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Post by Dahdo on Nov 29, 2012 11:46:41 GMT -5
Thank you Kirk for having the guts to open and continue this discussion in a respectful manner. And yes, “hairless, mule-footed, dwarfs”, was probably over the line, but at least your frustration was expressed as an attempt at humor. And thanks to all who have contributed in positive ways on both sides of the issue. It has helped me clarify own thinking on this issue.
I believe chondro is a special case of a genetic disease. Some people clearly think it is a beneficial, or at least, a useful genetic disease. It has been around a long time and people have made significant investments in carrier breeding stock. Some people think it makes a Dexter a Dexter. I have made a different choice, but I don’t think we can change the rules this late in the game. That said, I believe we all need to know with certainty which animals are chondro positive, and there should be a requirement to test or grant obligate status with parentage verification for every registered animal.
PHA on the other hand has no benefit to the breed. Far from it. Sure these animals also carry some fine genetics which should be retained, but why not save their non-carrier progeny, cull the rest, and let PHA die out within a generation?
Which brings me to future genetic mutations that Kirk very correctly points out WILL occur. What are we going to do? I haven’t even registered my first calf under my own farm name yet, but I can see that this is going to be a problem. We should assume that the current popularity of the breed is only going to grow and that the small group of experienced breeders is going to grow into a larger group of less experienced breeders over a short period. We need a plan so we don’t end up with another PHA where the disease contaminates our rich gene pool that you all have worked so hard to build.
I held off joining this conversation until now because I was not sure I had “standing”. But these discussions of genetic disease have made me think about the issue more than ever before and try and reach my own conclusions. I didn’t think I had standing because I am a small holder and relatively new to Dexters and cattle. Now I believe I do have standing because, number one, I am an owner: one of your customers. And number two: I am committed to becoming a good breeder and doing a small part to perpetuate this wonderful breed that we all love.
You all have helped me here many times in the past couple of years, but maybe never more than you have in the past few weeks by opening the lid on this issue and airing it out a little bit.
Thanks again to you all. Dave
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Post by Olga on Nov 29, 2012 12:00:28 GMT -5
You come across very strong, Kirk, knowingly or not, and that may have led me to perceive your ideas and proposals more radical than you may have intended. But if these initiatives have been around for many years, don't you think it's logical to conclude that they have failed to achieve general membership buy-in? Do some research, look up membership statistics. My hypothesis is that most breeders, however involved into the maintenance, improvement and preservation of the Dexter breed they may be, are ultimately guided by the market. They will not stop breeding what sells. As to ridicule, that recent statement of yours about breeding hairless mule-footed short-legged Dexter is ridicule in my book, deliberate belittling of anyone who doesn't agree with you at this point.
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Post by Cascade Meadows Farm - Kirk on Nov 29, 2012 12:27:35 GMT -5
From the ADCA site for breed standards: These standards existed before most, if not all of us became owners of the breed. I don't see where it mentions hairless, or mule-footedness in the breed standard. The standard simply says that dexters have a wide range of heights, with some having short legs and some having long legs. That's true, some dexters have short legs and some have long legs. Microcosm (AI Bull), for example has short legs, while there are some tall AI bulls with rather long legs. The standard says NOTHING about the chondrodysplasia dwarfism defect. It just talks about shorter dexters and taller dexters. If you set aside chondrodysplasia, you still have short-legged dexters and long-legged dexters. Further, there are many hog breeders who have capitalized on the mule-foot gene and there are show-wining mule-foot hogs. The hairless cat pictured earlier in the thread is a SHOW WINNER. You're right, the standard says NOTHING about syndactyly, or hypotrichosis, or Chondrodysplasia..... it neither supports nor discourages any defect. It's a fair question to propose to all registries, "What is our Genetic Defect Policy?" Will we allow all defects forever? some defects? no defects? (again, we're talking about serious genetic diseases). My guess is that the majority of dexter breeders would support a policy of NO Serious Genetic Defects (but allowing us plenty of time to get there in a very slow and planned approach). One way to get there, is to promote the use of AI bulls like Microcosm (or other true-shorts), who can give some breeders the shortness they prefer, without any serious genetic defects (after they are progeny-tested). Maybe after there are enough true-short dexters available, folks will drift away from the use of the chondrodysplasia defect gene.
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Post by lakeportfarms on Nov 29, 2012 12:49:19 GMT -5
"Standing" has little to do with common sense, and you show plenty of common sense in your analysis of the issue.
Rather than throw out the entire future progeny of any chondro or PHA carrier, it is entirely reasonable to implement a procedure to identify those carriers and post the information in the registry (I'm speaking of the ADCA, since I am more familiar with that being a member). I believe this has already been discussed on a prior thread. I don't care what date you set the deadline, it is still a deadline and I as well as many others will have chondro carrier calves born to our cows well past 2018 and beyond that no longer will have a registry to belong to, even out of registered parents.
I think it is also reasonable to work toward genotyping dams (and preserving tail hair samples) in order to maintain the integrity of the registry, and to allow better follow up if and/or when another genetic issue may occur, which was the original topic of this thread. It will involve expense to everybody proportionate to the size of their herds, but it will not place the entirety of the expense on owners who have made the decision, for whatever reason, to own or breed chondro (or PHA) carriers. They will already incur expenses above and beyond the non-carrier herd owners in the testing of their non-obligate calves, which is fair. I agree with Kirk on this, it's unfortunate that there are only 300 odd listed chondro carriers in the registry, the number is far higher than that. You'll also find quite a few of our Dexters on that list, so I'm not being a hypocrite.
So instead of making this a "throw out all the existing defective Dexters" lets get back to the subject of how we will be able to (economically) track and verify genetics that exist, or may or will crop up in the future. That, in my opinion is a worthwhile goal and worthy of more discussion.
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Post by lakeportfarms on Nov 29, 2012 12:54:14 GMT -5
Kirk, you're splitting hairs by trying to twist the words to suit your argument. I think it's pretty clear that the breed standard language is using short/long leg to describe chondrodysplasia, otherwise why include it in the first place.
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Post by Cascade Meadows Farm - Kirk on Nov 29, 2012 13:39:01 GMT -5
if these initiatives have been around for many years, don't you think it's logical to conclude that they have failed to achieve general membership buy-in? Do some research, look up membership statistics. My hypothesis is that most breeders, however involved into the maintenance, improvement and preservation of the Dexter breed they may be, are ultimately guided by the market. They will not stop breeding what sells. As to ridicule, that recent statement of yours about breeding hairless mule-footed short-legged Dexter is ridicule in my book, deliberate belittling of anyone who doesn't agree with you at this point. Most new ideas take decades to gain acceptance. If it was JUST chondrodysplasia, then I could learn to live with it. But it's not just chondrodysplasia. Now its 2 forms of chondrodysplasia, plus PHA, and the list will continue to grow. The last time folks considered doing something about Chondrodysplasia, PHA wasn't in the mix..... Now it is and that's changed everything. Even if we learn to live with 2 forms of Chondrodysplasia along with PHA, are we ready to add a 4th and 5th and 6th defect to the list and live with them too? A 4th one is out there, guaranteed (it's just a matter of time). Two of the largest cattle associations on earth implemented strong genetic defect policies because the free-market approach wasn't working. The free-market approach can actually help spread genetic diseases because it encourages people to hide their defects. It also encourages folks to market a defect (instead of marketing non-defect approaches). Now certainly a blend of good policy + a free-market approach might be best. For example, if true-short non-chondro dexters are well marketed to folks who like the "shorties", then they won't feel like they are losing very much to gradually switch to true-short genetics, and if policies are slow and gentle, then everyone will have plenty of time to switch. One concern I have, is that in trying to defend chondrodysplasia, breeders are unintentionally aiding the potential spread of other genetic problems. They may battle against a good genetic defect policy, in order to defend their beloved chondrodysplasia, and the lack of a good policy could have us swimming in defects in decades to come. PS. Mulefootedness and hairlessness are some of the most common defect mutations in mammals and they are PREFERRED for their uniqueness by MANY animal breeders. I used those genetic examples because they are on the list of common cattle defects monitored by other cattle breed associations. I used those examples because like chondrodysplasia,... mulefootedness and hairlessness have many fans in animal breeding (although, because those genes are not lethal, they can be less problematic than chondrodysplasia in some ways). PPS. Thanks to EVERYONE for offering opinions on this challenging subject and thank goodness that I have the world's thickest skin (and friendly smile).
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Post by kansasdexters on Nov 29, 2012 14:52:40 GMT -5
I believe that there is an obvious disconnect between the Dexter breeders that only have experience with, or preference for, Chondrodysplasia non-carriers (HN, homozygous normal) and the Dexter breeders that have a preference for, and intentionally choose, Chondrodyplasia-carriers (HC, heterozygous carriers) in their Dexter herds.
The breeders that see heterozygous carriers (one Chondrodysplasia gene/one normal gene) as highly desirable cattle have good reasons for doing so. However, that reasoning has not been articulated very well.
So here is my attempt at it. I will first use the example of a lethal gene (the sickle cell anemia gene) that is found in humans and that has been perpetuated for generations in parts of the world where malaria is common. In those areas, a heterozygous carrier (one sickle cell anemia gene/one normal gene) has a greater chance of survival than a homozygous normal (two normal genes) person. This is because the presence of the defective sickle cell gene in combination with the presence of the normal gene, confers on the carrier a greater resistance to malaria. When a heterozygous carrier (of sickle cell anemia) mates with another heterozygous carrier and produces offspring, the offspring that are homozygous for the sickle cell mutation (two sickle cell anemia genes) die, and the offspring that are homozygous for the normal gene die. It is heterozygous carrier offspring that survive and live to reproduce. Without the presence of that lethal sickle cell anemia gene, 100% of the offspring would potentially die without reproducing. But with the presence of that lethal gene, 50% of the offspring have a better chance to survive and reproduce, thereby adapting to the environment and sustaining the population. That is why the heterozygous carrier of sickle cell anemia continued to exist through the generations, it was an adaptation that had a selective advantage over the homozygous normal person, in the case of that particular lethal gene.
In a similar manner, with Dexter cattle, the heterozygous carrier (one Chondro gene/one normal gene) may have a selective advantage over the homozygous normal (two normal genes) Dexter in the following way:
1. A heterozygous carrier Dexter cow can produce offspring that are significantly larger than she is. That is because she can produce either a homozygous normal calf or a heterozygous carrier calf. For example, a 650 lb heterozygous carrier Dexter cow can give birth to a homozygous normal bull calf that achieves a weaning weight of 520 lb at 8 months of age, and thereby wean a calf that is 80% of her own weight. (I know this is achievable because I've done it with a heterozygous carrier Dexter cow, but I haven't done it (yet) with a homozygous normal Dexter cow). If a farmer sells his beef calves at weaning, by the pound, then this calf will be worth more than the smaller beef calf that would be weaned at the same age from a small "true-short" 650 lb Dexter cow. So there is a selective advantage for the farmer to have a herd of heterozygous carrier cows that produce weanling beef calves in this manner --- they get more pounds of calf per pound of cow.
2. A heterozygous carrier Dexter steer may have a live weight of only 650 lb when he is finished and ready for processing into beef. That same heterozygous carrier steer may also have nearly as many pounds of actual meat on his carcass as a 750 lb homozygous normal Dexter steer. However, you won't know this if you just compare the hanging weights of the two carcasses, because the hanging weight of the 650 lb heterozygous carrier steer will be around 325 lb and the hanging weight of the 750 lb non-carrier steer will be around 435 lb. But if you have both animals cut the same way, with mostly boneless cuts, there will only be about 10 pounds difference in the actual meat yield between these two carcasses. Since it doesn't take as much forage to finish (or maintain) a 650 lb animal as it does to finish (or maintain) a 750 lb animal, there may be a selective advantage for the farmer to produce and process the heterozygous carrier Dexter steers.
Completely eliminating the Chondrodysplasia gene from the Dexter breed could potentially result in the loss of the selective advantage that is found in the heterozygous carrier (HC) Dexters. So it really isn't just a matter of breeding small, cute cattle that have short legs and don't carry Chondrodysplasia. I believe that this is where the biggest disconnect in understanding comes from. Owners and lovers of heterozygous carrier Dexters appreciate and utilize a selective advantage that owners and lovers of homozygous normal (HN) Dexter don't utilize, and as an unintended consequence, don't fully appreciate.
Patti
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Post by wdd on Nov 29, 2012 15:02:12 GMT -5
Kirk first of all lets remember that there are around 350,000 registered Black Angus cattle in the US and who knows the number of unregistered. Dexter Cattle number around 5,000 registered animals (numbers I could find were a few years old so these are estimations). So the vast size difference in the herd would lend itself to a greater possibility of mutations to occur and we would expect it to take decades or centuries for the Dexters to match the number of offspring that the Angus produce in a relative short period of time.
The vast majority of all genetic mutations make the sperm or ova non-viable or the fetus is aborted before pregnancy is even known to have occured (I have heard upto +90%). Then there are the later term abortions and if the mutation affected fetus carries to full term most are self-culling (die) or are culled by the breeder (dominant and incomplete dominant could fall under the latter case). The exception are the recessive mutations that require two carriers to be bred together (50% carrier, 25% homo, and 25% non-carrier). 0.2% is the accepted percentage of human mutations occuring in a given population so lets assume the same with bovine. Lets say we start having 2500 registered Dexters per year (50% increase) that means we could expect 5 mutation per year (2500x.002). Of those five maybe 1 (20% survival to birth rather than 10% quoted above) could be born dead, die due to complications, be culled by producer, be steered (not even knowning it was a carrier), be sold as a pet that won't be bred, or may be sterile. Yes there can be environmental or other conditions that predispose the population to an increased number of mutations. However, I don't see where we need to be running around screaming the 'sky is falling' when there is not an emergency happening.
I have simplified my post leaving out many of the scientific terms and nomenclature so that others not as educated as yourself can follow what is being said. I am also at work with multiple deadlines screaming at me so can't take the tiime to fully refute your claims and exaggerations.
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Post by Cascade Meadows Farm - Kirk on Nov 29, 2012 15:19:20 GMT -5
You don't have to live with anything. It's America, where you have the freedom to choose. You've made your choice, now go live with it. You are the most vehement hater of short legged Dexter cattle I ADORE short legged cattle, and that's why I chose Dexters Here's a fine short-legged Dexter AI Bull at 39" (Lane's End Microcosm) he is free of the chondrodysplasia lethal dwarfing gene and free of PHA. Here's another short-legged Dexter bull that I like a lot (Brightlea Benjamin - 41ish inches) he is free of chondrodysplasia and free of PHA. He isn't in the AI catalog, but he sure is nice The only reason I like any bull, is if he can throw consistent, trouble-free offspring. The above two short-legged, non-chondro bulls can likely throw nearly 100% short-legged, non-chondro calves. I love short legged cattle so very much, that I'm willing to do battle against the genetic diseases that can plague any breed of cattle. I also love America where we can voice our opinions in a friendly and fair-minded way. I choose shorter dexters AND I choose NO GENETIC DISEASES (in the long haul). They are NOT in conflict with each other. PS. I know this is a sensitive subject for many, and I understand your strong reactions That's why I would vote for a very slow transition.
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Post by lakeportfarms on Nov 29, 2012 15:37:46 GMT -5
Thank you Patti and Gary for such clear explanations. I had a length conversation with Roberta Wieringa a couple of months ago and she also praised the chondro cow/offspring example Patti described. And to Gene for your photo that demonstrates the joy our "defective" cattle can bring. I hope this helps put the issue to rest. Time for me to go hug a Dexter or ten.
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Post by Cascade Meadows Farm - Kirk on Nov 29, 2012 16:16:01 GMT -5
Kirk first of all lets remember that there are around 350,000 registered Black Angus cattle in the US and who knows the number of unregistered. Dexter Cattle number around 5,000 registered animals (numbers I could find were a few years old so these are estimations). So the vast size difference in the herd would lend itself to a greater possibility of mutations to occur and we would expect it to take decades or centuries for the Dexters to match the number of offspring that the Angus produce in a relative short period of time. The vast majority of all genetic mutations make the sperm or ova non-viable or the fetus is aborted before pregnancy is even known to have occured (I have heard upto +90%). Then there are the later term abortions and if the mutation affected fetus carries to full term most are self-culling (die) or are culled by the breeder (dominant and incomplete dominant could fall under the latter case). The exception are the recessive mutations that require two carriers to be bred together (50% carrier, 25% homo, and 25% non-carrier). 0.2% is the accepted percentage of human mutations occuring in a given population so lets assume the same with bovine. Lets say we start having 2500 registered Dexters per year (50% increase) that means we could expect 5 mutation per year (2500x.002). Of those five maybe 1 (20% survival to birth rather than 10% quoted above) could be born dead, die due to complications, be culled by producer, be steered (not even knowning it was a carrier), be sold as a pet that won't be bred, or may be sterile. Yes there can be environmental or other conditions that predispose the population to an increased number of mutations. However, I don't see where we need to be running around screaming the 'sky is falling' when there is not an emergency happening. Nice posting and I agree with most of it. One thing to keep in mind is that all of our modern breeds of animals are relatively new. Angus and Dexters come from older British Isle breeds of cattle and share many common ancestors. When farmers relocated from one area to another, they took some of their cattle with them and that kept mixing the gene pools. Kerry/Dexters and Angus and Jerseys likely share most all of the same genes, but just at different frequencies and in different typical combinations. I'd even bet that the Dun (brown) gene in Dexters, is somewhere in Black Angus at VERY VERY low frequencies (and when it homozygously exhibits once in a blue moon, is quickly and quietly culled as a dirty little secret "red" mutant). Many of the defect genes that have been located in Angus could easily have started in ancestors to both Dexters and Angus and even chondrodysplasia could have started in the ancestors, but was easily culled out of Angus (because Chondrodysplasia (which is a co-dominant gene) can't hide well in Angus) Your idea that a large herd like Angus, will mathematically have more mutations, is VERY sound. But also, the larger breeders tend to find those mutations more quickly. An Angus AI bull bred on 5000 cows is far more likely to quickly find his mutations, than a dexter bull bred on 5 cows. That can allow a mutation in dexters to spread far and wide before being found. Since we haven't done a good job of looking for mutations in Dexters, we may already have a very long list of problems, with dead and deformed calves just being swept under the rug. Culling the mom only helps a very little bit, because the gene is likely also in the sire and in many other relatives. I agree that the sky isn't in danger of immediately falling. We've been talking about this for 10 years and in that 10 years we've only discovered 1 additional bad gene (pha in 2009) since the discovery of the chondro gene ten years ago. We may only discover one bad gene every 10 years..... but in 100 years, we'll have a very long list. Maybe we'll never agree on a full angus-like policy but..... Surely everyone agrees that we should at least implement procedures to report ALL defects, and to track ALL known carriers. Surely everyone agrees that we should at least attempt some level of progeny testing in AI sires to look for problems before they are widely spread. If we had done this with PHA, it could have been prevented from spreading so widely.
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Post by rezzfullacres on Nov 29, 2012 16:22:22 GMT -5
I hate to continue this BUT....Where do you draw the line when it comes to genetic defects/mutations.. There are people out there that would take that and run with it in an attempt to remove any condition they feel has or had been brought about by a genetic defect/mutation. Just wondering where the line in the sand would be? ??
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Post by Cascade Meadows Farm - Kirk on Nov 29, 2012 16:36:47 GMT -5
A few comments on Patti's well written posting regarding beef advantages of Chondros :
1. One of the world's largest Dexter beef producers who happens to post on this board (Clive) has experimented with chondrodysplasia and strongly rejects it.
2. Angus breeders do something similar to gain advantages with heterozygosity. They breed their Angus girls on Hereford bulls to get black baldy (heterozygous) calves. BUT THEY DONT REGISTER THE OFFSPRING, they eat them. They can't be registered because they are NOT purebred because they are HETEROZYGOUS (terminal crosses).
3. The eventual elimination of Chondrodysplasia from the Dexter registries, would NOT preclude folks from keeping production herds of chondro animals for the purpose of raising terminal crosses for beef. Now since Chondro has nothing to do with dexters, and is an independent stand-alone gene now found in many cross-breeds, it could be used in ANY breed to get the effects that Patti lists. I don't see the other breeds clamoring for it in their registered herds (even if they use it in their terminal crosses).
We're not talking about eliminating the gene from the planet, just eliminating it from registered dexters in the very very long haul. Angus folks tolerate black-baldies, but just not in the registry.
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Post by wdd on Nov 29, 2012 16:43:43 GMT -5
Most people refer to the benefit of outcrossing in #2 as hybrid vigor. Which isn't as strong in a second crossing thus the 'terminal cross'. (Just so common people can understand and relate to what your meaning was, not to correct you).
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Post by Cascade Meadows Farm - Kirk on Nov 29, 2012 16:50:35 GMT -5
I hate to continue this BUT....Where do you draw the line when it comes to genetic defects/mutations.. There are people out there that would take that and run with it in an attempt to remove any condition they feel has or had been brought about by a genetic defect/mutation. Just wondering where the line in the sand would be? ?? The list of serious genetic defects usually contains ALL lethal genes and any genes that interfere with important biological functions that cause deformity and pain and illness. This list has links to information about each defect. It's interesting to note that they list Double Muscling as a "defect". But it's because the calves are so large that the mothers cannot give birth without exceptional assistance. www.cdnangus.ca/breed/Genetic_Defects.htm
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