Some Very Sad News for GSDS...DR Clemmons - Page 2

I might question it too had I not seen the autopsy results of 3 GSD's that tested at risk and their pedigrees. So far I have not seen any proof to the contrary.  There are plenty of breedable GSD's in the world today and I would not use the results to eliminate any dog/s from breeding, so I see no reason to not use the DM DNA test as another tool in addition to hips, elbows, and probably cardiac, thyroid, and CERF depending on which lines I was working with. We'll have to agree to disagee on this one.

I am not familiar with Dr Clemmons or his research but Marjorie you poor thing!  I hope you are improving and getting some relief.  I got shingles last summer and then my Grandpa passed away unexpectedly the next day so it was very painful and stressful, physically and emotionally.  Only a small area of my body was involved (my face, and I have some scars unfortunately) but the sensation is really unbelieveable/indescribable and you cannot get any sleep which then makes you go insane. I cannot imagine your pain! Please take care of yourself, my thought are with you!

Blitzen 

First I find it interesting that you totally ignored my discussion of the testing results in breeds NEVER KNOWN TO HAVE DM.

Secondly why not name the dogs you are talking about IF in fact the results are public knowledge.

Thirdly, you dismiss my personal knowlege and acquaintance with a dog who tested N/N but displayed severe DM symptoms and on death was posted and found to have DM as mere hearsay but expect us to take your word for three individuals who tested A/A and not consider that hearsay. What we know for a FACT aside from your experiences or mine is that University of Missouri has ACKNOWLEDGED the prescence of N/N individuals who were confirmed with DM  to wit " a DNA test result of A/A in all but 2 individuals"  http://www.caninegeneticdiseases.net/DM/testDM.htm  This has been on their site since the test went public and the numbers have increased since them but neither UM or OFA chooses to publish THAT information.

The reality of any scientific hypothesis ( and that is ALL that the SOD1 gene theory is - an unproven hypothesis) the minute you get a case that disproves the hypothesis it suggests the hypothesis is wrong and needs to be reevaluated. We have far more than one case involving individual testing as N/N and N/A. In addition the promoters of this test have an additional obstacle trying to prove its SCIENTIFIC Validity in that they acknowledge many A/A are symptom free PLUS they are getting significant percentages of N/A and A/A's in breeds NEVER KNOWN to have DM. Please explain all these inconsistencies.

We have NO scientific proof the SOD1 CAUSES DM. What we KNOW is the SOD 1 gene has been present in SOME individuals who have the disease but it has NOT BEEN present in others who also have the disease. Mere presence of the gene in a diseased individual is not proof of causality or indeed any relation to the disease process ESPECIALLY when it can be shown that it is NOT present in other individuals with the disease. IAt that point it is simply a gene the dog has or doesn't have. You are putting your faith in snake oil.

What I especially find offensive in the individuals who developed and promoted this test is not only the fraudulent hope they are engendering in the dog community but the hubris to have published statements saying the cause and cure for ALS has been found. I suggest you do some research on ALS and the SOD1 gene. It will  be eye opening for you. LESS than 10% of ALS is presumed to be genetic and while there are some hypotheses about the role of SOD1 they are acknowleged to be just that and so far it involves much smaller percentages of the population affected by ALS ( I need to check but I believe somewhere around 1% of ALS cases so to make such sweeping pronoucements is unconscionable especially given the tradegy that ALS patients and their families face.

Do the numbers - over a million dollars has been made with this one dubious test. Do you really think they are going to acknowledge that there are problems with it???

Here's a thought if they truly believe in their very flawed hypothesis.

First any dog with a presumptive diagnosis of DM be given a free test ( not merely half cost which is what they currently do and is still probably a profit maker). This test MUST be done at a neutral lab NOT UM or OFA.

Any of those dogs who come back as N/N or N/A at death can be posted for Free - again at a neutral veterinary school - NOT UM. ALL results from both of these things MUST BE PUBLIC. IF one of these dogs is confirmed DM then OFA MUST retract and publicize that for any clear by parentage on that dog's progeny AND should seriously reconsider offering a clear by parentage.

Have a registry for symptom free A/A dogs where their info can be entered along with a confirming veterinary statement. AGAIN A PUBLIC DB .

As I noted above the original two dogs that gave the lie to this test are sufficient under the scientific method to disprove the hypothesis that Sod1 is the cause of DM however if you feel you need more data - this would be one way of acquiring it. NB I'm not holding my breath - the almighty dollar rules.

Tig, I'm not going to debate you about this. You have your experiences, I have mine. That's what each of us are basing our "opinions" on. It's not up to me to disclose the owners of these dogs or their pedigrees. I assure you it is true and anyone who has the time and desire to surf the OFA database can probably figure it out on their own.

A breeder should choose to test or not test based on as much information as they can learn and then make an informed decision that is right for THEM. I'm guessing the breed is split about 50/50. Some breeders I know and respect very much do not test for one reason or another, I don't judge them or try to discredit them on this database. I am not dismissing anything you have said, my experiences do not match yours; I never said you were wrong. I said I have had  different experiences to influence my opinion therefore I disagree.

I'm done with this now, I've said my piece.

Blitzen, You of course have the right to believe what you want to believe. I'm sure there are still some folks out there who believe that the moon is made of green cheese. But I expected better of you. You could of said that you know those are interesting facts and questions and I don't have the answers to the inconsistencies you have raised but I will do what I can to promote the idea of gathering greater knowledge on this issue since there does seem to be a number of problematic areas.

Instead you took the coward's way out as so many do on the db and for that matter in life that when presented with a fact or question that threatens what they believe they go off in a huff stamping their foot saying I believe in what I believe and god forbid you try to clutter up my mind with real facts and probing questions. By doing so you choose to support bad science and that is to the detriment of our breed.

For those that missed school on the day the scientific method of research and reasoning was introduced ( wh/ obviously includes certain DM researchers) here is a quick graphic.

The original hypothesis here was that the SOD1 gene was the cause of DM in dogs ( without first answering the question of are we dealing with one or more diseases since there are signficant differences in the expression across breeds - strike one). This hypothesis was modified to say that it places a dog "at risk" for the disease when the researchers were faced with the problem of A/A dogs who exhibit no symptoms of the disease. (oops - strike two)

So the logic to this hypothesis goes like this. If a dog carries to two copies of the SOD1 allele represented by A/A the dog will have DM ( now modified to be at risk for DM.) If a dog carries one copy of the allele N/A the dog will not have the disease but can pass the potentiallity of the disease on to his or her progeny. If a dog carries no copies of the SOD1 gene the dog is normal and unaffected by the disease, can not pass it to his progeny and is represented by N/N. This hypothesis implies that ALL DM dogs will be A/A and ALL N/N will be disease free. To be proven as a hypothesis testing would have to confirm this.

TESTING DID NOT CONFIRM THIS (strike three and your out). We have N/N and N/A's confirmed by necropsy to have the disease. We have A/As that are disease free. The hypothesis FAILS - see right hand purple box above which leads us to the Think - Try again box. THIS IS WHERE WE ARE AT FOLKS whether you choose to acknowledge it or not. The very sad part is the researchers KNEW THIS from their original test group of dogs. BEFORE they sold you the test - BEFORE they ripped of the dog community to the tune of a million dollars. Where is the outrage for this theft???? Where is the outrage for great dogs lost to our breeding programs prematurely???

The question that is unanswered and will be unless some serious research is done is - is the SOD1 gene implicated in any way in the disease process either as a comorbidity or perhaps a trigger or is it merely a hitchhiker we noticed because of his bright clothing while the driver was dressed in all black. The research team who foisted this bogus test upon us - bogus because NOT ALL DOGS WITH DM CARRY THE SOD1 GENE and not all A/A dogs are affected - owes us this research. If they truly believe it plays a role in SOME DM cases - prove what it does and how it does it and why only some dogs are affected by it IF IN FACT That is true. Or man up and admit it was a hitchiker that looked like a good prospect but turned out to be innocent and unrelated.

Meanwhile folks for the sake of our breed do NOT supprt junk science dancing with dollar signs!

Interesting reading - a cautionary tale for day when and IF a reliable test is ever developed. http://devinefarm.net/rp/bathw.htm

Geez, Marjorie, you scared me--I thought your news was going to be that Dr. C was no longer in this dimension with us!  As long as he's well, his work remains alive and viable with him; he just needs to find a location where he'll be appreciated for what he has contributed to date, and which will nurture what he can and will continue to contribute to the science today and tomorrow. Like Tig, I too used his early protocol to slow down the progression of DM in my first GSD, giving me an additional year with her--six months of it with her having regained her full mobility, retaining full use of her bodily functions and enjoying life as she helped me raise her successor until I lost her to hemangiosarcoma two weeks after her 14th birthday. Without Dr. C's generosity in offering to review videotape of my old girl's to establish a diagnosis of DM, I wouldn't have learned of the treatment protocol, and I would not have had that year at all. Should I ever find myself with another dog I suspect is showing early signs of the disease, I will not hesitate to use the regimen once again; I've been lucky so far [and I know it full well that it was nothing more than sheer luck].

YOU, however, owe it to not just yourself, but all your dogs, past and present, to slow down, catch your breath and devote all your time and energies to taking care of yourself for a change. I, too, an angry and sad and perplexed and frustrated that all of the research monies went to the SOD1 test, which I also doubt as to the applicability of the results to true DM of the German Shepherd Dog. But those emotions cannot change what has taken place, and they are not productive in moving other work on the disease forward, either. 

It's long been my suspicion that there's more than one type of degenerative myelopathy that occurs in GSDs--one is an early-onset version that I believe falls within the entire spectrum of immune-mediated disorders that affect this breed, while another is a late-onset manifestation that I think has some degree of immune-response activity included in the progression, and we see dogs as young as 4 years of age already showing early clinical signs.  But I feel is also related to an overall degeneration of neurofunction throughout the dog's body, and which is related to the factor that causes a greater incidence of bloating and torsion occuring in senior dogs which had no history of such before they reached 8-10 years of age--my DM dog was still active and jumping up on walls and furniture and into the back of a truck when she was 12-13 years of age...it was a few months before she turned 13 that she began to show signs of a degenerative myelopathy, with the reduction in sensory response of the toes and nails, with dragging of hind feet and inability to remain in a standing position for more than a few minutes, and eventually more than a few minutes. Within a span of three months, she went from poppin up onto her couch at will to not being able to stand long enough to eat her meals--and within three months of starting the vitamin & ACA protocol, she was able to remain standing, could climb up a step to get on her couch, and was able to complete a two mile walk every other day right up until two days before her death. 

One of these conditions is not like the other--but they clearly are related in some fashion.

Neither version bears any resemblance to ALS, though.The SOD1 testing, while I question it's predictive value as a DM test for GSDs, may well be providing us with data that WILL be of importance at some point, for some other health condition or risk in our dogs, and in truth I tend to view it more as a test result in search of the disease it will eventually predict or identify in our dogs. If it were an invasive test, I wouldn't even consider doing it; that it's but a cheek swab test makes it trivial to add it to the list of other testing one when collecting samples, although I'll concede that the $65 fee is hardly negligible when you're talking about multiple dogs.

I will be surprised if Dr. C is on the market very long before he's snapped up and back in the lab and/or lecture hall. His knowledge of Traditional Chinese Medicine, coupled with all his work on GSD DM, make him an excellent catch for a forward-thinking university or research facility, IMO.

I wish that the DM research would become a joint venture.

I hear that, Blitzen. Sadly, research has become completely about the shareholders, much to the scientists' chagrin, so unless a way is found to tie GSD DM to a condition that affects humans, the interest in finding out what triggers the condition or what will arrest it or prevent it will remain limited when it comes to getting funding.

My original reply above is too old to edit, and re-reading it just now I see that I mixed thoughts about different forms of DM in the GSD so as to make the point obscured. Below is how that paragraph SHOULD read:

"It's long been my suspicion that there's more than one type of degenerative myelopathy that occurs in GSDs--one is an early-onset version that I believe falls within the entire spectrum of immune-mediated disorders that affect this breed, and we see dogs as young as 4 years of age already showing early clinical signs. The other is a late-onset form, which doesn't begin to produce any clinical signalment before the dog is 10+ years of age, which I think has some degree of immune-response activity involved in the progression of the disease, but which I also feel is part of an overall degeneration of neurofunction throughout the dog's body, and which is related to the factor that causes a greater incidence of bloating and torsion occuring in senior dogs which had no history of such before they reached 8-10 years of age."