TrinityDobes
Novitiate
OK I took notes during Dr. Meurs presentation - so these are what I thought I heard 
I took the notes in shorthand and then transcribed so I may have not "translated" a thought or message correctly - and I appologize in andvance for any mistakes
PLEASE post it you heard something different or IF I haver captured something wrong - this should be a great place to capture FACTS about what we now KNOW after the presentation
Known Facts
Dobermans are the most common Dog Breed to be affected with DCM
Every breed has a different type of DCM
What causes each type of DCM is different for each breed
Cardio Myopathy = muscle disease and it is a very complex issue
Non affected (neg/neg) and affected (pos/neg and pos/pos) dogs can all die of Congestive Heart failure
On a normal echocardiogram beats should be normal and regular
20 % of Dobermans will show VPCs via holter monitor but will not get an enlarged heart
Some people have suggested that DCM can be traced back to the 7 sires, 3 of which died of heart disease Demossi, Emporer and ????
Breeders may need to breed affected (positive hetero and positive homo) dogs to neg/neg dogs to maintain enough genetic diversity in the lines for a while
Dr. Meurs looked at the human genes (24) that can cause DCM in people
If you have the gene mutation in just one of these you can develop DCM
The study needed to look at affected (positive) dogs from as many different un related dogs for 3 generations as possible, which allowed them to identify a larger genetic population to determine a consistent deviation (mutation)
This Doberman gene mutation causes not enough protein to be produced. Non affected genes produce a certain level of protein that goes into your heart to make it work normally.
Affected (positive-hetero) genes produce less of the normal amount of protein needed.
Affected (positive-homo) genes can produce a small amount of this protein but no where near enough.
In Dobermans the job of the protein is to move energy in and out of the cells. Normal mitochondria (sp) is affected with how the cells move the energy, so not enough protein affects the account of energy moving in the cell.
Factors Unknown
Cardio Myopathy is very complex – there are things that are not very well understood with DCM and there are still things that need to be found out over the next few years of research
Dr. Meurs first looked at the main coon cat as they have a form of cardio myopathy. There are 2 causal agents of CM in Maine coon cats. Some cats get the disease that is negative for the mutation.
Boxer's are quite different than Dobermans – and from her research it appears they have more than one causal agent as well as there are affected boxers out there that have a negative mutation test but have expressed clinical signs of and died from Cardio Myopathy.
There are also other infectious agents like viruses that can affect and enlarge the heart that mimic DCM
Will need to continue to follow dogs that are negative for this gene but end up getting heart disease so we can determine if they can identify any other consistent overlaying causal agents or reasons why these boxers who test negative for their gene mutation still end up with the disease. Dr. Meurs said we won’t ever have all the definitive answers
Another factor in Doberman DCM is Genetic Penitrance or how much the mutation penetrates (ie clinically expresses the disease) each animal varies and likely involves environmental or genetic factors such as Diet? Genetic Back Ground? and Daily Activities.
They don’t know what absolutely affects genetic penetrance. It might be something in dobes that have the mutation but some other overlaying gene modifies the effects of the genetic mutation – so that is what varies the amount of penetrance.
Going Forward
Start thinking about testing your dogs– not every body that has the gene mutation will show the same extent or clinical manifestation of the disease – you need to use the test as a tool.
Question: What % of dobes have this mutation? –the study looked at the dog samples sent in and those were mostly affected. 210 dogs tested for gene mutation 150 positives and 62 neg. Of the 62 dogs over ten y/o without DCM, 10 had a positive genetic test or (16%). When they are able to look at the first 1000 test results that will give you a better idea of the percentages (positive to negative) in the total population.
If you remove every dog that is positive from the breeding population would NOT be a good thing – no breed can afford to do that. For instance, there was another dog breed where they identified the gene mutation for blindness in puppies. By removing (spay/neuter) every positive dog they were left with a much bigger problem of seizures – when they removed all the blindness genes with the blind dogs, they were left with a much bigger and concentrated problem.
We need to be very careful about this, and not wholesale remove positive dogs from the breeding populations – you need to use this test as a tool – its not black and white - you can’t say its positive so remove from breeding gene pool
Recommended breeding options
Recommended using negative mutation dogs to guide your program incrementally forward to help increase the number of negative dogs and reduce the number of positive-homo dogs produced.
Test all your dogs; continue to study your pedigrees. Remember that the test is a tool to help you identify If your dog does or does not have the Doberman DCM gene mutation
We can’t say this is the only gene that causes DCM, because we do not know if there are other genetic causes for DCM, but we think there is a good chance there are probably other gene mutations that contribute to DCM.
Therefore this does not mean, at least for now in 2010, that you should stop testing even clinically affected dogs. As many dogs as possible that we can test will help identify other contributing factors. Continue to follow your lines with holtering and echoing for now. Testing will let you know which dogs in your lines are negative. So you can develop a strategy for going forward.
Positive-Heterozygous (1 mutated gene and one clear gene)
If the dog comes back Pos -hetero, ask yourself, Does this dog have a family history of heart disease? Are there any suspected sudden deaths? Are there any questionable echo or holter findings in this dog? If you answer YES then this would likely be a dog not to be used for breeding. On the other hand, if there is no family history of DCM, no clinical evidence of DCM, consider the individual dogs importance to the breed and to your program. Is this a wonderful example? If so then breed this dog to a mutation negative statistically then 50% pups will be negative and 50% will be positive hetero. Each parent will give 1 copy of this gene to the pups – so you could theoretically even end up with all negative if the Positive Hetero parent gave only the Negative genes. But even if some of the pups from this type of breeding are positive – hetero (1 copy of the gene) they can still be used in a program if bred to a negative partner, As always you will grade your litter, looking at those puppies decide which is the best to be retained. Hopefully there any puppies who are negative in this litter can replace the positive hetero parent so you will go forward into the next generation with a negative puppy. This will allow you to keep the good things out of that positive parent and still work towards all negative dogs within a couple of generations.
If a dog is Positive-Homozygous (2 copies of the mutant gene) I would not recommend breeding if at all possible as these dogs do tend to have the worst manifestation of the disease – Dr Meurs has not seen very many positive-homo, in boxers of the boxers tested so far 35% have been positives and only 4% of those were Positive-homo. Since both copies of the gene carry the mutation, these dogs should not be used for breeding except under extreme circumstances – such as the end of a line and then this pos-homo can only be bred to a neg/neg and select a pos- hetero puppy to continue the line to be eventually be bred to a negative to reach a neg/neg puppy in the 3rd generation
IMPORTANT TO NOTE - not every positive dog will get the disease because of the variable penetrance. If you would cull or discard all the positives within your breed you will change the gene pool and not for the betterment of the breed. You need to test and use it as a tool to work towards 5 to 10 years from now to reduce the positives in the gene pool – if you do this then you will have successfully chopped away a large chunk of the cause of DCM in Dobermans.
Results: You can decide if you want to publish results or not or just publish some and not all results, but if a sample is received and the sample is not signed they will assume that you don’t want information published. Testing is blind testing – They would like more information though on each sample, i.e. holter and echo history, and on bloodlines for further research but it’s not mandatory
Question: Did you find any difference while doing the research or in the testing that indicated whether a certain diet or supplements etc were identified in relation to DCM... Dr. Meurs: No Correlation found
Anecdotal comment: Some vets have used as a predictor that15 vpcs or greater would translate or predict that the dog would get DCM within the next 1 ½ years – Bobbie whose dobes were the first Dr. Meurs studied had a holter with 15 or over VPCs and she lived another 10 years – We need to not run out and be quick to spay and neuter dogs that have high vpcs yet no clinical manifestation of the disease. There are other things that can cause VPCs besides the onset of DCM. VPCs can be a sign of DCM but also can be caused by viruses – keep doing the holters – some vpcs go away and some never increase, and some that holtor every year and find VPCs never manifest the disease.
Question: Does Dr. Meurs see any benefit to supplementing with L-carnatine and Tarine? Dr. Meurs said she would not supplement with L-carnatine and taurine or anything else…. She specifically said not to do Taurine. But you *could* do L-carnitine
Question: What about EFA’s could they help? (EFA=essential fatty acids) She said she did not think they would specifically help with DCM, but they would not hurt either
Question: Is there any research ongoing for helping increase the protein needed that the mutation is lacking? Dr. Meurs indicated that yes some research is going on, the missing or lower level of protein was just one thing that is part of a cascade.
Question: What about antioxidants supplements = Dr Meurs does not think that will affect the cascade to increase protein
Question: Age to start testing – whenever you want – nursing puppies should be careful to do after nursing so no mothers dna from milk does not contaminate the cheek cells.
Question: Can Frozen Semen be tested? YES Frozen semen can be tested!
Question: Will can people outside the USA be able to send in for test results. Absolutely the lab will test samples from out of the country
OK - so everyone else please add to this the things I missed - Thanks!
I took the notes in shorthand and then transcribed so I may have not "translated" a thought or message correctly - and I appologize in andvance for any mistakesPLEASE post it you heard something different or IF I haver captured something wrong - this should be a great place to capture FACTS about what we now KNOW after the presentation
Dr. Meurs Presentation on identifying
“A” gene mutation responsible for DCM
“A” gene mutation responsible for DCM
Known Facts
Dobermans are the most common Dog Breed to be affected with DCM
Every breed has a different type of DCM
What causes each type of DCM is different for each breed
Cardio Myopathy = muscle disease and it is a very complex issue
Non affected (neg/neg) and affected (pos/neg and pos/pos) dogs can all die of Congestive Heart failure
On a normal echocardiogram beats should be normal and regular
20 % of Dobermans will show VPCs via holter monitor but will not get an enlarged heart
Some people have suggested that DCM can be traced back to the 7 sires, 3 of which died of heart disease Demossi, Emporer and ????
Breeders may need to breed affected (positive hetero and positive homo) dogs to neg/neg dogs to maintain enough genetic diversity in the lines for a while
Dr. Meurs looked at the human genes (24) that can cause DCM in people
If you have the gene mutation in just one of these you can develop DCM
The study needed to look at affected (positive) dogs from as many different un related dogs for 3 generations as possible, which allowed them to identify a larger genetic population to determine a consistent deviation (mutation)
This Doberman gene mutation causes not enough protein to be produced. Non affected genes produce a certain level of protein that goes into your heart to make it work normally.
Affected (positive-hetero) genes produce less of the normal amount of protein needed.
Affected (positive-homo) genes can produce a small amount of this protein but no where near enough.
In Dobermans the job of the protein is to move energy in and out of the cells. Normal mitochondria (sp) is affected with how the cells move the energy, so not enough protein affects the account of energy moving in the cell.
Factors Unknown
Cardio Myopathy is very complex – there are things that are not very well understood with DCM and there are still things that need to be found out over the next few years of research
Dr. Meurs first looked at the main coon cat as they have a form of cardio myopathy. There are 2 causal agents of CM in Maine coon cats. Some cats get the disease that is negative for the mutation.
Boxer's are quite different than Dobermans – and from her research it appears they have more than one causal agent as well as there are affected boxers out there that have a negative mutation test but have expressed clinical signs of and died from Cardio Myopathy.
There are also other infectious agents like viruses that can affect and enlarge the heart that mimic DCM
Will need to continue to follow dogs that are negative for this gene but end up getting heart disease so we can determine if they can identify any other consistent overlaying causal agents or reasons why these boxers who test negative for their gene mutation still end up with the disease. Dr. Meurs said we won’t ever have all the definitive answers
Another factor in Doberman DCM is Genetic Penitrance or how much the mutation penetrates (ie clinically expresses the disease) each animal varies and likely involves environmental or genetic factors such as Diet? Genetic Back Ground? and Daily Activities.
They don’t know what absolutely affects genetic penetrance. It might be something in dobes that have the mutation but some other overlaying gene modifies the effects of the genetic mutation – so that is what varies the amount of penetrance.
Going Forward
Start thinking about testing your dogs– not every body that has the gene mutation will show the same extent or clinical manifestation of the disease – you need to use the test as a tool.
Question: What % of dobes have this mutation? –the study looked at the dog samples sent in and those were mostly affected. 210 dogs tested for gene mutation 150 positives and 62 neg. Of the 62 dogs over ten y/o without DCM, 10 had a positive genetic test or (16%). When they are able to look at the first 1000 test results that will give you a better idea of the percentages (positive to negative) in the total population.
If you remove every dog that is positive from the breeding population would NOT be a good thing – no breed can afford to do that. For instance, there was another dog breed where they identified the gene mutation for blindness in puppies. By removing (spay/neuter) every positive dog they were left with a much bigger problem of seizures – when they removed all the blindness genes with the blind dogs, they were left with a much bigger and concentrated problem.
We need to be very careful about this, and not wholesale remove positive dogs from the breeding populations – you need to use this test as a tool – its not black and white - you can’t say its positive so remove from breeding gene pool
Recommended breeding options
Recommended using negative mutation dogs to guide your program incrementally forward to help increase the number of negative dogs and reduce the number of positive-homo dogs produced.
Test all your dogs; continue to study your pedigrees. Remember that the test is a tool to help you identify If your dog does or does not have the Doberman DCM gene mutation
We can’t say this is the only gene that causes DCM, because we do not know if there are other genetic causes for DCM, but we think there is a good chance there are probably other gene mutations that contribute to DCM.
Therefore this does not mean, at least for now in 2010, that you should stop testing even clinically affected dogs. As many dogs as possible that we can test will help identify other contributing factors. Continue to follow your lines with holtering and echoing for now. Testing will let you know which dogs in your lines are negative. So you can develop a strategy for going forward.
Positive-Heterozygous (1 mutated gene and one clear gene)
If the dog comes back Pos -hetero, ask yourself, Does this dog have a family history of heart disease? Are there any suspected sudden deaths? Are there any questionable echo or holter findings in this dog? If you answer YES then this would likely be a dog not to be used for breeding. On the other hand, if there is no family history of DCM, no clinical evidence of DCM, consider the individual dogs importance to the breed and to your program. Is this a wonderful example? If so then breed this dog to a mutation negative statistically then 50% pups will be negative and 50% will be positive hetero. Each parent will give 1 copy of this gene to the pups – so you could theoretically even end up with all negative if the Positive Hetero parent gave only the Negative genes. But even if some of the pups from this type of breeding are positive – hetero (1 copy of the gene) they can still be used in a program if bred to a negative partner, As always you will grade your litter, looking at those puppies decide which is the best to be retained. Hopefully there any puppies who are negative in this litter can replace the positive hetero parent so you will go forward into the next generation with a negative puppy. This will allow you to keep the good things out of that positive parent and still work towards all negative dogs within a couple of generations.
If a dog is Positive-Homozygous (2 copies of the mutant gene) I would not recommend breeding if at all possible as these dogs do tend to have the worst manifestation of the disease – Dr Meurs has not seen very many positive-homo, in boxers of the boxers tested so far 35% have been positives and only 4% of those were Positive-homo. Since both copies of the gene carry the mutation, these dogs should not be used for breeding except under extreme circumstances – such as the end of a line and then this pos-homo can only be bred to a neg/neg and select a pos- hetero puppy to continue the line to be eventually be bred to a negative to reach a neg/neg puppy in the 3rd generation
IMPORTANT TO NOTE - not every positive dog will get the disease because of the variable penetrance. If you would cull or discard all the positives within your breed you will change the gene pool and not for the betterment of the breed. You need to test and use it as a tool to work towards 5 to 10 years from now to reduce the positives in the gene pool – if you do this then you will have successfully chopped away a large chunk of the cause of DCM in Dobermans.
Results: You can decide if you want to publish results or not or just publish some and not all results, but if a sample is received and the sample is not signed they will assume that you don’t want information published. Testing is blind testing – They would like more information though on each sample, i.e. holter and echo history, and on bloodlines for further research but it’s not mandatory
Question: Did you find any difference while doing the research or in the testing that indicated whether a certain diet or supplements etc were identified in relation to DCM... Dr. Meurs: No Correlation found
Anecdotal comment: Some vets have used as a predictor that15 vpcs or greater would translate or predict that the dog would get DCM within the next 1 ½ years – Bobbie whose dobes were the first Dr. Meurs studied had a holter with 15 or over VPCs and she lived another 10 years – We need to not run out and be quick to spay and neuter dogs that have high vpcs yet no clinical manifestation of the disease. There are other things that can cause VPCs besides the onset of DCM. VPCs can be a sign of DCM but also can be caused by viruses – keep doing the holters – some vpcs go away and some never increase, and some that holtor every year and find VPCs never manifest the disease.
Question: Does Dr. Meurs see any benefit to supplementing with L-carnatine and Tarine? Dr. Meurs said she would not supplement with L-carnatine and taurine or anything else…. She specifically said not to do Taurine. But you *could* do L-carnitine
Question: What about EFA’s could they help? (EFA=essential fatty acids) She said she did not think they would specifically help with DCM, but they would not hurt either
Question: Is there any research ongoing for helping increase the protein needed that the mutation is lacking? Dr. Meurs indicated that yes some research is going on, the missing or lower level of protein was just one thing that is part of a cascade.
Question: What about antioxidants supplements = Dr Meurs does not think that will affect the cascade to increase protein
Question: Age to start testing – whenever you want – nursing puppies should be careful to do after nursing so no mothers dna from milk does not contaminate the cheek cells.
Question: Can Frozen Semen be tested? YES Frozen semen can be tested!
Question: Will can people outside the USA be able to send in for test results. Absolutely the lab will test samples from out of the country
OK - so everyone else please add to this the things I missed - Thanks!
