khalswitz
Well-Known Member
The thing not captured in this chat though is the effect that excluding horses who are carriers of recessive disease alleles from breeding has at a population level especially in small effective population size populations.
Its fine to say stop breeding Warmbloods with FFS (it’s been found in TBs as well so there’s a push to stop referring to it purely as a Warmblood disease), because there’s so many thousands of them and they are a large admixed population anyway. But the Connemara and New Forest pony examples, and even smaller breeds like Eriskay, Dales or Cleveland Bay that are all closed populations - excluding carriers of recessive disease alleles means significantly reducing population genetic diversity, which in turn just gives rise to even more recesssive diseases due to inbreeding over time.
There was a lovely study done in Australian TBs that demonstrated an effect of genetic purging in historically inbred TBs - ie, high inbreeding coefficients from further back in the pedigree actually didn’t negatively affect performance, because accumulating recessive disease alleles that affected performance were selected against over time. So it was recent inbreeding that actually had the most negative impact (inbreeding depression) on performance traits.
Personally, I’d be less concerned about a theoretical link between heterozygosity for the FFS allele and hypermobility in WBs than I would be about a disease like PSSM1 where age of onset is older and the type of horse being affected is more likely to be a leisure horse than a performance horse (and thus potentially bred from and selected for despite disease).
Regarding EMS - it’s my pet hypothesis that there’s a genetic component, and I’ve been trying very hard to get a project funded to continue research into it, but not had any takers yet!
Its fine to say stop breeding Warmbloods with FFS (it’s been found in TBs as well so there’s a push to stop referring to it purely as a Warmblood disease), because there’s so many thousands of them and they are a large admixed population anyway. But the Connemara and New Forest pony examples, and even smaller breeds like Eriskay, Dales or Cleveland Bay that are all closed populations - excluding carriers of recessive disease alleles means significantly reducing population genetic diversity, which in turn just gives rise to even more recesssive diseases due to inbreeding over time.
There was a lovely study done in Australian TBs that demonstrated an effect of genetic purging in historically inbred TBs - ie, high inbreeding coefficients from further back in the pedigree actually didn’t negatively affect performance, because accumulating recessive disease alleles that affected performance were selected against over time. So it was recent inbreeding that actually had the most negative impact (inbreeding depression) on performance traits.
Personally, I’d be less concerned about a theoretical link between heterozygosity for the FFS allele and hypermobility in WBs than I would be about a disease like PSSM1 where age of onset is older and the type of horse being affected is more likely to be a leisure horse than a performance horse (and thus potentially bred from and selected for despite disease).
Regarding EMS - it’s my pet hypothesis that there’s a genetic component, and I’ve been trying very hard to get a project funded to continue research into it, but not had any takers yet!
