|Topic Review (Newest First)|
|05-13-2014 11:58 PM|
My veterinarian is an expert in endocrinology he wrote the book that everybody else reads from you can check out his website I'll give you the address:
He's been doing research on endocrinology and cortisol for the last 50 years if he doesn't have the answers then nobody in the country does.
Most veterinarians do not know how to test cortisol levels. I am not the expert. Do not shoot me I'm only the messenger.
|05-13-2014 11:08 PM|
|Doc||Is there any advantage using pre and probiotics along with enzymes when treating for EPI?|
|05-12-2014 10:36 PM|
|Doc||interesting approach to EPI khawk. Your example illuminates the complexity of the disorder. I have a line bred dog that is effected by EPI. Luckly, his is controled by Prozyme. 1/4/tsp per cup food. So far so good.|
|05-06-2014 08:55 PM|
EPI--Exocrine Pancreatic Insufficiency
I've noticed a couple of threads about EPI recently, one old thread being resurrected and a new poster with an EPI dog and some one thought there ought to be a new thread about Epi, so I thought I'd post the things I've managed to pull together on the topic.
This is one of the 3 genetic conditions that make up the triad of Toxic Gut Syndrome. EPI means that the pancreas fails to produce enough of the digestive enzymes and chemicals it secretes into the small intestine to allow the dog to digest enough food to live. This is called becoming symptomatic. Most dogs do not reach this point until age 3 at the earliest and some do not become symptomatic until age 6 or even 7. This makes trying to eliminate affected dogs from the breeding population difficult, and carriers almost impossible to identify in a timely manner so as to keep them out of the breeding population.
Recent discoveries in canine DNA have found that EPI is made up of 4 alleles and 2 epigenes in close proximity on the chromosomal string. To get an idea of the genetic construct, think of the chromosomal string as a rope ladder twisted into a spiral. Two of the rungs of the ladder carry the affective alleles, one affixed to each side of the rung. It will help if you think of the rung as the epigene. This is, of course, a gross over-simplification, but it's a useful visual to help understand the arrangement.
One side of the ladder is donated to the pup by Dad, the other by Mom. At conception the two sides of the ladder join to make a whole ladder, and if all 4 alleles are affective for EPI, then the likelihood is that at some time during the pup's life, its pancreas will fail and the pup will become symptomatic with EPI.
The epigenes which determine whether the alleles affect the pancreas are themselves affected by environmental stressors. The usual suspects, malnutrition, pediatric spay and neuter which affects the dog's hormone production, over-vaccination, exposure to pesticides and toxins from plastics, air, soil and water contaminants all come into play here. Epigenes in the active position are heritable. That is, if Mom or Dad is symptomatic for EPI, it may create a situation where the pup is also born with epigenes which will allow the alleles to affect the pup's pancreas and there fore the pup becomes symptomatic upon weaning.
The majority of pups who will eventually develop EPI inherit epigenes in the inactive positions. As environmental stressors act on the epigenes, they deteriorate and no longer control the affective alleles. Slowly, but surely, the dog's pancreas begins shutting down and when enzyme production drops below 20% the dog becomes symptomatic. The life of the dog can then be prolonged by feeding artificial enzymes and adding regular vitamin B12 shots. For some dogs with bacterial overgrowth of the small intestine, antibiotics may be needed.
The process for feeding the dog is to mix the enzymes with a small amount of wet food, feed it to the dog, and then wait half an hour. Then feed the remainder of the dog's ration. The purpose of the wait is to allow the enzymes to get situated in the small intestine before the food arrives to be digested.
EPI is an artifact of in-breeding, for the most part, and is endemic in German Shepherd Dogs. The first dog to be identified with this condition was Alex v Westfalenheim, and he was born in 1914. Unfortunately for the breed, Alex was the son of Sieger Hettel Uckermark and the grandson of Sieger Roland v Starkenburg. Alex was also the father of Sieger Erich v Grafenwerth, the grandfather of 1925 Sieger Klodo v Boxberg (who became symptomatic with EPI at age 6) and great grandfather of Sieger Utz v Haus Schutting, double great grandfather of Siegers Odin v Stolzenfels and Hussan v Haus Schutting. Additional Sieger descendants, Ferdl v d Secretainerie, Ingo v Piastendamm, Rolf v OsnabruckerLand and Siegerins Rena and Reina v OsnabruckerLand passed on the condition. This line became the MAIN line of German Shepherd dogs in Germany, Czechoslovakia, Great Britain and the US. The result is that not only do all German Shepherds carry Alex in their ancestry, most Gsds carry multiple lines to Alex, often numbering in the hundreds.
Because of the complexity of this inheritance system, we are not going to have a 'health' test to identify affected and carrier dogs soon. And as far as carriers are concerned, what do you consider a 'carrier'? Any dog with 1 affective allele? You may be talking about the entire breed. 2 affective alleles? How many of those 'titled' dogs are you willing to drop out of the breeding population? How many can you drop out of the breeding population before the numbers of that population become genetically unviable? And what about the other stuff? Some of it a lot more deadly, and/or painful than EPI? What about DM, Cardiomyeopathy, JRD, Anal fistulas and the aforementioned SIBO and IBD?
If there comes a time when we can identify how many affective alleles a dog has, maybe we may want to eliminate the dogs with 3 affective alleles, even tho they will never exhibit EPI. Maybe. Just bear in mind that when you eliminate one set of genes, many breeders have found that something a lot worse takes its place.
One obvious answer, of course, is to not breed dogs who are affected by EPI, but that is not as easy as it sounds, given that dogs may not become symptomatic until age 5 or 6 and we have no other way of knowing that they contain all 4 alleles for EPI. Not breeding a pair of dogs who have produced an EPI dog in the past may also be a good idea, but given that it is possible that one member of the pair may only be contributing 1 allele to the mix, trying a different combination is not out of the question.
The bottom line is that getting rid of EPI is not going to be either simple or easy, and there are no easy answers. khawk