I didn’t want to hijack the EIC thread, but it has brought a question to my mind. I will try to keep this from running too long. There seems to be a movement toward breeding clears to clears, or at least breeding carriers to clears with the goal to breed only clears and eliminating the affected from this part of the gene pool. I understand the back yard breeders will continue the poor genetics, but there we are.
I cast this against the discussions on hip dysplasia. There appears to be a concerted effort to make hips look as good as you can on film to get a good rating and if we get a good film and the resultant good rating, we breed. This doesn’t seem to be the same conservative philosophy I am seeing with the CNM and EIC discussions.
There is some evidence that we haven’t made any real headway on reducing the occurrence of CHP despite the years of testing and breeding practices. There is an argument that PennHip which measures laxity of the joint provides a better method of identifying the potential for the resulting arthritis and remodeling. This also seems to have its limitations. There is that group in the study with DI’s between 0.30 and 0.70 that is not real clear yet, except that the occurrence of DJD increases.
Comments about having 2nd and 3rd opinions, retaking x-rays, doing x-rays without chemical restraint so the muscles hold the joint together better, etc. begins to sound like “I will keep asking until I get the answer I like.” Yes, I know there is a lot going into this evaluation that is difficult, we don’t want to eliminate based on poor diagnostic technique, etc, and I can agree with that. The question still has to be asked though, how conservative is this approach? There at least on first look appears to be plenty of room for making it all about the hip rating and not about the hips. Just because we can get film that doesn't show the laxity, does it remove it or wasn't it really there? Even if the muscles in the real world keep the joint together and there isn't any problems develop, does it remove the genetics that producted it?
Is it that we still don’t have enough understanding of the disease to make better decisions? Are we just left with two imperfect diagnostic tools to use together and make the “best decisions” we can until we have better information? I will be the first to admit I do not have the answers, but I am interested in others take on this. As you can tell from this recitation, I am struggling with this issue and would appreicate your point of view.
I cast this against the discussions on hip dysplasia. There appears to be a concerted effort to make hips look as good as you can on film to get a good rating and if we get a good film and the resultant good rating, we breed. This doesn’t seem to be the same conservative philosophy I am seeing with the CNM and EIC discussions.
There is some evidence that we haven’t made any real headway on reducing the occurrence of CHP despite the years of testing and breeding practices. There is an argument that PennHip which measures laxity of the joint provides a better method of identifying the potential for the resulting arthritis and remodeling. This also seems to have its limitations. There is that group in the study with DI’s between 0.30 and 0.70 that is not real clear yet, except that the occurrence of DJD increases.
Comments about having 2nd and 3rd opinions, retaking x-rays, doing x-rays without chemical restraint so the muscles hold the joint together better, etc. begins to sound like “I will keep asking until I get the answer I like.” Yes, I know there is a lot going into this evaluation that is difficult, we don’t want to eliminate based on poor diagnostic technique, etc, and I can agree with that. The question still has to be asked though, how conservative is this approach? There at least on first look appears to be plenty of room for making it all about the hip rating and not about the hips. Just because we can get film that doesn't show the laxity, does it remove it or wasn't it really there? Even if the muscles in the real world keep the joint together and there isn't any problems develop, does it remove the genetics that producted it?
Is it that we still don’t have enough understanding of the disease to make better decisions? Are we just left with two imperfect diagnostic tools to use together and make the “best decisions” we can until we have better information? I will be the first to admit I do not have the answers, but I am interested in others take on this. As you can tell from this recitation, I am struggling with this issue and would appreicate your point of view.
