red-list categories (from Least Concern after near extinction, to Vulnerable), and also a range of demographic histories. Put together, the Alpine ibex wins the overall competition for being the most bottlenecked (down to 100 individuals), having the least nucleotide diversity and having a considerable part of the genome in runs of homozygosity (ROH).

So let’s focus on the Alpine ibex from now on. Grossen et al. used demographic records to estimate long-term effective population sizes and compared these to the estimates of nucleotide diversity, concluding that nucleotide diversity decreased with smaller long-term population size. The same goes for heterozygosity, while the inbreeding (from ROH) showed inverse pattern.

Next, the authors estimated high-confidence deleterious mutations based on a) GERP analysis of conserved regions, b) transciptomic analysis and genes missing evidence of transcription, and for some analyses also c) functional annotation of each variant in snpEff. Grossen et al. used a whole battery of genetic load tests, starting with the proportion of segregating, highly deleterious mutations. This was inversely correlated with nucleotide diversity, and thus, most pronounced in the most bottlenecked populations – the Alpine ibex, Iberian ibex, and Markhor.

Site frequency spectra (SFS) analyses were used to look for evidence of purging selection.

“Both Alpine and Iberian ibex experienced severe bottlenecks due to overhunting and habitat fragmentation. We first analyzed evidence for purifying selection using allele frequency spectra. We focused only on derived sites that were polymorphic in at least one of the two sister species. … We found that frequency distributions of high and moderate impact mutations in Alpine ibex were downwards shifted compared to modifier (i.e. neutral) mutations, which strongly suggests purifying selection against highly deleterious mutations. … We found no comparable frequency shifts in Iberian ibex (Fig. 2b). This is consistent with purifying selection acting more efficiently against highly deleterious mutations in Alpine ibex compared to Iberian ibex.” (Grossen et al. 2020)

They also calculated the relative number of derived alleles Rxy, comparing the Alpine ibex to the Iberian ibex across the spectrum of different mutation impact categories, using a set of intergenic SNPs for standardization. It turns out that the Alpine ibex, compared to the Iberian ibex has a minor excess of low to moderate impact mutations however, it has a strong downward allele frequency shift in the highly deleterious mutation category. Together with the observation of a lower individual allele count at highly deleterious sites and lower number of homozygous sites with highly deleterious mutations, this provides a good evidence of purging in the Alpine ibex.

Zooming in, the authors looked at the genetic load across populations, focusing on whether the genetic load increases with the number of bottlenecks that the population went through.

“Bottlenecks affect the landscape of deleterious mutations by randomly increasing or decreasing allele frequencies at individual loci. We find that individuals from populations that underwent stronger bottlenecks carry significantly more homozygotes for nearly neutral and mildly deleterious mutations (i.e. modifier, low and moderate impact mutations Fig. 4a). In contrast, individuals showed no meaningful difference in the number of homozygotes for highly deleterious (i.e. high impact) mutations across populations. The stability in the number of homozygotes for highly deleterious mutations through successive bottlenecks despite a step-wise increase in the number of homozygotes for weaker impact mutations, supports that purging occurred over the course of the Alpine ibex reintroductions.” (Grossen et al. 2020)

I could continue, but I guess that you get the picture. The take-home message is that mutational load accumulates in bottlenecked populations through mildly deleterious mutations, while highly deleterious mutations can be purged under extreme bottlenecks.

I really liked how the authors formulated the conclusions, so I will leave the last words to them:

“Our empirical results are also in line with predictions that populations with an effective size below 100 individuals can accumulate a substantial burden of mildly deleterious mutations. Such mutation load constitutes long-term extinction risks in contrast to short-term risks associated with highly deleterious mutations. The burden of deleterious mutations evident in Iberian ibex supports the notion that even population sizes of

1000 still accumulate mildly deleterious mutations. High loads of deleterious mutations have been shown to increase the extinction risk of a species. Thus, conservation efforts aimed at keeping effective population sizes above a minimum of 1000 individuals are critical for the long-term survival of managed species.” (Grossen et al. 2020)

P.S.: This paper has truly beautiful figures. I had to restrain myself from using them all, so go check out the paper.


Grossen, Christine, Frédéric Guillaume, Lukas F. Keller, and Daniel Croll. 2020. “Purging of Highly Deleterious Mutations through Severe Bottlenecks in Alpine Ibex.” Nature Communications.

Feng, Shaohong, Qi Fang, Ross Barnett, Cai Li, Sojung Han, Martin Kuhlwilm, Long Zhou, et al. 2019. “The Genomic Footprints of the Fall and Recovery of the Crested Ibis.” Current Biology.

Hedrick, Philip W., and Aurora Garcia-Dorado. 2016. “Understanding Inbreeding Depression, Purging, and Genetic Rescue.” Trends in Ecology and Evolution.

Robinson, Jacqueline A., Caitlin Brown, Bernard Y. Kim, Kirk E. Lohmueller, and Robert K. Wayne. 2018. “Purging of Strongly Deleterious Mutations Explains Long-Term Persistence and Absence of Inbreeding Depression in Island Foxes.” Current Biology.

Rogers, Rebekah L., and Montgomery Slatkin. 2017. “Excess of Genomic Defects in a Woolly Mammoth on Wrangel Island.” PLoS Genetics.

Valk, Tom van der, David Díez-del-Molino, Tomas Marques-Bonet, Katerina Guschanski, and Love Dalén. 2019. “Historical Genomes Reveal the Genomic Consequences of Recent Population Decline in Eastern Gorillas.” Current Biology.

Xue, Yali, Javier Prado-Martinez, Peter H Sudmant, Vagheesh Narasimhan, Qasim Ayub, Michal Szpak, Peter Frandsen, Yuan Chen, Bryndis Yngvadottir, and David N Cooper. 2015. “Mountain Gorilla Genomes Reveal the Impact of Long-Term Population Decline and Inbreeding.” Science 348 (6231): 242–45.


Resistance assays

We found that inbreeding significantly increased susceptibility to parasitism. In the first study, there was a significant effect of inbreeding treatment (Table 1): prevalence of infection among the inbred F[5] flies was significantly higher compared with outbred flies (Fig. 1). Logistic regression, using a reduced data set, revealed no effect of body size on the probability of infection ( = 0.47, P = 0.49), while inbred status remained a significant predictor of infection ( = 4.74, P < 0.05). No linear relationship using regression analysis was revealed between body size and the number of mites per fly (F[1,522] = 0.99, P = 0.32).

Source SS DF MS F P
Study 1
Trtmt† 0.171 1 0.171 10.96 0.005
Line 0.349 14 0.025 0.76 0.700
Jar (line) 0.280 13 0.022 4.57 0.005
Trtmt × line 0.227 14 0.016 3.44 0.016
Error 0.061 13 0.005
Study 2
Trtmt† 0.923 3 0.308 6.49 0.0007
Line 2.439 21 0.116 1.32 0.1952
Jar (line) 3.996 59 0.068 2.43 0.0001
Trtmt × line 3.024 63 0.048 1.72 0.0030
Error 4.930 177 0.028
  • SS, sum of squares DF, degrees of freedom MS, mean square, †Trtmt = inbreeding treatment levels: F[0], F[5] (study 1), and F[0], F[1], F[3], F[5] (study 2).

In the second study, inbred flies pooled across F[1], F[3] & F[5] levels of inbreeding were significantly more susceptible to parasitism than outbred flies (F[1,221] = 24.44, P < 0.0001). In an expanded analysis, in which all levels of inbreeding were represented separately, there was a similarly strong effect of inbreeding treatment (Table 1), such that mean prevalence of infection among the outbred flies was significantly lower compared with either the F[1], F[3] and F[5] inbred categories, but these inbred groupings did not differ from each other (Tukey–Kramer's tests, P > 0.05, Fig. 1). Importantly, in both studies, there was a significant treatment-by-line interaction (Table 1), indicating a heterogeneous response to inbreeding among the genotypes.

Outcross experiment

We found significant differences in the prevalence of infection among groups in both the first (F[4,45] = 6.51, P < 0.001) and second (F[4,45] = 8.50, P < 0.0001) replicates (Fig. 2). The mean prevalence among hybrid lines was significantly lower compared with their respective parental-inbred lines (Tukey–Kramer's tests, Fig. 2). This elevated level of resistance in hybrids was comparable with the outbred populations, confirming the causative link between expected heterozygosity because of hybridization and enhanced resistance, i.e. heterosis ( Lynch & Walsh, 1998 Tompkins et al., 2006 ).

Prevalence of infection for outbred (Outb), inbred (Inb1, Inb2) and hybrid lines (F1, F1r). The two inbred lines in the first replicate are independent of the two inbred lines in the second replicate. Error bars indicate ±1 SE. Within each replicate study, means not sharing a letter are statistically different (α < 0.05) by way of Tukey-Kramer's post hoc testing.

Host stamina and parasite resistance

Mean hover time to exhaustion was 61 % less for inbred [back-transformed least-square mean (lsmean) ±SE = 73.5 min ±1.21, n = 19] compared with outbred flies (lsmean, 186.4 min ±1.31, n =9 F[1,23] = 7.65, P = 0.01). In the second endurance study, mean hover times for the high susceptibility lines were less than both the low susceptibility and outbred lines, which themselves were not significantly different from each other (Fig. 3). Differences among lines were strongly significant (F[4,113] = 13.45, P < 0.001). All lines, including the outbred population, were equally likely to initiate hovering ( = 0.738, P = 0.95), and body size was not significantly associated with hover time (F[1,89] = 0.15, P = 0.70). These results demonstrate that inbred flies become exhausted sooner.

Mean hover time for outbred and inbred lines. Based on Tukey–Kramer's post hoc analysis, the average endurance was significantly lower in the two F[5] inbred-high susceptible lines (H1 & H2) compared with the two inbred-low susceptible (L1 & L2) and outbred lines. Means not sharing a letter are statistically different (α < 0.05). Data represent log10-transformed means ±1 SE. Numerals inside bars indicate the number of individuals.

Next, across the 43 assay chambers in which one exhausted fly and one control fly were simultaneously exposed to mites, the mean elapsed time to parasitism was 41.7 min ±2.8 SE (n = 43). In four (9 %) of all trials, both members of a pair recovered from a chamber carried one or more mites. In 34 (87.2%) of the 39 exposure trials that resulted in a single fly becoming parasitized, it was the exhausted fly that became parasitized (Fisher's exact test, P < 0.0001). Multiple logistic regression indicated that the treatment effect (i.e. exhausted or not) on the probability on parasitism was strong ( =28.80, P < 0.0001), but that there was no effect of day ( = 1.20, P = 0.3). Moreover, among the infected flies, the median mite burden for the exhausted category (6.5 mites, range = 38, n = 39) was significantly greater than that for rested controls (2.0 mites, range = 11, n = 9 Wilcoxon Z = 2.50, P = 0.01). Thus, host exhaustion (via tethered flight) significantly increases susceptible to parasitism by mites.

Finally, we found that exposure to mites in the infestation chambers had a significant negative effect on host stamina. Overall there was a significant effect of treatment (F[2,45] = 5.98, P < 0.01) and block (F[3,45] =8.96, P < 0.0001) on time to exhaustion. The effects of sex (F[1,45] = 0.75, P = 0.39), treatment x block (F[6,45] = 1.73, P = 0.14) and treatment x sex (F[2,45] = 0.46, P = 0.63) were nonsignificant. Time to exhaustion did not differ significantly between flies in the control vials (134.1 ± 16.0, n = 18) and those in the control chambers (137.8 ± 14.3, n = 22 Tukey–Kramer, P = 0.98), but flies from the control groups had significantly longer hover times than flies from the infestation chambers (73.0 ± 14.9, n = 20 Tukey–Kramer, P = 0.008 and 0.02, respectively) flies that interacted with mites experienced approximately a 50% reduction in time to exhaustion compared with controls. Thus, exposure to mites resulted in an increased rate of exhaustion during the subsequent hovering trials, demonstrating that interactions with mites are energetically expensive. All flies initiated hovering, and body mass did not influence hover time (F[1,56] = 0.14, P = 0.71).

Three key strategies to reduce genetic disorders

Every dog – in fact, every animal – has mutations that could potentially cause disease, and don’t let anybody try to claim that their dogs are any different. The key to producing healthier dogs is breeding in a way that reduces the chance that an animal will inherit two copies of the same mutation. Doing the available DNA tests for a breed then producing a litter with an inbreeding coefficient of 20% is self-defeating and just asking for trouble. Money to identify mutations, develop tests, and screen potential breeding stock is all for naught if we are using breeding strategies that are specifically designed to increase homozygosity of the genes for desirable traits, because homozygosity of mutations will necessarily increase as well. You cannot do one without the other.

If we’re serious about reducing genetic disorders in dogs, the things we must do are simple and clear. It is responsible breeders, not researchers and DNA tests, that will reduce the burden of genetic disease in dogs.

Online course starts 1 February 2016
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— 10 weeks, $125


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Inbreeding avoidance mechanisms have evolved in response to selection against inbred offspring. Inbreeding avoidance occurs in nature by at least four mechanisms: kin recognition, dispersal, extra-pair/extra-group copulations, and delayed maturation/reproductive suppression. [2] [10] Of note, these mechanisms are not mutually exclusive and more than one can occur in a population at a given time.

Kin recognition Edit

Kin recognition is the mechanism by which individuals identify and avoid mating with closely related conspecifics. There have been numerous documented examples of instances in which individuals are shown to find closely related conspecifics unattractive. In one set of studies, researchers formed artificial relative and non-relative mate-pairs (artificial meaning they preferentially paired individuals to mate for the purposes of the experiments) and compared the reproductive results of the two groups. In these studies, paired relatives demonstrated reduced reproduction and higher mating reluctance when compared with non-relatives. [10] [11] [12] [13] For example, in a study by Simmons in field crickets, female crickets exhibited greater mating latency for paired siblings and half-siblings than with non-siblings. [11] In another set of studies, researchers allowed individuals to choose their mates from conspecifics that lie on a spectrum of relatedness. In this set, individuals were more likely to choose non-related over related conspecifics. [10] [12] [14] For example, in a study by Krackow et al., male wild house mice were set up in an arena with four separate openings leading to cages with bedding from conspecifics. The conspecifics exhibited a range of relatedness to the test subjects, and the males significantly preferred the bedding of non-siblings to the bedding of related females. [12]

Studies have shown that kin recognition is more developed in species in which dispersal patterns facilitate frequent adult kin encounters. [10]

There is a significant amount of variation in the mechanisms used for kin recognition. These mechanisms include recognition based on association or familiarity, an individual's own phenotypic cues, chemical cues, and the MHC genes. In association/familiarity mechanisms, individuals learn the phenotypic profiles of their kin and use this template for kin recognition. [10] Many species accomplish this by becoming "familiar" with their siblings, litter mates, or nestmates. These species rely on offspring being reared in close proximity to achieve kin recognition. This is called the Westermarck effect. [15] For example, Holmes and Sherman conducted a comparative study in Arctic ground squirrels and Belding's ground squirrels. They manipulated the reared groups to include both siblings and cross-fostered nestmates and found that in both species the individuals were equally aggressive toward their nestmates, regardless of kinship. [16] In certain species where social groups are highly stable, relatedness and association between infants and other individuals are usually highly correlated. [10] [17] Therefore, degree of association can be used as a meter for kin recognition.

Individuals can also use their own characteristics or phenotype as a template in kin recognition. For example, in one study, Mateo and Johnston had golden hamsters reared with only non-kin then later had them differentiate between odors of related and non-related individuals without any postnatal encounters with kin. The hamsters were able to discriminate between the odors, demonstrating the use of their own phenotype for the purpose of kin recognition. [18] This study also provides an example of a species utilizing chemical cues for kin recognition.

The major histocompatibility complex genes, or MHC genes, have been implicated in kin recognition. [19] One idea is that the MHC genes code for a specific pheromone profile for each individual, which are used to discriminate between kin and non-kin conspecifics. Several studies have demonstrated the involvement of the MHC genes in kin recognition. For example, Manning et al. conducted a study in house mice that looked at the species's behavior of communal nesting, or nursing one's own pups as well as the pups of other individuals. As Manning et al. state, kin selection theory predicts that the house mice will selectively nurse the pups of their relatives in order to maximize inclusive fitness. Manning et al. demonstrate that the house mice utilize the MHC genes in the process of discriminating between kin by preferring individuals who share the same allelic forms the MHC genes. [20]

Post-copulatory inbreeding avoidance in mice Edit

Experiments using in vitro fertilization in the mouse, provided evidence of sperm selection at the gametic level. [21] When sperm of sibling and non-sibling males were mixed, a fertilization bias towards the sperm of the non-sibling males was observed. The results were interpreted as egg-driven sperm selection against related sperm.

Human kin recognition Edit

The possible use of olfaction-biased mechanisms in human kin recognition and inbreeding avoidance was examined in three different types of study. [22] The results indicated that olfaction may help mediate the development during childhood of incest avoidance (the Westermarck effect).

Inbreeding avoidance in plants Edit

Experiments were performed with the dioecious plant Silene latifolia to test whether post-pollination selection favors less related pollen donors and reduces inbreeding. [23] The results showed that in S. latifolia, and presumably in other plant systems with inbreeding depression, pollen or embryo selection after multiple-donor pollination may reduce inbreeding.

Natural History

The only people who think it is good don’t know what they are talking about– or they have been so severely indoctrinated into the dog culture that they can’t see it.

In virtually all of these dog registry and competition systems, there is a strong desire to produce a high level of homozygosity in either behavior or conformation. You win more consistently if you have more homozygosity in your lines. It doesn’t matter if we’re talking shih-tzus or trial border collies. The tendency is to breed tightly and to breed to the dogs that win.

No one sits back and thinks about what this does to the dog populations in the long-term, because no one is really in it for the long term. You’re in it to win it.

This means that dogs will continue to lose genes over time. At the very same time, it will be these breeders who are forcing them down these tight genetic bottlenecks who will say they are improving the dogs.

They might be improving in one sense, but in another, they are impoverishing their animals with each successive generation.

The least obvious way in which they are impoverishing their dogs has to do with the immune system. You can’t see immune systems or the genes associated with them, but by golly, you can lose immune system genes.

The genes associated with the immune system are called the Major Histocompatibility Complex, which are called the dog leukocyte antigen (DLA) system. These genes are very easily lost when one is inbreeding or very tightly line breeding.

Now, in most domestic dog populations, breeders are operating within a closed registry system. These closed registries rarely allow new blood in, and if they do, it will most often be from dogs that derive from the same founding population– so it’s not really a new infusion of genes at all.

Then, you have another nice problem within closed registry systems. They demand that people breed only from the best dogs within that system. So certain winning stud dogs wind up siring a huge proportion of the puppies in each generation. Over time, many of these dogs wind up with very similar paternal ancestors, which means it’s very hard to produce dogs within the breed that are not highly inbred.

So you essentially have a system set up for the destruction of the domestic dog as an organism. Over time, the immune system will continue to weaken, coefficients of inbreeding will continue to increase, and the health and reproductive ability of the dogs will continue to fail.

Do we seriously want dogs to end up here?

Do we think all of these breeds are so unique that we can never allow a gene flow to exist between them?

If we think all of these things are true, then we have to accept the obvious consequence– the total collapse of many breeds.

And this analysis doesn’t even account for the tendency for deleterious and lethal recessives to be inherited in a homozygous fashion as a result of inbreeding.

If we are to be honest about saving dogs, we need to tell these people who promote this toilet science of blood purity and who sanctify consanguinity that they are very wrong– and what they are doing is ultimately dangerous.

I don’t care if some breeder or some half-assed geneticist says it’s okay.

It’s going to destroy dogs.

Someone might get good results from a very tight breeding.

That’s not what I’m talking about.

I’m talking about population genetics and population genetics over time.

If everyone is doing that sort of breeding over a long period of time within a closed registry system, it is guaranteed to fail.

But the institutionalized fancy and its token prostitute scientists continue to promote inbreeding and make apologies for its use that are so twisting of the actual science of dog biology that one wonders if these people might be closet creation scientists.


We thank customers of Embark whose participation made this work possible, in particular the Doberman Diversity Project. We also thank all of the Embark employees who made this work possible, particularly Ryan Boyko, Matt Barton, Erin Chu, Adam Gardner, Tiffany Ho, Andrea Slavney, and Samuel H. Vohr. We also thank the Embark scientific advisory board (in particular Carlos Bustamante for comments on this manuscript), Cornell University, and the Kevin M. McGovern Family Center for Venture Development in the Life Sciences, for their guidance and encouragement. This study was funded by the participants and by Embark.