Artificial Insemination

[andyhilt27]

Please describe all that you know on this subject. And pretend that I am a total idiot in explaining it. That shouldn't be too difficult.:D I need each and every detail. Well I do know where the semen comes from, you can leave that unsaid. I dealt with A.I. on the hog farm but forgot a lot of it in terms of storage and such.

[dobesign]

First there is a boy dog, and he has a cell that grows up and becomes a sperm which looks like a ping pong ball with a tail...sorry I couldn't resist this one Andy!!!:p After breeding pigs, this should be EASY!:D

[andyhilt27]

Fine....I'll google it!:D

[tosca]

Hey Andy - I've had 2 litters through use of Artificial Insemination. A total of 15 puppies were born - 8 in the first litter; 7 in the 2nd litter. Both litters were with the same dam; both litters were surgical implants of frozen semen. The key to successful AI breeding is timing - with my first litter, we did 6progesterone tests prior to the breeding to properly time the implant, done on Day 12 of her heat cycle. With the 2nd litter, we ended up with 6 progesterone tests; the implant was done on Day 17 of her heat cycle.

With both surgical implants, we had no problems; no ill effects and both pregnancies were normal, with puppies born on Day 60 after the implants.

[andyhilt27]

cathy thanks. What about storage? The temps it has to be frozen etc....

[tosca]

With my breedings, the semen was stored in 2 different locations/2 different states. The semen is stored at the semen bank until shortly before it's needed. Then, it's shipped (at great expense, mind you) to the vet who is doing the implant. The shipment includes a storage vessel which should keep the semen in frozen state for 3-5 days - this is another aspect of the timing, particularly when you run up against a weekend. If the implanting vet doesn't have storage facilities, you have to rely on the storage vessel/shipment to ensure that the semen remains frozen until use.

I don't know anything about temperatures, etc., it's not like I kept it in the freezer! :)

[sorthund]

Cathy, what did it approx. cost? I know people charge different for the semen, but what is a ball park $? and the shipping?

[Elaine]

Artificial Insemination allows breeders to do breedings of choice; they are not restricted to breedings of geographic convenience. Frozen semen opens the door to world class breedings that were only dreamed of a few short decades ago. We’ve used frozen semen in both the dogs and the horses.

I can't think of a single one of the world's top Warmblood sires that is available via live cover. All breedings are fresh chilled or frozen. In the horses we imported the semen directly from Paul Schockemöhle in Germany http://www.schockemoehle.com/englisch/s333906.html ... where the world’s finest Dressage sires reside and had the semen shipped to our vet in Pennsylvania.

We purchased the shipping tank for the semen in England (about $800 US) had them ship it to Germany... Schockemöhle’s people filled it with the coolant for maintaining the correct temperature (our tank will hold the temp constant for about 45 days) then filled our order (Sandro Hit and Lord Sinclair) and passed it off to an agency that is licensed to carry the tank through customs at JFK Airport (which is one of the few airports in the country that will allow foreign semen shipments). The agency then had it Fed Ex’d to Dr Hurtgen clinic in New Freedom PA http://www.nandivet.com/ Dr. Hurtgen is by far the best with frozen semen and embryo transfers in North America. He is a Repo vets’vet. By far the most credible, skilled and successful veterinary professional we have ever encountered. The venture cost about $10K... and produced 6 foals... a gamble.. that turned out to be a HUGE bargin.

Success with frozen semen is a function of how many times the vet does the procedure. It is a waste of time and money to use someone who does not specialize in the techniques. My understanding is that equine vets can earn a Ph.D. in theriogenology. There is no doctorate of theriogenology in canines, so breeders can be misled that a vet knows what they are doing, when in fact they don’t.

Obviously the Kafka breeding was a frozen semen breeding. We were originally using a vet in Beavercreek, Ohio and at the last minute switched to Dr. Hutchinson’s Animal Clinic North View in Ohio. Dr. Hutchinson was good and we were lucky. (In contrast, the first vet was simply wasting our time and money, he did not have the expertise he claimed). After speaking with Cathy, we realized we were on the wrong track. We almost missed the breeding altogether, but Arthur was able to draw a vile of blood and we were able to drive Lizabeth in a snow storm up to Hutchinson’s clinic... she was inseminated the next day. The blood draw and the timing were absolutely perfect (which was sheer luck), she had 7 puppies. The vet costs were about $600 - $700 as I recall.

[andyhilt27]

I am trying to go somewhere with the A.I. approach. If we had a coalition of dobe breeders to form a dobe sperm bank we could have a plan of attack against DCM. We wouldn't breed until the dog has a confirmed death at 10 years old or so. IF DCM is polygenetic we could reduce the chances. Obviously this approach won't work with every breeding but it could help. Thoughts????

[tosca]

Cathy, what did it approx. cost? I know people charge different for the semen, but what is a ball park $? and the shipping?

Well, the cost for the semen should bed the same as a 'normal' breeding to any stud dog. The general rule of thumb for a stud fee is the purchase price of a pet quality puppy. In my instance, I had shown both of the studs I used, so no hard cost for the semen itself - phew! :D

The progesterone tests were done by my vet in Puyallup - about $56 each test. The surgical implant itself cost $250. The shipping cost close to $200.

One thing to know: the progesterone test cost varies substantially by vet; it can be as much as $90+; my vet seems to have the lowest cost for the progesterone testing. So, if you're looking at AI, do check around for the cost - the tests are all done at the same lab, so the cost should be essentially the same!

[tosca]

I am trying to go somewhere with the A.I. approach. If we had a coalition of dobe breeders to form a dobe sperm bank we could have a plan of attack against DCM. We wouldn't breed until the dog has a confirmed death at 10 years old or so. IF DCM is polygenetic we could reduce the chances. Obviously this approach won't work with every breeding but it could help. Thoughts????

Essentially, that's one of the reasons I did the AI - the first dog I bred to, died at 10+ after eating poison mushrooms. The 2nd dog had died at almost 10, from cancer. He had actually had a number of heart tests and had no signs of DCM.

[Elaine]

I am trying to go somewhere with the A.I. approach. If we had a coalition of dobe breeders to form a dobe sperm bank we could have a plan of attack against DCM. We wouldn't breed until the dog has a confirmed death at 10 years old or so. IF DCM is polygenetic we could reduce the chances. Obviously this approach won't work with every breeding but it could help. Thoughts????

Andy,

In a nut shell, a plan of attack on DCM would have to be based on science. We could freeze dogs till hell froze over and that won’t tell us they are DCM free. Simply because a dogs dies of something other than DCM does not mean he wouldn't have developed it if he'd lived longer or that he couldn't / didn't transmit it. Even an autopsy confirming that a given dog died of some other cause will not tell us that they could not also transmit DCM and that they would not have developed DCM if they had simply lived longer. How many other ways do you think I can say the same thinig here? :p

As of 2008 we believe that DCM is autosomal dominant trait with incomplete penetrance. Dogs that never exhibit symptoms can transmit the disease. Also, regardless of how and when a dog dies, we have no way to know that it wouldn’t have developed DCM had it just lived longer. The dog that died at 10 years of age of cancer, choking, liver failure, was hit by a car, had a stroke etc., may still have developed DCM at 11. We can not identify which dogs will not develop the disease and we can not identify which dogs will transmit the disease.

So including or excluding a dog based upon its DCM status at any point in its life is not based upon credible science. We have no way to tell that a given dog will not transmit DCM. The testing we have in June of 2008 allows some breeders to smugly and sanctimoniously claim some fantasy High Ground about their dogs DMC status, which is based on their hope and ignorance of how the disease is transmitted (and opens the door to them getting sued like Ms. Babbitt did in Skaer v Babbitt, where Skaer was awarded treble damages because she [Skaer] allegedly relied on Babbitt’s claims of health testing and expected to be purchasing a genetically perfect dog and then after-the-fact dogs in the pedigree died of DCM. ).

Breeders smug ignorance accounts for why we are making no progress at all towards eradicating DCM. What we have are breeders who formerly claimed that they had "DCM free pedigrees" suddenly raising their hand and admitting, “Opps! Sorry folks, we have it too.”

It’s not that they were lying before, it’s that they do not understand what you can claim about transmission of DCM based on the dog in front of you.

And here is a big one... Offspring and littermates of the dogs with DCM who do not develop DCM may have some genetic mechanism to inhibit the development of DCM and they may be the very dogs we should include in our pedigrees if we want to control DCM.

There are something like 23 genetic markers in humans that are connected to the transmission of DCM. We suspect there are even more in dogs, and veterinary science hasn't found a single one yet. Not a single one. We are no where near being able to eradicate DCM based upon medical science. At best we can diagnose and treat it.

[andyhilt27]

Andy,

In a nut shell, a plan of attack on DCM would have to be based on science. We could freeze dogs till hell froze over and that won’t tell us they are DCM free. Simply because a dogs dies of something other than DCM does not mean he wouldn't have developed it if he'd lived longer or that he couldn't / didn't transmit it. Even an autopsy confirming that a given dog died of some other cause will not tell us that they could not also transmit DCM and that they would not have developed DCM if they had simply lived longer. How many other ways do you think I can say the same thinig here? :p

As of 2008 we believe that DCM is autosomal dominant trait with incomplete penetrance. Dogs that never exhibit symptoms can transmit the disease. Also, regardless of how and when a dog dies, we have no way to know that it wouldn’t have developed DCM had it just lived longer. The dog that died at 10 years of age of cancer, choking, liver failure, was hit by a car, had a stroke etc., may still have developed DCM at 11. We can not identify which dogs will not develop the disease and we can not identify which dogs will transmit the disease.

I understand that they may transmit the DCM genes without exhibiting DCM. Am I understanding correctly that DCM being polygenetic means the younger the dog dies of DCM the more "affected" they were by it?

[andyhilt27]

And here is a big one... Offspring and littermates of the dogs with DCM who do not develop DCM may have some genetic mechanism to inhibit the development of DCM and they may be the very dogs we should include in our pedigrees if we want to control DCM.

If a dog were to live to 10+ I would say he may be one of these offspring or littermates.:D What are you basing this theory on???? Not that I don't like it.....is there scientific evidence backing this? I think the bottom line is that DCM is polygenenitic and every Doberman has it in their genetics. Breeding it out may be impossible. Reducing the chances of it at this time is the only plan of attack.

And how do we do that? Well breeding to a stud that is 2 or 3 years old leaves one open to whatever he may develope in the next few years of his life. For instance, all the big time breeders are using this hot young stud. He is young, a phenominal dog, has won BISS BIS, top 20 contender, etc. He dies at age 5 of DCM. There is frozen semen at your disposal. Will you use it???? I say Hecky NAH!!! Now this same dog lives to be 12 or 13 with no signs of DCM and gets hit by a Mack truck. Would you use his semen? I say Hecky Yeah!!!

[Elaine]

If a dog were to live to 10+ I would say he may be one of these offspring or littermates.:D What are you basing this theory on???? Not that I don't like it.....is there scientific evidence backing this? I think the bottom line is that DCM is polygenenitic and every Doberman has it in their genetics. Breeding it out may be impossible. Reducing the chances of it at this time is the only plan of attack.

And how do we do that? Well breeding to a stud that is 2 or 3 years old leaves one open to whatever he may develope in the next few years of his life. For instance, all the big time breeders are using this hot young stud. He is young, a phenominal dog, has won BISS BIS, top 20 contender, etc. He dies at age 5 of DCM. There is frozen semen at your disposal. Will you use it???? I say Hecky NAH!!! Now this same dog lives to be 12 or 13 with no signs of DCM and gets hit by a Mack truck. Would you use his semen? I say Hecky Yeah!!!
There are stud dogs who have lived to 10 and then were diagnosed with DCM. There is no magic cut off age upon which we can base a credible claim that a given dog is DCM free and will not transmit DCM. We have no way to know that a dog will not transmit DCM regardles of whether or not he/she ever shows symptoms. And, yes, I might use the frozen semen of the DCM dog. Would you breed to Monty (Ch. Eastwicks Meadow Monster)? Would you breed to Ch. Dabney's Phenomenon (Agador)? Would you breed to any of Ch Cactus Cash (Eddie's) children and grandchildren? Of course you would, if it was the right dog for your bitch... even though these dogs all have DCM in their pedigrees. There is no such thing as a DCM free pedigree.

My larger point is that if we truly want to make progress with eradicating DCM, then we need to be guided by credible science... not well meaning guess work. At this time there is no way to determine that a given dog will not transmit DCM,. because of incomplete penetrance. It has nothing to do with being "polygenetic."

[dobesign]

Another piece of the puzzle is that DCM is a rather generic term for a host of conditions causing cardiac dilation. Myocardial tissue can be corrupted in a variety of ways: genetic, viral, traumatic, bacterial....on and on ad nauseum. My point here is that until we know which kind of DCM we are dealing with, presuming it is genetic and heritable that we are trying to eliminate, we cannot know who carries what. There are conditions that cause arterial isuuse, ones that affect the cardiac tissue, others the nerves that feed the vessels that in turn feed the cardiac tissue. Until we can specifically name the issue, it seems to rather "put the cart before the horse" to say we are "eliminating DCM". It is akin to saying that by eliminating an allergy to cats that we have abolished all allergies. Let's put an effort into finding the marker, isolate it, then see who has it. Otherwise we might as well say that we will eliminate DCM in the Doberman by eliminating the Doberman itself. I for one, do not believe in throwing away the baby with the bath water! Besides, I LOVE my babies, even the one with DCM (Faith), dirty bath water and all. :cool:

[andyhilt27]

Credible science is great, but what if it goes against inbreeding and linebreeding? Let's really look at why the dobermans in particular are dying of DCM. There must have been a dog early on that had DCM. Maybe the dog was used as an outcross for a desired trait. Then came inbreeding after inbreeding. The frequency of these DCM affected genes were condensed. The gene pool needs to be diluted of this genetic defect. Eradication will never happen. Too many genes can carry the defect. That is credible science. That is reality. I am probably wrong of course.

We have one option right now. To dilute the DCM in our gene pool. We can only do this with phenotypical, loose line, and outcross breedings in terms of DCM since it is in every pedigree somewhere and there are zero genetic markers.

[andyhilt27]

This is from Elaines post on Oppenheimer's 20 rules to breeding better dogs:

"10. Inbreeding is a valuable tool, being the fastest method to set good characteristics and type. It brings to light hidden traits that need to be eliminated from the breed."

My take of this is that inbreeding sure has brought DCM to light. Now what? Do we keep breeding the same way to increase the frequency of this? I would love to do a close linebreeding with Eva. I believe I may have talked myself out of it. Eva is an outcross. In terms of producing champion quality puppies I need to do a tight linebreeding. But what will that produce? In my humbled, uneducated opinion it will indeed increase the chances of DCM.

[andyhilt27]

This is from the article on the UDC webesite.

Increasing Hereditary Health Problems in the Breeding of Purebred Dogs: A Comparative Overview Using Dobermans in Germany, Europe and in the USA as Examples
by Dr. Reinhard Haberzettl

"Affected Dobermans can die at 2 months, 12 months, 3 years, 7 years or 11 years –the age of DCM death in any individual affected Doberman depends upon how many of the DCM genes he has received from his sire and dam (van der Zwan 1987). Quantitatively, DCM has a polygenetic mode of inheritance (Table 1). The greater the number of DCM genes inherited, the earlier the dog will die, less than 5 years old. If he has inherited only a few of the DCM genes, then he will not die of it till he is an old dog (over 9 years old) or perhaps not showing DCM at all, dying of something else first."

[tosca]

Inbreeding of itself does not raise the incidence of DCM. I know of breeders who always outcross who have produced dobermans who have died of DCM. Failure to disclose cause of death; breeding dogs whose pedigrees are riddled with early DCM death - those 2 factors, in my opinion, are contributing substantially to what seems to be an extraordinary upsurge in DCM in our breed.

With regard to 'one dog' being the cause - I am of the understanding that of the 7 sires, 5 died of DCM. It's in the breed.

[andyhilt27]

With regard to 'one dog' being the cause - I am of the understanding that of the 7 sires, 5 died of DCM. It's in the breed.

I think I read 3 of the sires died of DCM. 3 or 5 it makes no difference. I was referring to an outcross of grey hound, weimeraner, rottweiler, etc. earlier on.

I am not bashing inbreeding....we wouldn't have purebreds without it. And sure you could have DCM with an outcross breeding. I do think it would be less likely. We have the DCM lottery at this point. I know we will not be able to claim a DCM free pedigree. Breeding is a game of odds....We as breeders place two together to increase the odds of desireable traits, yet there are no gurantees. The same applies for the converse.

[Elaine]

You can produce DCM in an outcross pedigree just the same as with a line breeding. And, inbreeding or linebreeding does not create problems, these kinds of breedings simply bring the problems in the breeding line to the fore, so you will see what is in your line. Inbred (or linebred) animals are generally speaking desirable as breeding animals because their genetic contribution in a breeding combination is predictable.

About outcrossing to a Weimaraner, Rottie or Greyhound, in my opinion, that would be a going backwards. It has taken decades and decades to refine the influence of the various breeds that originally made up the Doberman. Adding more Weimaraner, Rottie, Greyhound or whatever at this date would be chaos... and make no mistake, these breeds suffer from as many health issues as Dobermans.

Look at any breed of dog, they all have health problems listed. Is that because in 2008 they have more health problems? Or, is it because we are more aware and better able to track what has always been going on? For that matter, is DCM on the rise, or is it simply that we are better able to accurately diagnose a DCM death and we talk about it more because of the internet? Another consideration, people seldom do autopsies on their dogs, so some deaths attributed to DCM may not be DCM. Without an autopsy we simply do not know for sure, one way or the other.

All living organisms have frailties that will eventually lead to their demise. Arguably mixed breed dogs have as many genetic problems as purebreds, but no organization tracks data on mix breed dogs. And, owners of mixbreeds typically don’t do health testing. Think about it, when you’ve only spent $35 on the dog, what is the likelihood that you will get the mixbreed OFA’d, Michigan State Thyroid tested... etc.? What organization would be tracking the test results if you did them? If/when a mixed breed dog dies of DCM, how does the owner know? No organization tracks that kind of data.

There are so many good sounding but utterly wrong approaches to addressing health issues. Before we go down yet another wrong path... let’s concentrate on trying to find the 23 plus genetic markers for DCM in canines... and then let’s see if we can come up with a test to determine which dogs will NOT transmit DCM.

[andyhilt27]

About outcrossing to a Weimaraner, Rottie or Greyhound, in my opinion, that would be a going backwards. It has taken decades and decades to refine the influence of the various breeds that originally made up the Doberman. Adding more Weimaraner, Rottie, Greyhound or whatever at this date would be chaos... and make no mistake, these breeds suffer from as many health issues as Dobermans.

I didn't say to do this....I said this could have been where the breed devoloped DCM early on . Could have been any of the breeds used for the formation of this breed.

[andyhilt27]

Before we go down yet another wrong path... let’s concentrate on trying to find the 23 plus genetic markers for DCM in canines... and then let’s see if we can come up with a test to determine which dogs will NOT transmit DCM.

The reality is that DCM is polygenetic with incomplete penetrance and there is no way to determine which dogs will transmit it. There never will be a way because of so many genes that can carry it. My opinion is that there needs to be more outcrossing to dilute the gene pool.

[andyhilt27]

You can produce DCM in an outcross pedigree just the same as with a line breeding. And, inbreeding or linebreeding does not create problems, these kinds of breedings simply bring the problems in the breeding line to the fore, so you will see what is in your line. Inbred (or linebred) animals are generally speaking desirable as breeding animals because their genetic contribution in a breeding combination is predictable.

With many traits being polygenetic, inbreeding increases the likelyhood of them appearing in the phenotype. Both good and bad traits. DCM is in every pedigree correct? Therefore inbreeding will increase the frequency of it.

[Elaine]

There never will be a way because of so many genes that can carry it.

You are so wrong here... we need science... we need to fund and focus on credible science, not fantasy. We can find the answers... but we have to approach the solution in a scientifically sound principled manner. As for outcrossing, you are making an incorrect assumption that outcrossing will only bring in desired characteristics... that is a fallacy. For starters, we will still have no way to determine if these outcrossed animals have achieved the goal of not being able to transmit DCM. We need the genetic markers, whether we use the info on an inbred dog or an outcrossed dog.


Also, I said we have no way to determine which dogs will not transmit DCM... that is not the same as "we don't know which dogs WILL transmit it with a predictiable statistical probability." We can not say we have a DCM free pedigree. But, it is possible to say that dog X was diagnosed and dog Y was diagnosed and there is a predictable statistical probability that some number of the offspring will have it too. The question remains, for the littermates that do not develop DCM... do they have some mechanism that inhibits the development of DCM. We need to study this... in a credible manner... not guess at it.

[Elaine]

Therefore inbreeding will increase the frequency of it.
Again, you are wrong.

If a breeder inbreeds two animals that have some mechanism to inhibit the development of DCM then the breeder may have produced a dog preponent for not passing on DCM. Before we go down the wrong path yet again, we need credible science to guide us, otherwise we’re just chasing our tails... and eliminating great dogs (with great breed type and other attributes) out of sheer ignorance.

[andyhilt27]

Again, you are wrong.

If a breeder inbreeds two animals that have some mechanism to inhibit the development of DCM then the breeder may have produced a dog preponent for not passing on DCM. Before we go down the wrong path yet again, we need credible science to guide us, otherwise we’re just chasing our tails... and eliminating great dogs (with great breed type and other attributes) out of sheer ignorance.

How can you state that I am wrong with no credible science to prove your claim of bionic genes? Oh the Earth is round by the way.:D:D:D Mechanism inhibiting the developement of DCM. That's crazy talk. You're wrong. I still like you though.:D

[andyhilt27]

Before we go down the wrong path yet again, we need credible science to guide us, otherwise we’re just chasing our tails... and eliminating great dogs (with great breed type and other attributes) out of sheer ignorance.

Ok give me a male and a female of a great dog whose sire died early of DCM. I will house them for scientific study and inbreed the hell out of them until DCM appears in every one of their offspring. It will happen. Will you believe this theory then?

[Elaine]

Ok give me a male and a female of a great dog whose sire died early of DCM. I will house them for scientific study and inbreed the hell out of them until DCM appears in every one of their offspring. It will happen. Will you believe this theory then?

Andy,
To understand DCM and how to prevent transmitting it we need credible science... not antidotal data from a few breedings. We would need credible research, conducted in an academic or institutional setting, by trained, qualified medical researchers, that conforms to the scientific method (i.e. that the results are replicatable, verifiable and falsifiable). For just a general idea of what I’m referring to, here is what Wikipedia says about the Scientific Method. http://en.wikipedia.org/wiki/Scientific_method

We need to fund and support credible scientific research. We need accurate data generated from a well designed research protocol that would guide us towards achieving our goal. Having you raise a few litters in some informal ad hoc approach would prove nothing.

[Elaine]

How can you state that I am wrong with no credible science to prove your claim of bionic genes? Oh the Earth is round by the way.:D:D:D Mechanism inhibiting the developement of DCM. That's crazy talk. You're wrong. I still like you though.:D


We know that some dogs develop DCM, yet their litter mates and offspring do not. It may be very useful for us to understand why... and our understanding needs to be based upon credible science... not speculation and hunches.

[Elaine2]

How can you state that I am wrong with no credible science to prove your claim of bionic genes? Oh the Earth is round by the way.:D:D:D Mechanism inhibiting the developement of DCM. That's crazy talk. You're wrong. I still like you though.:D

Andy, thanks for the morning laugh. I am rolling on the floor here. Notice how she ignores you and just keeps on going like the ever-ready bunny? She ignores me too!
LMAO!!!
Just teasing E1;)
E2

[Elaine]

Andy, thanks for the morning laugh. I am rolling on the floor here. Notice how she ignores you and just keeps on going like the ever-ready bunny? She ignores me too!
LMAO!!!
Just teasing E1;)
E2
Actually, I had to attend to life, a home, 22 acres of snakes and crap... a brush fire that's been going all night... stalls to clean, animals to feed.... power tools to return to rental companies... running to the feed store... because I am responsible for 9 horses, including two stallions and a mare and foal... and at least one or two dogs [insert violin music] ... and I am solving world hunger and establishing peace in the Middle East... all before 9:00 am ... so I didn't finish. Here is the rest of the answer:

Andy, I am not claiming anything about "bionic genes." Rather, I am advocating an intelligent, scientifically sound, credible approach to solving the health problems that we face, be it DCM or any other health problem. In human medicine we make advances based upon credible research and science. We need to do the same in canines. To date, we are sorely lacking in our understanding of most of the health problems we face, in part because we don't have the basic science... we are still at the very infancy of understanding. And, if you speak with researchers, they will tell you it is near impossible to get funding for the kind of research we need. There is no will and no funding for the kinds of research we would need to address the problems we see.

Stir hinted at this in her post, any study is funded by some interest... and sometimes the true agenda of the funder is antethical to our goals and even our long term health. Most often the funding is tied to the expectation of being able to market a product... most especially to market a drug.

IF you read the Meurs study that was recently halted, I think you can see why. The data was not useful, in part because so many dogs had disappeared from the study, the results would have been questionable at best. I suspect that the reason they pulled the plug on the study was that they realized it was going no where... and that the protocal was flawed from the get go.

We don't need just any research.. we need something specifically tailored to the ability to identify which dogs will not transmit DCM (and of course, we will then have to hope like all hell that these dogs don't instead transmit an increased likelihood of some other hideous health disorder). And btw, I am not saying that all research is of the same value or that we need a billion dollar budget. I think the key is the protocol itself. As a Bio Chem undergrad at the U of W Arthur worked on a multi institutional research project to use self-assembled monolayers of bio-recognition groups on gold surfaces to promote healing. Forget the name of the study... it went on for years and years... may still be going on... I always suspected that its true purpose was to create reason to build a new Chem building on the U of W campus. :D

In canines, I would suspect that one reason research is expensive is that we need a breeding population of affected individuals and a control group of unaffected individuals... that would live at a research facility and be available for necropsy. That thought is almost beyond comprehension to all of us, but we may have to face the fact that if we want to understand any health disorder, we may need to make the sacrifices for the science.

[andyhilt27]

most universities refuse to honor wikipedia as a source of information. But I will look at.

[andyhilt27]

Andy, thanks for the morning laugh. I am rolling on the floor here. Notice how she ignores you and just keeps on going like the ever-ready bunny? She ignores me too!
LMAO!!!
Just teasing E1;)
E2

Yes, she is persistant and repetetive. Credible science and bionic genes. :D Elaine perhaps you are correct on the bionic genes.....but there is evidence of Dobermans with lower frequencies of DCM in Eastern Europe. Perhaps they weren't inbred as much or they may have these bionic inhibitors. Regardless, back to the topic of my thread. You breed your bionic genes and I will dilute the gene pool. Either way I need the semen in my sperm bank.

[andyhilt27]

We need to fund and support credible scientific research. We need accurate data generated from a well designed research protocol that would guide us towards achieving our goal. Having you raise a few litters in some informal ad hoc approach would prove nothing.

Oh no!!! I am moving to North Carolina and building a kennel to house over 100 Dobermans. It is gonna be the real deal. Lab coats and all. All nonprofit. North Carolina you say? That's right, I have a lab coat with your name on it Elaine. You can house 50 of the dogs believed to carry the magical inhibitors. It will take many years and many dogs. Don't worry though many of the inbred dogs will die early of DCM so we can make room for the diluted gene study.:D

[andyhilt27]

I just looked at a recent issue of Backyard Poultry. They have instructions on how to build an automated chicken plucker!!! I don't have any chickens yet but I will begin construction soon. I am curious if the chickens are dead before they enter this amazing machine.

[Elaine]

Yes, she is persistant and repetetive. Credible science and bionic genes. :D Elaine perhaps you are correct on the bionic genes.....but there is evidence of Dobermans with lower frequencies of DCM in Eastern Europe. Perhaps they weren't inbred as much or they may have these bionic inhibitors. Regardless, back to the topic of my thread. You breed your bionic genes and I will dilute the gene pool. Either way I need the semen in my sperm bank.
You have evidence of a lower incidence of DCM in Dobermans Europe... really? Credible evidence... not just antidotal, unsubstantiated hype to promote someone’s kennel or breeding line? Really? Where (i.e., in what peer reviewed journal) has this claim been published. Not to disparage anyone, but this kind of reminds me of the German Women’s Olympic Swim team’s claims that they didn’t use steroids, they were just genetically superior (with handle bar mustaches and Adam’s apples). :D:D:D If you are not doing autopsies on your dogs, how can you say what they died of?

As for understanding DCM and how to avoid transmitting it, first we need a way to identify dogs that will not develop it. Doesn’t matter if they are line bred dogs or outcrossed mutts, Born in the USA or imported, we need a credible way to identify which dogs will not pass on DCM. As of June 17, 2008 we have no way to do this, whether in a line-bred dog, some import or in your Dr. Frankenstein- Dobie-Weimaraner-Rottie-Greyhound outcross.

We know for a fact that in a given litter some dogs will develop DCM and we believe that some dogs do not. Among other avenues of inquiry, it is worth exploring (in a credible scientific manner) why some dogs do not develop DCM. It is possible that the dogs who do not develop DCM have some inhibitor for the expression of DCM; understanding that process may be of value towards eradicating DCM. Overall, I think that research is something the DPCA and the AKC Canine Health Foundation might consider funding... with the help of private donations.

But if you have other research ideas, hey, by all means have at it. Neither Arthur nor I are medical researchers, though we were both involved in medical research projects as undergraduates at the U of W in the late 1990's. It is not a field for amateurs. Research projects that lead us in productive directions are based upon credible science and are undertaken by trained and educated researchers. In my opinion, well-meaning theory, anecdotal stories, self-serving claims about a given pedigree and/or amateur guesswork, most especially something like a Weimaraner, Greyhound, Rottie outcross lead us no where. Your Wei-Rot outcross experiment isn’t grounded in credible science, it would never get funded, it would involve producing numbers of unwanted animals and it simply won’t lead us in any useful direction.

But if you feel differently... go for it.:)
most universities refuse to honor wikipedia as a source of information. But I will look at.

Before you launch into your Dobe-Wei-Rotti Import cross research project, you should know, The Scientific Method is not a creation of Wikopedia... it is the GOLD STANDARD for research. And the purpose of being published and reviewed by peers in a credible journal of your particular discipline is that the research and the claimed results can be scrutinized by peers... with the goal of exposing faults and identifying strengths in the research methodology and the results... all with the broader goal of leading to understanding, and, ideally, to useful scientific advances.

[andyhilt27]

Before you launch into your Dobe-Wei-Rotti Import cross research project, you should know, The Scientific Method is not a creation of Wikopedia... it is the GOLD STANDARD for research. And the purpose of being published and reviewed by peers in a credible journal of your particular discipline is that the research and the claimed results can be scrutinized by peers... with the goal of exposing faults and identifying strengths in the research methodology and the results... all with the broader goal of leading to understanding, and, ideally, to useful scientific advances.

I did not say that we as breeders should do a freakin cross breeding to Wei-Rotti!!!!!!! FOR THE LAST TIME. I stated this could have been why we have high frequencies of DCM....One of the EARLY cross breeding to one of these breeds could have and most likely did have a canine that was affected by DCM. From there many many inbreedings compounded the genes that carry it. Thus why we in terms of dobermans have such a high frequency in comparison to other breeds. GEEZ. I am in no way trying to solicit the use of frankenstein dobermans. They would look funny with the bolts sticking out of their necks.

[andyhilt27]

You have evidence of a lower incidence of DCM in Dobermans Europe... really? Credible evidence... not just antidotal, unsubstantiated hype to promote someone’s kennel or breeding line? Really? Where (i.e., in what peer reviewed journal) has this claim been published. Not to disparage anyone, but this kind of reminds me of the German Women’s Olympic Swim team’s claims that they didn’t use steroids, they were just genetically superior (with handle bar mustaches and Adam’s apples). :D:D:D If you are not doing autopsies on your dogs, how can you say what they died of?

Again from the UDC website,

Increasing Hereditary Health Problems in the Breeding of Purebred Dogs: A Comparative Overview Using Dobermans in Germany, Europe and in the USA as Examples
by Dr. Reinhard Haberzettl

Brief C.V. of the Author: Dr. Reinhard Haberzettl was born in 1952. He obtained his doctorate in biology (equivalent to Ph.D.) in USA) from the prestigious Humboldt University Berlin. He did additional work that focused on animal genetics. In that field, he achieved a Diplom-Biologe (equivalent to USA M.S) from Martin-Luther University in Halle/Wittenberg.
After completing his formal education, Dr. Haberzettl worked for 5 years in the pharmaceutical industry as a genetic and toxicological scientist and published in the journal “Chemical and Pharmacological Factory Fahlberg-List Magdeburg” (today part of Hexal AG). From 1980-90 he worked at the Institute of Animal Breeding of Humboldt Berlin, doing agricultural-animal breeding research. Since 1991, returning to the pharmaceutical industry, he has worked for Celltech Pharma AG Essen.
In 1990, he served as Breed Warden for the East German Dobermann Verein, the same year that the East and West German Dobermann Verein were reunited. He bred Dobermans from 1970 until about 1990. At the present time he is an active member of the SV and is an ardent breeder of German Shepherd Dogs

Now what does Dr. Reinhard Haberzettl stand to gain from publishing his findings of Eastern European Dobermanns? Look at the man's credentials.....

[tosca]

Andy, what does listing this fellow's credentials have to do with anything?

[andyhilt27]

credible science

[Elaine]

Andy,

As Tosca tried to point out... you have listed a C.V.

A C.V. is not "credible science" ... and it may have nothing to do with a published peer reviewed article. Is there one?

To put your fellows C.V. in a context, when I was at the University of Washington I was fortunate to be a student of (and do undergrad research with) Dr. Elizabeth Loftus. Dr. Loftus is a world renown expert on human memory and eye witness testimony. She was on the faculty of the U of W’s Department of Psychology and she was an adjunct professor of law at the University of Washington’s’ School of Law. She was one of the founding members of Innocence Project Northwest... she has testified in dozens of lawsuits around this country and around the world. Last I heard, she is back at Stanford. Dr. Loftus’ C.V is over 50 pages long. Still, each and every research project she is involved with is published in a credible scientific journal and reviewed by her peers. And each must stand on its own merit.

[robinb]

Yes, she is persistant and repetetive. Credible science and bionic genes. :D Elaine perhaps you are correct on the bionic genes.....but there is evidence of Dobermans with lower frequencies of DCM in Eastern Europe. Perhaps they weren't inbred as much or they may have these bionic inhibitors. Regardless, back to the topic of my thread. You breed your bionic genes and I will dilute the gene pool. Either way I need the semen in my sperm bank.

Andy,

There is NO evidence of lower frequencies of DCM in Eastern Europe. Go look at many of the Eastern European kennels advertising 'cardio clear' which is total BS, as no one can honestly make that claim. Perhaps it was based on talking to those breeders! I actually like some of the Euro bred dogs, even owned one, but they have the same problem and frequency with DCM that we do. Also just like the DPCA has articles linked to the DPCA website so does the UDC. It's just something that some member read, found interesting and linked it. I'm a member of the UDC and it's certainly not some official position of the UDC.

Robin

[andyhilt27]

Ok....I will admit that I have pushed this thread a little further than it should have been. I did get a great rise out of Elaine though. Did you like the bionic genes terminology? :D I do agree we need credible science but it is far from being a reality. Like I am really going to start a sperm bank...:rolleyes: I was bored for crying out loud.....trying to liven this joint up a little. It gets quiet on mondays in here.

[Athy]

I was bored for crying out loud.....trying to liven this joint up a little. It gets quiet on mondays in here.

Andy, honey, we LIKE it quiet on Mondays. Gives us a bit of time to recover from the weekend.... ;)

[Elaine]

Hey... this is a discussion forum... Andy gets a Gold Star for his love of "discussion." Can’t fault him for that. :)

[robinb]

Hey... this is a discussion forum... Andy gets a Gold Star for his love of "discussion." Can’t fault him for that. :)

:) I agree Elaine.

However it really irks me when I see 'cardio clear' or 'cardio free' listed on MANY of the Euro dogs. I presume they did a holter or echo at sometime and base it on that. Just a pet peeve of mine as the current testing we have is diagnostic and good for the day it was done only. I see people listing the testing results here too in the context of breeding which imho is wrong, but in Europe they have taken it a step further and just list them as cardio free.:(

[andyhilt27]

I too agree with all that you have said. One serious question though:

Why does DCM affect dobermans more than other breeds? In your opinion...

[andyhilt27]

Hey... this is a discussion forum... Andy gets a Gold Star for his love of "discussion." Can’t fault him for that. :)

At least I started my own thread to do it.:D I bet your are thinking, "Well start your own website to do it!"

[tosca]

IWhy does DCM affect dobermans more than other breeds? In your opinion...

I don't think it does necessarily - it's just talked about a lot. It's been rampant in other breeds for some time. Interestingly, it's now becoming a significant problem even in whippets.

[andyhilt27]

I don't think it does necessarily - it's just talked about a lot. It's been rampant in other breeds for some time. Interestingly, it's now becoming a significant problem even in whippets.

I downloaded a 185 page study, I believe it may have been a thesis by Polana Stabej. It has a crap load of medical jargon that I am trying to decipher at this point. "Molecular Genetics of Dilated Cardiomyopathy in the Dobermann Dog." Perhaps Elaine or Arthur could read it and translate it.:D It is not very new, written in 2002 I believe. So no new findings I assume.

[Athy]

Why does DCM affect dobermans more than other breeds? In your opinion...

I think it is prevalent in our breed because of the incidence in the seven sires. Whatever makes it is in every line it seems.

I read somewhere that something like 90% of report DCM deaths occurred in these eight breeds: Doberman Pinschers, Boxers, Great Danes, Irish Wolfhounds, Saint Bernards, Cocker Spaniels, Golden Retrievers and German Shepherd Dogs. I have no evidence to support that claim though.

[Elaine]

moved this to the DCM Studies Thread - Admin

[andyhilt27]

information overload.....need headache meds stat!!!!

[Elaine]

information overload.....need headache meds stat!!!!

Actually, these articles are well worth reading... :) and not too difficult... I will try to fix the formatting.

[mosso]

so am I understanding this to mean that current thinking is autosomal dominant transmission BUT incomplete penetrance?

what studies are going on now? (do you know?) (hope I'm not asking something that was covered....)

stir

[andyhilt27]

so am I understanding this to mean that current thinking is autosomal dominant transmission BUT incomplete penetrance?

what studies are going on now? (do you know?) (hope I'm not asking something that was covered....)

stir

poloygenetic autsomally dominant believed to be incomplete penetrance. Has not been proven yet to be incomplete in my understanding of it. I think there are theories of it being partly x chromosomal due to a higher incidence of males being affected. I haven't read all of these studies yet that Elaine posted. I won't be reading them today as I have a nasty hangover thanks to my boss.:D

[Elaine]

so am I understanding this to mean that current thinking is autosomal dominant transmission BUT incomplete penetrance?

what studies are going on now? (do you know?) (hope I'm not asking something that was covered....)

stir
Stir,
I have moved the DCM part of the discussion to a new thread... because it is important and really has little to do with artificial insemination. About incomplete penetrance, here is what the Meur's study says:


There is substantial interest in the development of a genetic test for familial canine DCM to allow for early detection of affected animals. A linkage analysis approach was previously performed in a family of Newfoundland dogs with DCM.33 It is regrettable that statistical analysis did not identify a chromosomal region that was statistically linked to DCM in that Newfoundland family or the Doberman Pinscher family presented here. A simulated linkage analysis program with assumptions of a fully penetrant autosomal dominant inheritance with 100 replications was performed in this study to predict the likelihood of successful linkage analysis. This predicted an average LOD score of 1.5 with a maximum score of 4.18. Although this analysis was used as a starting point for the study, it has some limitations. The penetrance of DCM in the Doberman Pinscher is unknown, but it is incomplete in human beings.34 Therefore, the calculations in this study may have been a bit optimistic. The high LOD score of 1.31 identified here was close to the average predicted by the simulation but we did not come close to the maximum predicted score. In the study performed here we completed the analysis after evaluating just under 400 markers over the 38 autosomomal chromosomes. Almost 20% of the markers were nonpolymorphic for this family. A higher LOD score might have been identified if additional markers were evaluated and if the family was more powerful (larger number of animals, fewer animals of indeterminate status).
[omitted]

... In conclusion we have demonstrated that DCM in the Doberman Pinscher dogs is a familial disease inherited as an autosomal dominant trait. Due to the autosomal dominant nature, genes that have been found to be involved in the development of X-linked DCMmay be deemphasized in future studies. A genome wide scan with microsatellite markers of Doberman Pinscher DCM has limitations due to the adult onset nature of this disease and the likely incomplete penetrance. In the future, association studies with single nucleotide polymporphism array technology may prove to be more valuable. Further investigations remain necessary to identify the causative gene(s) responsible for this condition.