- EPIC trial results are scheduled to be announced at ACVIM Forum in Denver in June -- Feb. 2, 2016
- Too many cavaliers are too fat! -- October 25, 2015
- Cardiologists focus on bionic fixes to the leaking mitral valve -- October 14, 2015
- Heart failure in the MVD-affected cavalier King Charles spaniel -- July 1, 2015
- The CKCSC,USA makes part of its ethics code optional -- April 30, 2015
- “Purebred breeding” is a euphemism for accelerated genetic entrophy -- April 19, 2015
- The EPIC trial ends on schedule, but could a whitewash be in the works? -- March 25, 2015
- Is it 'Back to the Future' for the American Kennel Club? -- March 19, 2015
- All that cavalier owners need to know about the “Reverse Sneeze” or “Cavalier Snort” -- Feb. 10, 2015
- Just Asking: What’s up with Vetmedin's ‘EPIC Trial’? -- October 20, 2014
- So your cavalier has a heart murmur. What do you do next? -- October 13, 2014
- Do MVD-affected cavalier King Charles spaniels really need taurine supplements? -- October 11, 2014
- When NOT to start giving your cavalier pimobendan (Vetmedin). -- July 12, 2014
- Do-it-yourself diagnosing of congestive heart failure in your cavalier. -- June 18, 2014
- Dog food companies may be turning a grain-free corner. -- March 10, 2014
- The accordion-muzzled cavalier King Charles spaniel. -- December 12, 2013
- All that cavalier owners need to know about primary secretory otitis media. -- September 23, 2013
- All that cavalier owners need to know about their dogs' blood platelets. -- August 26, 2013
- What if the American Kennel Club ceased to exist? -- August 10, 2013
- All that cavalier owners need to know about natriuretic peptides tests (ANP & BNP). -- July 9, 2013
- The cavalier King Charles spaniel is pre-disposed to ... -- July 7, 2013
- CKCSC,USA embarks on an offensive “charm offensive” -- March 26, 2013
- AVMA’s House of Nannies aims at homeopathic vets -- December 18, 2012
- Dog food companies lie, and allergic dogs may die -- September 27, 2012
- Update on Hill's Science Diet junk food. -- September 26, 2012
- The US cavalier clubs contemptuously keep whistling past our breed's graveyard. -- August 3, 2012
- The insidious mind control over clueless veterinarians by Hill's Pet "Nutrition". -- June 14, 2012
- Congratulations to Her Majesty, lover of cavaliers! -- June 3, 2012
- When ignorance (stupidity?) guides cavalier PSOM research -- May 9, 2012
- AKC's CHIC program is a farce for cavaliers -- March 14, 2012
- Pedigree Dogs Exposed: The Sequel, or The End? -- March 1, 2012
- Will the next SM breeding protocol be BAD FOR THE BREED? -- December 24, 2011
- What do the two USA CKCS clubs have against breeding healthy cavaliers? -- October 14, 2011
- A neurologist answers our August 13 questions -- September 13, 2011
- Plucking the MVD genes: The first shoe has dropped! -- August 29, 2011
- Will the CSF-space gap predict future syringomyelia in cavaliers? -- August 18, 2011
- Okay, syringomyelia researchers: What now? Where do we go from here? -- August 13, 2011
- AKC Chairman Ron Menaker condemns "Pedigree Dogs Exposed" -- July 24, 2011
- How the SM breeding protocol could lead to the Popular Sire Syndrome -- June 13, 2011
- CKCSC,USA board admits its ignorance ... but not its stupidity! -- May 11, 2011
- Beware the pimobendan/Vetmedin "EPIC clinical trial": There is no upside -- April 23, 2011
- Chiari-like malformation HAS been re-defined! -- January 30, 2011
- Maybe cavaliers don't even have Chiari-like malformation (CM)! -- January 28, 2011
- CKCSC,USA's board reinstates a third of the REAL MVD breeding protocol -- December 28, 2010
- To CKCSC,USA's board: Reinstate the REAL MVD breeding protocol! -- October 7, 2010
- How self-absorbed can the CKCSC,USA board be? -- September 10, 2010
- CKCSC,USA dumps the MVD breeding protocol -- September 7, 2010
EPIC trial results are scheduled to be announced
at the ACVIM Forum
in Denver in June
15 months from the end of the trial to publication of its results
Why wait so long?
The results of the EPIC* Trial, a five-year study of up to 360 dogs suffering from pre-heart-failure MVD, will be announced at ACVIM’s annual forum in Denver, Colorado on June 9, 2016. All three lead researchers, Drs. Adrian Boswood, Sonya Gordon, and Jens Haggstrom, are scheduled to participate in the “EPIC Trial Results” session that morning.
The EPIC Trial, fully funded by Boehringer Ingelheim, the manufacturer of pimobendan (Vetmedin), began in 2010 as a placebo-controlled clinical trial evaluating the effectiveness of pimobendan in the prevention of the onset of signs of congestive heart failure in dogs with cardiac enlargement secondary to pre-clinical MVD. Thirty-six veterinary cardiologists from all over the globe participated, each examining ten MVD-affected dogs over the following five years, ending March 1, 2015.
The boastful March 2015 announcements were unethical and premature
Since publication of three clearly unethical**, premature public announcements*** in March 2015 of non-peer-reviewed “interim analysis”, claiming “clear evidence of benefit of the administration of pimobendan in prolonging the time to the primary endpoint of the study”, a lid has been firmly placed upon the actual results of the study.**** It will have been an extraordinary length of time -- over fifteen months to be exact -- between the March 1, 2015 end date of the study and the June 9, 2016 release of the actual (and presumably) peer-reviewed results. The scheduled date of the release reportedly has been postponed twice, without explanation.
The March 2015 press releases had manufacturer Boehringer Ingelheim’s desired effect, because numerous veterinarians -- specialists and general practice vets alike -- have been ignoring the FDA guidelines which forbid the administration of pimobendan to MVD-affected dogs prior to heart failure. When questioned about the lack of any evidentiary support for violating the FDA ruling, many such veterinarians have referenced the March 2015 announcements as their sole justification. Thus, if the full report includes any conditions or qualifications to the press releases’ bold asssertion of “clear evidence of benefit”, then the lead researchers will have a lot of explaining to do.
Why wait so long to publish?
A burning question remains: Why have the lead researchers waited over 15 months to disclose the peer-reviewed results of the EPIC Trial?
Obviously, in the interim, manufacturer Boehringer Ingelheim has been getting exactly what it has been paying for.
* "Evaluation of Pimobendan In dogs with Cardiomegaly caused by preclinical mitral valve disease".
** See, "What is Ethics in Research & Why is it Important?", by David B. Resnik, J.D., Ph.D. National Institute of Health website, 2011: “There are many other activities that the government does not define as ‘misconduct’ but which are still regarded by most researchers as unethical. These are called ‘other deviations’ from acceptable research practices and include: ... Bypassing the peer review process and announcing your results through a press conference without giving peers adequate information to review your work.”
**** Dr. Boswood's March 7, 2015 press release was supplemented a month later with this addition in bold font: "Please note – quantitative analysis of these results will not be discussed until the full results are available."
Too many cavaliers are too fat!
Feed the fat cavalier less and exercise it more!
Unfortunately, but perhaps not surprisingly, cavalier King Charles spaniels are pre-disposed to obesity. In other words, for whatever reason, it is easier for cavaliers to gain excess weight than nearly any other breed. Their pleading eyes and sweet demeanor are nearly impossible for many owners to resist. The CKCS’s only serious competition in this area are Labrador retrievers, boxers, Cairn and Scottish terriers, and Cocker spaniels.
Obesity in dogs is considered to be a medical disorder and is the canines’ most common nutritional disease. Its estimated prevalence, species-wide, ranges from 30% to 50%, with the percentage of fat cavaliers probably even higher. Obesity is defined as “an accumulation of excessive amounts of adipose tissue in the body. ” While some other health disorders may cause cavaliers to gain too much weight, scientifically speaking, it usually is the result of either eating too much and/or not exercising enough. Veterinary specialists call this “overnutrition”.
Obesity is unhealthful because it can lead to other disorders and accelerate the effects of still more of them. For instance and most importantly, it can shorten their life spans. It can have severe effects upon the dogs’ respiratory system function, especially as an added risk factor for breathing difficulties due to brachycephalic airway obstruction syndrome (BAOS), another disorder to which cavaliers are pre-disposed due to their shortened muzzle lengths. It can affect cardiac function, cardiac rhythm, and left ventricular volume, all of particular concern to the CKCS because of the breed's prevalence of mitral valve disease (MVD). It can be a major risk factor for hip dysplasia and intervertebral disc disease, two other disorders more common in cavaliers than the average purebred.
What to do? Feed the fat cavalier less and exercise it more! It usually is as simple as that. It may not be easy, because maybe you already have conditioned your dogs and yourself to feeding them upon their demand. But the remedy is simple. Don’t feed as much per meal. Eliminate junky treats; if you must treat, do so infrequently and only as a reward for good behaviors, and use healthful, nutritious dog food as that reward. And, most importantly, walk your fat dogs – every day. If you already walk them, then take them on longer walks.
What should be your goal – an ideal weight? The weight is not as important as the shape of the body. Veterinarians have devised a couple of charts called “Body Condition Scoring” or “Body Condition System”, showing either five or nine different shapes of the canine body, from extremely fat to far too thin. The goal is to reach the middle number of, essentially, an hour-glass figure. See the two charts below:
Cardiologists focus on bionic fixes
to the leaking mitral valve
Four man-made devices are in the works
Since the first realization that some purebred dogs, particularly cavalier King Charles spaniels, regularly develop mitral valve disease, veterinary cardiologists have dealt with MVD-caused congestive heart failure by trying to “manage” its consequences with drugs. They started with digoxin, a relative of the 18th century herbal digitalis from the foxglove plant. Then they added diuretics (and ACE-inhibitors, to offset the negative side effects of the diuretics). And now we have pimobendan, which its manufacturer anxiously is trying to get approved for use as a preventative of heart failure in dogs.
In the past decade, veterinary surgeons, particularly in Japan and the USA, have tried their hand at replacing defective mitral valves with transplants from pigs, or even mechanical valves. But serious drawbacks to such surgeries include the need to by-pass the heart’s pumping system during the procedures and the requirement that the patient be young and otherwise healthy enough to endure the operation and recovery without dying from stress or transplant rejection. And, it has gone without saying that the costs of such procedures, from thirty thousand dollars and up, is prohibitive to all but the wealthiest of cavalier owners.
So now, some inventive cardiologists are focusing upon simplified surgeries which would not require by-passing the heart during the brief procedure and are designed to prevent the deteriorating mitral valve from allowing blood to backflow through it.
All four of these quick-fixes involve inserting man-made devices onto or into the heart while it continues to beat normally. The first of these, with the full name of “epicardial mitral annuloplasty device” but nicknamed “Mitrex”, is essentially a U-shaped clamp (right) which is wrapped around the mitral valve leaflets and tightens them so that they are prevented from allowing blood to backflow through the valve. The Mitrex clamp reportedly has been inserted on dogs’ beating hearts in less than 30 seconds. The device currently is being tested by veterinary cardiac surgeons at clinics in California and Florida on MVD-affected dogs in congestive heart failure.
Veterinary cardiologist Dr. George Kramer, is researching the viability of a balloon device, called the Tucker valve (left), which is inserted through either the mitral or the tricuspid valve in order to block regurgitation of blood through the valve back into the atrium.
Veterinary cardiologist Simon Swift has begun research on a valvular prosthesis that is to be implanted but does not require the use of cardiopulmonary by-pass during the installation procedure. While he has not yet publicly published details of the device, he proposes to reduce the cost of the prosthesis by manufacturing his own valves.
In June 2013, a team of California medical cardiologists reported that they had found that injecting alginate hydrogel directly into the left ventricle (LV) of the hearts of 7 dogs in advanced heart failure, increased the thickness of the LV wall, and LV structure and function improved. Alginate is a naturally derived polysaccharide that is used in drug delivery and as cell encapsulation material. (See a diagram of the injection at right.)
For more information about these devices, see our section on them on our MVD webpage.
Heart failure in the MVD-affected
cavalier King Charles spaniel
What it is, and what it is not
The terms “heart failure” and “congestive heart failure” are used almost interchangeably by many veterinary cardiologists when discussing mitral valve disease (MVD) in the cavalier King Charles spaniel. Nevertheless, there can be a difference between the two.
What is “heart failure”?
In the ACVIM’s 2009 “Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease” (ACVIM Consensus Statement), it claims to be providing a definition of “heart failure”, but it really does not. The ACVIM introduces its “new system” of “4 basic stages of heart disease and failure”, and yet the ACVIM uses the term “heart failure” in them without defining it. Nevertheless, the ACVIM’s Consensus Statement gives us hints as to what that definition might be.
First, by way of introduction to the topic, it states:
“Heart failure is a general term that describes a clinical syndrome that can be caused by a variety of specific heart diseases, including CVHD [chronic valvular heart disease]. Heart failure from any cause is characterized by cardiac, hemodynamic, renal, neurohormonal, and cytokine abnormalities.”
So from that, we learn that heart failure is a “clinical syndrome”, characterized by “abnormalities”.
The Consensus Statement goes on to cite the 2001 American College of Cardiology/American Heart Association [ACC/AHA] classification system for the treatment of heart disease and failure in human patients*, stating the ACVIM has adapted that human classification system to the management of canine MVD. Fortunately, the ACC/AHA does provide a useable and understandable definition of heart failure. It states:
“Heart failure [HF] is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. ... Because not all patients have volume overload at the time of initial or subsequent evaluation, the term ‘heart failure’ is preferred over the older term ‘congestive heart failure’.
“... HF is defined as a clinical syndrome that is characterized by specific symptoms (dyspnea and fatigue) in the medical history and signs (edema, rales) on the physical examination. There is no single diagnostic test for HF because it is largely a clinical diagnosis that is based on a careful history and physical examination.”
So essentially, within reasonable limits, a veterinary cardiologist can “call it as he sees it” in terms of diagnosing heart failure in an MVD-affected cavalier.
To get back to the ACVIM Consensus Statement, even though it fails to adequately define “heart failure”, it is crystal clear that only dogs in either Stage C or Stage D are in heart failure, and that dogs in Stages A or B1 or B2 are not. Therefore, a dog with a loud murmur and an enlarged heart is not in heart failure unless it also displays some specific clinical symptoms and signs, such as coughing, dyspnea/orthopnea (difficulty breathing / shortness of breath while lying down), anorexia / cachexia (lack of appetite/involuntary weight loss), ederna / ascites (fluid collecting in cavities and tissues), restlessness especially at night; tire easily, reluctance to exercise, less playful, lethargic, depressed, collapse / syncopal (fainting or nearly fainting). It is for this reason that counting respiratory rates is so important in being able to identify the onset of heart failure.
Is “congestive heart failure” different from “heart failure”?
Yes, it can be, in the context of MVD. The term “congestive” often mistakenly is assumed to refer to fluid from the heart, which collects in the lungs. However, medically speaking, “congestive” simply means that the heart is unable to pump adequate blood to the body, and as a result, the blood that is not being pumped out of the heart is being retained within the heart. Some of that fluid may also back up into the lungs, and so fluid detected in the lungs can be a sign of congestive heart failure.
What are “systolic dysfunction” and the “ejection fraction”?
“Systolic dysfunction” occurs when the heart muscle does not contract with enough force to pump enough oxygen-rich blood throughout the body. It also is referred to as “diminished contractility”. During an echocardiogram, the cardiologist is able to calculate the “ejection fraction”, which measures how well the heart pumps with each beat. That ejection fraction determines whether there is systolic dysfunction.
For many years, heart failure has been considered by many veterinarians to be synonymous with a systolic dysfunction, despite research evidence to the contrary.** Cardiologists have discovered that some MVD-affected dogs – particularly among toy breeds and especially many CKCSs – display classic signs and symptoms of heart failure without having a low ejection fraction or systolic dysfunction or diminished contractility. Dogs in heart failure but which nevertheless have an ejection fraction greater than about 50% are considered to be adequately “compensating” for their MVD condition or have a “preserved ejection fraction”.
This distinction is particularly important when deciding when to begin medicating the MVD-affected dog in heart failure. Some standard MVD drugs for dogs in heart failure are designed to compensate for systolic dysfunction and to increase the ejection fraction. In particular, pimobendan (Vetmedin, Cardisure) is one of those drugs. But if the cavalier in heart failure is adequately compensating for its condition with a normal ejection fraction and therefore no systolic dysfunction, those drugs could over-stimulate the heart muscle and cause damage, rather than manage the dog’s heart failure.
Guidelines for the Evaluation and Management of Chronic Heart Failure in the
Adult: Executive Summary. A Report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J.
American College of Cardiology. July 2001;38(7):2101-2113.
** Myocardial function in small dogs with chronic mitral regurgitation and severe congestive heart failure. Kittleson MD, Eyster GE, Knowlen GG, Bari Olivier N, Anderson LK. JAVMA. February 1984;184(4):455-459. (“This study suggests that the contractile performance of the left ventricle in most dogs with chronic mitral valve fibrosis and clinical evidence of severe congestive heart failure is either normal or mildly depressed. This suggests that congestive heart failure in these patients is due to severe regurgitation and subsequent volume overload of the left ventricle and atrium. Heart failure secondary to mitral regurgitation can be due not only to myocardial failure, but also to severe regurgitation by itself or in combination with myocardial failure.”).
The CKCSC,USA makes part of its ethics code optional!
It’s real motto: “Forever Guardians of the Cavalier BREEDERS!”
The Cavalier King Charles Spaniel Club, USA (CKCSC,USA), like all other nationwide cavalier clubs, has a Code of Ethics.* Traditionally, ethics codes, like the Ten Commandments, command breeders either to always do something or to never do something. For instances, the CKCSC,USA’s code has stated:
“If I decide to breed a litter, I will ...”
“As the owner of a stud dog, I realize that I must exercise exemplary conduct in the use of my dog in order to abide by the standards set forth in this Code of Ethics. Therefore I will ...”
“As the owner of a brood bitch, I realize that I must exercise exemplary conduct in breeding from her in order to abide by the standards set forth in this Code of Ethics. Therefore I will not: ...”
But no longer. As of March 14, 2015, the CKCSC,USA has made portions of its ethics code optional! Specifically, it has added this non-mandatory (and therefore meaningless) statement to the ethics code section on breeding brood bitches**:
“The CKCSC,USA recommends a minimum breeding age of 2½ years, and following the health testing guidelines as published on the CKCSC,USA website.”
It is bad enough that the club’s so-called “health testing guidelines” do not even include the MVD breeding protocol, but to make health testing optional in its ethics code shows that, in reality, the CKCSC,USA is Forever Guardian of the Cavalier BREEDERS!
* Note that CKCSC,USA's
website has not yet been updated to include the March 14, 2015 amendments.
**Not even this recommendation applies to stud dogs!
“Purebred breeding” is a euphemism
for accelerated genetic entrophy
Toss out that closed studbook now!
Researchers estimate that more than 50% of cavalier King Charles spaniels (CKCSs) may have the genetic neurological disorder called syringomyelia (SM), also known as “neck scratcher’s disease”. And, they estimate that up to 95% of CKCSs may have Chiari-like malformation (CM), which purportedly is at least part of the cause of SM. And, we know from statistics that more than half of all cavaliers may be expected to develop mitral valve disease by their fifth birthday. So what are we doing wrong? And what do these severe genetic problems – among several others* -- foretell about the future of our breed?
* To name the rest: various hereditary eye disorders, progressive hereditary deafness, low blood platelets (idiopathic asymptomatic thrombocytopenia), cerebellar infarcts (strokes), chronic pancreatitis, brachycephalic airway obstruction syndrome (BAOS), curly coat syndrome, intervertebral disk disease (IVDD), diabetes mellitus, eosinophilic stomatitis, idiopathic epilepsy, episodic falling syndrome, fly catchers syndrome, primary secretory otitis media (PSOM) – glue ear, chronic kidney disesase, masticatory muscle myositis (MMM), muscular dystrophy, obesity, patellar luxation, hip dysplasia (HD), and pneumocystis pneumonia.
For starters, it means that the breed clubs’ proverbial “closed studbook*” is destined to fail, and bring the entire breed down with it.
* In the parlance of dog breeding, the “studbook” is the list of pedigrees of the dogs of a particular breed. In turn, “pedigree” means the record of the ancestors of a breed, showing that it is “purebred”. “Purebred” means that all of the dogs in the breed descended from other dogs of the same breed. Therefore, no dogs of any other breed (or multi-breed) are allowed entry into a breed club’s closed studbook. If a mating occurs between a purebred dog and a dog of some other breed, their offspring are ostracized by that breed club, banned from participating in purebred activities, especially conformation shows, much less being allowed to mate with any other dogs of that breed.
The second law of thermodynamics applies to closed studbooks
A basic tenet of physics is Rudolf Clausius’ and Lord Kelvin’s statement of the Second Law of Thermodynamics:
“The amount of energy available for useful work in a given isolated system is decreasing. The entropy is always increasing. Therefore, closed systems cannot perpetually sustain themselves.”
In other words, a closed system inevitably always is expending its store of energy and is constantly winding down. An isolated system has no additional source of energy with which to replenish itself. And no system is more “isolated” than a dog breed club’s closed studbook. Its “energy” component is its pool of genes. Every breeding decision results in eliminating more and more genes from the very limited pool which a closed studbook contains at its start. Therefore, in no way can the closed studbook be capable of perpetually sustaining itself. From the beginning of the concept of “purebred” breeding, the closed studbook has been destined to degrade into accelerated, irreversible exhaustion.
The breed standard does not mention “pedigree” or the “studbook”
The stated goal of purebred breeding has been to produce dogs which meet a defined “breed standard”, which mainly pertains to appearance, structure, and temperament. Breed standards typically do not even mention a requirement that the dogs be descended only from dogs listed in the breed’s studbook.
The closed studbook has never really been a necessary corollary to achieve that goal. For example, it is possible to mate together a variety of “mongrels” – note how class snobbery so easily seeps in to the purebred vocabulary – and produce, within as few as three or four generations, a dog which actually meets the breed standard of the cavalier King Charles spaniel. Indeed, if the CKCS breed standard included a “health clause” – that is, requiring that the dog not have certain genetic disorders, such as Chiari-like malformation or mitral valve disease – it would be easier to produce a dog matching the CKCS breed standard from mongrels than it would be by mating purebred cavaliers.
Because the national kennel clubs decreed that their breeds’ studbooks be closed, the second law of thermodynamics kicks in and guarantees a foreseeable end point to those breeds’ existence. As evidence, the American Kennel Club, founded in 1884, has been predicted to run itself into the ground within the next ten years. This is based upon the rate of declining annual puppy registrations, from a high of over 1,500,000 in 1992 to around 400,000 in 2014*, a decline of over 75% in only the last twenty-two of its 131 years. And just why is that? Pure irrational snobbery, perhaps.
* The AKC was so embarrassed by the declining registrations that it stopped publicizing their numbers in 2008.
So, why not toss out the closed studbook, or at least open it up to outsiders, and let the offspring of any parents vie for matching the breed standard?
Case Study: The low uric acid (LUA) Dalmatian
A tragic example: Up to 2011, all AKC-registered Dalmatians reportedly carried a mutated version of the SLC2A9 gene, which causes exceedingly high levels of uric acid – about ten times that of a normal dog. In research studies, high majorities of males were found to have uric sediment in their bladders, and an estimated 13% to 34% produce potentially painful urate stones which can cause blockages and which may require repeated surgeries to remove.
In an effort to come to the rescue of that breed, in 1973 a very knowledgeable and courageous breeder, Dr. Robert Schaible, cross-bred a Dalmatian bitch with a German shorthaired pointer (not affected with the mutated SLC2A9 gene), producing a litter half of which also did not have the dreadful mutation. These dogs since have been labeled “low uric acid” or LUA Dalmatians. Within three generations after back-crossing those healthy offspring, only the most biased Dalmatian fanciers could detect which dogs were from that cross breeding when compared to champion purebred Dals.
Nevertheless, the ever so particular members of the AKC's parent club, the Dalmatian Club of America (DCA), voted twice – in 1984 and 2008 (by then, the tenth generation of LUA Dals had been produced) – to reject these healthy dogs’ bids to obtain AKC registrations. In the meantime, all AKC Dalmatian breeders necessarily produced only litters of dogs with the version of the gene which was certain to cause exceedingly high levels of uric acid. They all did this intentionally!
Finally, by the twelfth generation of LUA Dals, which were 99.97% purebreds (see Fiona, at right), even the AKC board of directors had reached the limit of its patience. In November 2010, the AKC board warned the Dalmatian parent club that if its membership did not vote to approve admission of the LUA Dals into the AKC within the following six months, then AKC would take the matter into its own hands and rule on admitting the LUA dogs into the breed’s studbook. The parent club read the signals and finally voted to admit the LUA Dals in 2011, after 38 years of irresponsible foot-dragging, during which the club’s breeders gleefully continued to produce Dals suffering this potentially agonizingly painful genetic urinary disease.
So, almost invariably the purebred dog clubs’ studbook fetish trumps the genetic health of generation after generation of the dogs their breeders produce. Thus, these degenerate offspring continue to be bred, and their reputations for sever genetic health defects grow and grow. The recent BBC documentary television program “Pedigree Dogs Exposed” is evidence of that. As a consequence, the dog owning public is turned off, repulsed even, by the selfish, snobbish, anti-health policies of the national kennel clubs.
The cavalier clubs still irresponsibly ignore the MVD and the CM/SM breeding protocols
Added to that is the fact that purebred breed clubs often refuse to recognize either the severity of the genetic disorders their breeding practices have brought upon their dogs, or the often simple solutions to dealing with those disorders. For example, both of the CKCS national breed clubs in the United States have refused to endorse the Mitral Valve Disease Breeding Protocol, designed by cardiologists and geneticists to eliminate early-onset MVD in the breed. And, both clubs refuse even to acknowledge the existence of the SM Breeding Protocol, designed by neurologists and geneticists to reduce the incidence of CM/SM in the breed.
So, we have a combination of (a) the inevitability of the second law of thermodynamics to waste away an isolated system, like the ubiquitous and totally unnecessary closed studbook, and (b) the breed clubs’ persistent denial of the reality of at least a partial solution to some of the severe genetic health disorders which their closed studbooks have brought about. All this is wrapped in the breed clubs’ tuxedo-dressed attitude of elitism, snobbery, and condescension towards anyone who dares to suggest that the clubs could be doing something terribly wrong and also could be refusing to do something absolutely necessary. The victims, of course, are these purebred dogs, as their genetic health deteriorates with each future generation.
Perhaps as predicted, by the year 2025 the purebred dog will be put out of its misery, as the closed studbooks of these miserable dog clubs follow the second law of thermodynamics and degrade into total exhaustion.
The EPIC trial ends on schedule,
but could a whitewash be in the
Study's objective is changed and findings are disclosed prior to peer review
Such advance disclosures normally are unethical and unprofessional
In 2010, Boehringer Ingelheim, the manufacturer of Vetmedin (a brand name for pimobendan) announced the start of the EPIC Trial, a 360-dog study by 36 veterinary cardiologists around the world, to determine if the drug could be effective in delaying the onset of clinical signs of congestive heart failure in dogs with mitral valve disease. In that announcement, Boehringer Ingelheim's senior brand manager is quoted stating:
“The EPIC trial will definitely answer the question: Does pimobendan delay the onset of clinical signs?”
In a press release issued by EPIC Trial co-lead researcher Dr. Jens Häggström* on March 16, 2015, it was announced that “The EPIC study has been terminated”. No surprise there, because from the beginning of the EPIC Trial back in 2010, it was announced that it would end in early 2015. But, really! A press release to announce the end of a drug study which was scheduled to end anyway? Could that announcement have been just an excuse for issuing a press release at all?
What is surprising is this comment included in that press release:
“The interim analysis indicated that there was clear evidence of benefit of the administration of pimobendan in prolonging the time to the primary endpoint of the study, which was a composite of the development of left-sided congestive heart failure, or death presumed to be cardiac in origin. The interim analysis did not raise any concern over the safety of pimobendan administration.” (Emphasis added.)
Unfortunately, there is a lot wrong with that dreadfully vague statement.
Can you spell p-e-e-r r-e-v-i-e-w?
First of all, in the world of scientific research, it is unusual for research data, much less any results, to be leaked publicly before peer-reviewing and the official publication of the peer-reviewed article. Further, it is unheard of for there to be an official public release of any such premature information, over the name of one of the researchers. Any such prior disclosure normally is considered unethical and unprofessional in the scientific research arena.**
So, what is so special about the EPIC Trial that this seemingly unethical, unprofessional, and unheard of press release has been issued? It is far from clear, within the four corners of that press release.
The answer may be tucked into the highlighted portion of that quote above – “or death presumed to be cardiac in origin.” You see, from the outset, it never was intended that the EPIC Trial's pre-heart-failure administration of pimobendan end at death.
Here is how the EPIC trial researchers originally stated the objective of their study:
“Investigators will determine if chronic oral administration of pimobendan in dogs with evidence of increased heart size secondary to preclinical MMVD can delay the onset of signs of CHF. Complete EPIC results will be published and distributed, regardless of the outcome.
“Does chronic oral administration of pimobendan in dogs with evidence of increased heart size secondary to preclinical MMVD delay the onset of signs of congestive heart failure?”
In other words, pimobendan would be given to dogs with Stage B2 mitral valve disease (dogs with a loud murmur and some enlargement of the heart but not in heart failure), and once congestive heart failure signs appear, the study ends for that dog. There is nothing there about intending to give the dogs pimobendan until they die, or that doing so would “benefit” the dog.
Now, granted, in the FAQs on the EPIC Trial website, it does state that “The primary endpoint is a composite of the development of left-sided congestive heart failure (CHF) or cardiac death.” (All that means is that a particular dog's testing ends either when the dog reaches CHF or if the dog dies instead of reaching CHF.) But surely that did not mean that cardiac death prior to CHF meant that the pimobendan treatment had been a success. It meant the opposite -- that the pimobendan had failed to allow the dog to reach CHF at all. In other words, there would be no “evidence of benefit” if the pimobendan killed a dog which otherwise would have reached CHF.
Since one of the main concerns about administering pimobendan prior to heart failure always has been that it can cause death, and since death before the usual progression to heart failure always has been considered to be a bad thing and not a desirable one, it would be very curious if death prior to heart failure has been added to the EPIC Trial’s objective as a normal, desirable end point. ***
A bad smell pervades this EPIC Trial
This press release is very troubling because it reeks of an effort to placate the manufacturer of Vetmedin. We feared this from the beginning, when we urged cavalier owners to not particpate in the EPIC Trial in our Blog entry, “Beware the pimobendan/Vetmedin ‘EPIC clinical trial’: There is no upside.”
Hopefully, between now and when the actual (presumably peer-reviewed) article on the EPIC Trial is published, responsible professionals will re-take control of this process back from the manufacturer and not suggest that death before reaching congestive heart failure is an acceptable end result of giving their dogs pimobendan.
Adrian Bosworth issued a nearly identical
press release on March 17, 2015. Co-lead researcher Sonya Gordon
issued an even more egregious
press release on March 24, 2015.
** See, "What is Ethics in Research & Why is it Important?", by David B. Resnik, J.D., Ph.D. National Institute of Health website, 2011: “There are many other activities that the government does not define as ‘misconduct’ but which are still regarded by most researchers as unethical. These are called ‘other deviations’ from acceptable research practices and include: ... Bypassing the peer review process and announcing your results through a press conference without giving peers adequate information to review your work.”
*** In the "Pimobendan in Congestive Heart Failure (PICO) trial", a 1996 study of 317 human patients, the researchers found that: "In both pimobendan groups combined the hazard of death was 1.8 times higher than in the placebo group."
Is it 'Back to the Future' for the American Kennel Club?
A degenerate breeding program masquerading as the dogs’ champion
The new Chairman of the Board of the American Kennel Club is the same old chairman who led the AKC into its decline earlier in this millennium. Ron Menaker (right) was re-elected chairman by AKC’s board of directors this month, after a three year hiatus while interim chairman Alan Kalter fiddled around trying to figure out how a million or so “Likes” on Facebook could reverse AKC’s rapid decline.
Yes, the same Ron Menaker whom we chided in a July 2011 blog entry for not only condemning the factually accurate (as far as cavalier King Charles spaniels are concerned) 2008 BBC television program “Pedigree Dogs Exposed” (PDE), but also actually petitioned the UK Parliament to have the BBC do a documentary attacking PDE’s producer, called “Jemima Harrison Exposed”!
To re-hash a bit, Mr. Menaker described PDE as a “piece of sensationalist fiction and tabloid journalism masquerading as a documentary” and an “exercise in media sensationalism”. Ironically, he pretty much could have used similar words to describe the AKC these days:
“A degenerate breeding program masquerading as the dogs’ champion.”
It should come as no surprise that closed studbooks have led to rapid declines in genetic diversity and the production of sicker and more exaggerated versions of each purebred breed of dogs. AKC's mantra should be something more like “Cross-breed or die”, but Mr. Menaker appears incapable of seeing that viewpoint.
So, the question becomes: Will Chairman Menaker’s tired old head-in-the-sand ideas speed up AKC’s annual double-digit drop in litter and puppy registrations? We all must wait and see, although perhaps not have to wait as long as the statistically predicted death date of 2025.
All that cavalier owners need to know about
the “Reverse Sneeze” or
Occasionally, excited cavalier King Charles spaniels will suddenly stand still and start making a very loud snorting sound, over and over, as if they are gagging and having difficulty breathing. In cavalier circles, this is known as the “Cavalier Snort” or the “Reverse Sneeze”. A YouTube video of a cavalier making this sound is here.
In cavaliers, this gagging sound usually is due to the dog having an elongated soft palate. The palate is the roof of the mouth. It is divided into two parts, the front bony hard palate, and the rear fleshy soft palate. The soft palate separates the nasal passage from the oral cavity. (See the soft palate at the top of the sketch to the right.)
An elongated soft palate is too long for the length of the mouth, so that its tip protrudes into the front of the airway and may get sucked into the laryngeal opening where it may obstruct the normal passage of air into the trachea. This is because the CKCS has a shorter muzzle than the average dog, and therefore all of the dog’s breathing apparatus is compressed into a shorter space than the average dog.
When the elongated soft palate protrudes and partially or totally blocks the airway, the dog no longer can breathe through its nose. Since dogs normally breathe through their noses, they continue to try to do so, thereby causing the gagging or snorting sound.
Block the dog’s nostrils and make it breathe through its mouth
If the palate is only moderately elongated and does not totally block the airway, most cavaliers are able to pull out of these blockages by themselves. Snorting may be relieved by forcing the cavalier to breathe through its mouth instead of its nose. This may be done by holding the dog's head down and mouth open with one hand while blocking air from entering the nose with the other hand.
In severe instances, the dog may collapse if the airflow is obstructed completely for too long. In such cases, surgical removal of excess tissue from the palate may be necessary. One of those procedures is called “folded flap palatoplasty” (FFP), which both shortens and thins the soft palate. Post surgery prognosis is good for young dogs. They generally may be expected to breathe much easier, with significantly reduced respiratory distress, and display more energy and stamina. Older dogs may have a less favorable prognosis.
In all cases, it is strongly recommended that only board certified veterinary surgeons who also are very experienced at airway surgery, be permitted to perform any type of airway surgery on cavaliers.
(This article has been excerpted from “Brachycephalic Airway Obstruction Syndrome (BAOS) in the Cavalier King Charles Spaniel” on this website.)
Just Asking: What’s up with Vetmedin’s ‘EPIC Trial’?
It’s due to end next year, but some recent indications are ominous
When the EPIC Trial was announced in 2010 by the manufacturer of Vetmedin (a brand name of pimobendan), we did not think it was a wise approach for studying whether the drug could safely delay the onset of heart failure in dogs with mitral valve disease (MVD). We went so far as to warn all cavalier owners to “Beware the pimobendan/Vetmedin ‘EPIC clinical trial’: There is no upside” in an April 2011 blog entry on this page.
The trial, of up to 360 dogs with MVD murmurs and enlarged hearts (but not yet in heart failure), is scheduled to end in 2015. Each dog was to receive either two pimobendan tablets or placebos daily until the dog reached heart failure. Since the trial started over 4 years ago, presumably many of those dogs by now have reached the heart failure stage of MVD, and their reports should be piling up in the in-boxes of the study’s leaders, including Dr. Sonya Gordon of Texas A&M University in the USA and Professor Adrian Boswood in the UK.
We may assume that the 36 cardiologists participating in the EPIC Trial are sworn to secrecy until the final report, which entails drafting, review, approval by at least a majority of them, and peer review before publication in a veterinary journal. However, there are curious indications that some of the results are known and do not look so good for the wannabe peddlers of early-use Vetmedin.
Owners of some of the dogs in the trial are reporting that their dogs died suddenly, shortly after its start. Some cardiologists who are among the 36 participants now are talking with renewed emphasis about the importance of waiting for signs of heart failure before starting Vetmedin. At least one other cardiologist recently has openly attacked the trial as being risky. The EPIC Trial’s own website – epictrial.com -- with its videos and graphics and list of names of those 36 cardiologists and its map showing their locations around the globe and all of its optimistic hype about Vetmedin before heart failure, has disappeared from the Internet*. Inquiries to Vetmedin’s manufacturer, Boehringer Ingelheim GmbH, go unanswered.
Are these indications that the EPIC Trial has been an epic failure? Just asking ...
* Finally, as of early December 2014, the Epic Trial website is back on line.
So your cavalier has a heart murmur. What do you do next?
The ACVIM says: Get an x-ray, not an ultrasound!
Since over half of all cavalier King Charles spaniels may be expected to develop mitral valve murmurs by age 5 years, it should come as no surprise when your veterinarian tells you that your cavalier has one. But there is no reason to panic. The American College of Veterinary Internal Medicine (ACVIM*) has a sensible list of steps to take once a murmur is first detected in your CKCS.
For the record, the ACVIM recommends that cavaliers be screened annually by “auscultation” (examination by stethoscope) by board certified cardiologists. Specifically, ACVIM** states:
“Owners of breeding dogs or those at especially high risk, such as Cavalier King Charles Spaniels, may choose to participate in yearly screening events at dog shows or other events sponsored by their breed association or kennel club and conducted by board-certified cardiologists participating in an ACVIM-approved disease registry.”
For that reason, CavalierHealth.org has a list of upcoming heart screening clinics in the USA and Canada, which is updated weekly.
Once a murmur is detected by the vet, the first thing to realize is that you do not need to rush your dog to have an ultrasound (echocardiograph) of its heart. In fact, rarely does a cavalier with a mitral valve murmur ever need an ultrasound before the disease reaches heart failure. Instead of an ultrasound, the ACVIM recommends that you get your dog’s heart x-rayed to be a “baseline” for measuring the heart size against future x-rays after any heart enlargement takes place. The ACVIM states:
“Thoracic radiography [chest x-ray] is recommended in all patients to assess the hemodynamic significance of the murmur and also to obtain baseline thoracic radiographs at a time when the patient is asymptomatic for CVHD [chronic valvular heart disease].”
The ACVIM does not recommend that cavaliers with new murmurs be ultrasounded unless the auscultation and the x-ray do not adequately satisfy the cardiologist about the true cause of the murmur. Specifically, this is what the ACVIM states about ultrasounding cavaliers once a mitral valve murmur is detected:
“In small breed dogs with typical murmurs, echocardiography is recommended to answer specific questions regarding either cardiac chamber enlargement or the cause of the murmur if those questions are not answered adequately by auscultation and thoracic radiography.”
Note that the only “baseline” that the ACVIM recommends for cavaliers with new murmurs is an x-ray and not an ultrasound, as long as the cardiologist is satisfied that the stethoscopic exam and the x-ray confirm the cause of the murmur.
* The ACVIM certifies
veterinary cardiologists. A list of them in the
USA and Canada is available here.
** See the ACVIM's "Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease", page 1144.
Do MVD-affected cavalier King Charles spaniels
really need taurine
There is a popular notion that dogs with mitral valve disease will benefit from adding taurine (right) to their daily diets. Taruine (2-aminoethanesulfonic acid) is essential for cardiovascular function as well as for playing a variety of other fundamental roles in keeping animals functioning. Fortunately, most all dogs produce sufficient taurine themselves, as long as they ingest an adequate amount of animal-based protein. There is no published evidence that dogs with mitral valve disease are deficient in taruine or would benefit from supplementing it.
There were a couple of reports published in 1997 that found that American Cocker spaniels affected with dilated cardiomyopathy (DCM) became taurine-deficient and in need of taurine supplementation. Apart from the fact that American Cockers and cavaliers have the same last name, there is no established connection between the CKCS and a need for added taurine. Cavaliers are not inherently taurine-deficient, and as a breed, they are not known to develop DCM. Mitral valve disease (MVD) and DCM both affect the dog’s heart, but otherwise, they are not related.
Nevertheless, many canine heart supplements include taurine, and even some cardiologists recommend adding taurine to the diets of dogs with mitral valve disease. We are not sure why, because research studies have shown that MVD-affected dogs tend to have higher plasma taurine concentrations than unaffected dogs. In a 1995 study by George A. Kramer, Mark D. Kittleson, Philip R. Fox, Julia Lewis, and Paul D. Pion, for example, they found:
"[P]lasma taurine concentrations were highest in dogs with AVD [acquired valvular disease, e.g, MVD] ... We conclude that plasma taurine concentrations may be increased in dogs with AVD."
Even DCM-affected dogs other than American Cockers usually have no taurine deficiency. In board certified veterinary cardiologist Dr. Rebecca E. Gompf's 2005 article on nutritional therapies, she wrote:
“Because dogs readily make taurine from free sulfur amino acids, only lose a small amount in their bile acids, and can maintain normal blood levels of taurine despite their diets, they do not tend to develop taurine-deficient DCM.”
"Taurine supplementation is indicated whenever plasma or whole blood taurine concentrations are found to be low. ... [S]upplementation is generally only recommended after discovery of deficiency."
So, the bottom line is that, if you are thinking about giving your cavalier a taurine supplement, check its blood first to see if the dog needs it. The odds are great that no MVD-affected cavaliers will be low in taurine, and remember the old saying: “Too much of a good thing is not a good thing!”
When NOT to start giving your cavalier
Unfortunately, a few veterinary cardiologists, and a huge number of general practice vets, have been prescribing pimobendan (brand names Vetmedin and Cardisure) to cavaliers which have mitral valve disease (MVD) murmurs but definitely are not yet in heart failure. This is very disturbing because the premature dosing of pimobendan can kill the dog which does not need it.
Even some dogs already in heart failure cannot tolerate pimobendan, because one of its consequences is that it strengthens the heart muscle and enables it to pump harder. This is called improving the heart’s contractility. If a dog in heart failure still has a strong heart muscle, it does not need to be strengthened, and the pimobendan thereby forces the heart to work much harder than it should.
This is what happened to one of our cavaliers. We noticed that his heart was beating so hard after being given pimobendan that we could see the beats causing his chest hair to vibrate. So we cut back the dosage by half, and then by half again, so that he was getting a quarter of the typical dosage. Finally we discontinued it completely. He had an enlarged heart and he was in heart failure, but the heart muscle remained strong and was doing its job.
Premature administration of pimobendan can overwork the heart to the point of shredding some of its chordae tendineae and thereby causing instant death.
Ask your vet, "WHY?"
So, if you have a cavalier with a mitral valve disease murmur but has no symptoms of heart failure, and your veterinarian recommends starting pimobendan, the first thing you should do is ask him "Why?".
And, show him the manufacturer's warning on the box, about not prescribing it prior to heart failure. It states:
“Contraindications: Vetmedin should not be given ... in cases of hypertrophic cardiomyopathy, aortic stenosis, or any other clinical condition where an augmentation of cardiac output is inappropriate for functional or anatomical reasons.
“Warnings: Only for use in dogs with clinical evidence of heart failure.”
See for yourself:
And, point out that Vetmedin's website has this warning:
“The safety of VETMEDIN has not been established in dogs with: Asymptomatic heart disease.
“Use only in dogs with clinical evidence of heart failure.”
And, show him the ACVIM consensus statement, which states (on page 1145, top of second column):
“A few panelists considered the use of the following medications for patients in Stage B2 under specific circumstances: pimobendan, ... . The panel felt in general that these treatment strategies needed additional investigation into their efficacy and safety in this patient population before a consensus recommendation could be made.”
And, ask him about the current “EPIC study” of 360 pre-heart-failure dogs, being sponsored by Vetmedin's manufacturer and not due to end until 2015, to determine whether or not Vetmedin should be given to pre-heart-failure-dogs. On the EPIC Study website, it specifically states:
“Currently there is no treatment licensed to delay the onset of CHF [congestive heart failure].”
Elsewhere on the EPIC Study website it states:
“There is currently no treatment licensed for the management of preclinical, myxomatous mitral valve disease (MMVD).”
And still on another page of the EPIC Study website it states:
“Treatment of CHF due to MMVD begins when the dog shows clear clinical signs of heart failure, and is tailored for the individual dog.”
As you see, pimobendan's own manufacturer repeatedly warns against giving the drug to dogs before they are in heart failure.
In other words, ask your veterinarian to satisfy you that his way is better than ALL of the evidence against premature dosing of pimobendan! As Ricky Ricardo would say to Lucy, "You got some splainin' to do!"
Do-it-yourself diagnosing of congestive heart failure
cavalier King Charles spaniel
“Only respiratory rate predicted the presence of CHF with high accuracy.”
Veterinary cardiologists’ current consensus about medicating cavalier King Charles spaniels with mitral valve disease (MVD) is to wait until the dog enters “congestive heart failure” (CHF), or just “heart failure” (to avoid having to define “congestive”). They tell us cavalier owners that our dogs with MVD should be brought in and re-examined regularly – be it every six months or as frequently as every three months – so that if and when the dog is on the cusp of CHF, the vet will be ready and able to prescribe a combination of medications – usually a diuretic, an ACE-inhibitor, and pimobendan – immediately.
If it is so important to know exactly when our cavaliers enter CHF, so the drugs may be given promptly thereafter, then exactly how is CHF diagnosed? Can only a veterinarian make that diagnosis? Do only the vets have the necessary equipment? If so, what will happen to our dog if CHF shows up sometime between those periodic visits to the vet?
We know that vets, especially cardiologists, have some very expensive diagnostic equipment for our dogs’ heart problems. They include x-ray machines, Doppler echocardiographs (ultrasounds), and electrocardiograph devices (ECG or EKG), all of which may be used to detect CHF. In addition, the vets have expensive blood tests (cardiac biomarkers) to detect CHF. But what good are all of these tools and equipment if our dog enters CHF between visits to the vet?
Simply count the dog's breaths for 15 seconds
The answer is counting the dog’s “respiratory rate”, which is something that cavalier owners can do anytime they are with their dogs. As fancy and complex as all of the cardiologists’ electronic devices may be, and as sophisticated as their cardiac biomarkers may be, the best single means of determining when a cavalier enters congestive heart failure is when the dog’s respiration rate consistently exceeds 30 breaths per minute.
Top cardiologists in the UK and USA have concluded that respiration rate counts are more accurate in predicting the onset of CHF than any other means. In a 2011 study at Ohio State University’s veterinary school, Dr. Karsten Schober and a team of researchers compared the respiratory rates of 45 dogs with MVD (including 13 CKCSs) with their cardiac biomarkers and their Doppler echocardiographic indices, and they found that “Only respiratory rate predicted the presence of CHF ... with high accuracy.” They concluded that “home monitoring of respiratory rate is simple and very useful in the assessment of CHF in dogs with ... MVD.”
In a 2012 study conducted by an international team of cardiologists, they found that “apparently healthy adult dogs generally have mean sleeping respiratory rates [less than] 30 breaths/min and rarely exceed this rate at any time.”
As a result of these studies, several cardiologists are recommending that owners become familiar with their MVD-affected cavaliers’ normal resting breathing rate and effort and keep logs of their sleeping respiratory rates, to establish a baseline rate for each dog, and report when the dogs’ rates increase to consistent rates approaching or above 30 to 40 breaths per minute. For example, the University of Pennsylvania’s veterinary school advises in a handout available on-line:
“When your dog is at rest, watch their sides rise and fall as they breathe normally. One rise and fall cycle is equal to one breath. Count the number of breaths they take in 15 seconds, then multiply this number by 4 to get total breaths per minute. For example, if you count 8 breaths in 15 seconds, that is equal to 32 (8 x 4) breaths per minute. A normal dog at rest should have a respiratory rate less than 40. If you notice this number increasing consistently, or notice an increase in the effort it takes to breathe, contact your veterinarian.”
The vet school at Texas A&M University also has published a handout (right) explaining how to keep track of dogs’ respiratory rates. An excellent YouTube video shows when and how every cavalier owner can count the breaths of their MVD-affected dogs while they are sleeping or at rest.
Bottom Line: Ask your cavalier’s cardiologist (you do have one, don’t you?) whether and how you should monitor your dog’s respiratory rate for congestive heart failure.
Dog food companies may be turning a grain-free corner
Some truths about carbohydrate-laden kibbles ooze out of
the petfood industry magazine's March 2014 issue
Petfood Industry magazine’s March 2014 issue has a picture of a wolf on its cover. It’s cover story is “Should domestic dogs really eat like wolves?” It’s subhead asks “Bio-appropriate petfoods are often meat-first and grain-free, but are they based on nutrition science?”
Considering that Petfood Industry is the marketing association of the USA's commercial petfood industry, and that the petfood manufacturers’ bread-and-butter has been machine-extruded, carbohydrate-laden dry kibble for the past fifty years, one would expect the answer to both of those questions is “No!” – “No, dogs should not eat like wolves” and “No, biologically-appropriate petfoods are not based upon nutrition science”.
Well, think again. Petfood companies’ “conventional wisdom” is turned on its head in this remarkable issue of the industry’s magazine. The wolves article lays waste to the “validity” of feeding dogs carbohydrate-laced kibble, making such heretical politically-incorrect statements as:
“According to ‘The Biologically Appropriate Food Concept’, conventional dry dog and cat foods appear to be created on the premise that the digestive system of the dog and cat is similar to humans -- with an emphasis on grains and carbohydrates. While some would argue that dogs and cats have adapted since kibble foods were introduced, bio-appropriate petfood makers would counter that their digestive systems remain unchanged.
“‘Such evolutionary adaptations require much more time than a mere hundred years or so, and the evolutionary change -- from gross anatomy down to the molecular level -- that would be required for the development of such different digestive capabilities would take much longer than the time that dogs have been living with humans,’ the Champion Pet Foods whitepaper points out.
“In the short digestive systems of dogs and cats, plant proteins are far less digestible than meat proteins. High levels of trypsin inhibitors in grain legumes can cause substantial reductions in protein and amino acid digestibilities (up to 50%) in rats and pigs. Certain protein sources are better than others by providing a richer blend of amino acids. These proteins have a high biological value (BV). BV refers to how well the body can actually use the protein.”
Veterinary nutritionists' "Pet Humanization" slur is turned against them
In addition, the March issue’s second article, “Grain-free petfood: A top trend in the US pet market” (subhead: “Desire for natural products, pet humanization drive this growing segment”) reports that discerning pet owners finally are having an impact on the petfood industry by choosing more grain-free foods for their dogs and cats. Admittedly, the author of this article uses the more demeaning slur of “pet humanization” to describe the pet owners’ choices of meat protein over corn and other grains. She writes:
“Pet humanization is still a hot topic in the petfood industry today and is characterized by exactly what it sounds like -- pet owners increasingly taking the well-being of their furry companions every bit as seriously as that of any other member of their family. ‘Consumers are clearly comfortable splurging on pets because they see them as valued family members, not just everyday animals,’ said [Maria Lange, senior product manager for GfK Retail and Technology].”
The fact is that if anyone is guilty of “pet humanization”, it is the kibble manufacturers and their bought-and-paid-for "board certified veterinary nutritionists", who have falsely contended that the digestive systems of dogs have evolved to be similar to humans and less wolf-like.
Grain-free pet food sales increased 32% in 2013
The bottom line of the second article is that grain-free pet food sales increased 32% in the United States in 2013. Pet owners spent US$1.4 billion on grain-free dog food products at US pet stores in 2013, according to GfK. Perhaps, within a year or two, the Science Diet kibbles and their ilk will become just a nasty experience of the past.
A follow-up question is: What will all of those pro-corn and anti-meat "board certified veterinary nutritionists" do for a living?
The accordion-muzzled cavalier King Charles spaniel
Why do cavaliers have so many unique disorders of the head?
The cavalier King Charles spaniel breed suffers from some fairly unique hereditary disorders in their beautiful heads, including Chiari-like malformation (CM), primary secretory otitis media (PSOM), progressive hearing loss, dry eye syndrome, cerebellar infarcts (strokes), episodic falling syndrome (EFS), and fly catchers syndrome. CKCSs may not be the only breed with these disorders, but they clearly have more than their fair share, particularly of CM, PSOM, dry eye, strokes, and EFS.
What is there about the cavalier that explains this uniqueness?
There has been much discussion of late about “brachycephalic” breeds of dogs. The term "brachycephalic" means short-nosed and refers to dogs with short muzzles, noses, and mouths. "Brachy" means short and "cephalic" means head. The throat and breathing passages in brachycephalic dogs often are undersized or flattened. The head's soft tissues are not proportionate to the shortened nature of the skull, and the excess tissues tend to increase resistance to the flow of air through the upper airway (nostrils, sinuses, pharynx and larynx). The consequent disorders are labeled "brachycephalic airway obstruction syndrome" (BAOS).
Many cavalier fanciers will argue, vehemently, that cavaliers are not brachycephalic. They point out that most CKCS muzzles are significantly longer than such breeds as the English bulldog, pug, King Charles spaniel (English toy spaniel), French bulldog, and Pekingese. And, indeed, they have an obvious point; the muzzle of the average cavalier appears to be proportionally longer than those other breeds.
Nevertheless, cavaliers seem to have at least their share of brachycephalic disorders – inhalation issues caused by their compressed breathing apparatus – especially an elongated soft palate – not to mention sets of very jumbled teeth and gums. Also, veterinary researchers have unanimously classified the cavalier King Charles spaniel as brachycephalic in their research articles on the subject.
The CKCS's head has been treated like an accordion!
Apart from their relatively longer muzzle, cavaliers’ brachycephalism stands apart for one other reason: The cavalier is the only brachycephalic breed that was created by purposefully elongating an already snub-nosed snout. While the English bulldog, pug, King Charles spaniel (KCS), French bulldog, and Pekingese were fashioned by generation after generation of selective breeding to shorten the muzzle, the CKCS was bred to lengthen the already quite snub-nosed King Charles spaniel. Thus, the cavalier’s head has been treated as if it was an accordion – first shortening it to attain the King Charles spaniel breed standard (see KCS skull at near right), and then, beginning in the 1920s, selecting KCS breeding stock, and perhaps out-crossing, to produce longer snouts (see CKCS skull at far right).
(Specimens from the collections of the Albert HeimFoundation, Museum of Natural History, Bern.)
If you consider that breeding to shorten the head will compress the dog’s breathing apparatus, what happens when those jumbled contents then are stretched out again? Certainly, there can be no assurance that the end result would be perfectly relocated airway passages and teeth in the exact position they would have been had no bunching had taken place to begin with. Unlike an accordion, the dog's skull is not equipped with a built-in spring. Once jumbled by compression, it is very possible that the decompressed airways remain confusingly jumbled but just in some other manner. We know that to be the case just by looking in the cavalier’s mouth. Despite a longer muzzle than the KCS, many of the cavalier’s overcrowded teeth are in anything but a functional position.
We also know that the CKCS’s hereditary head disorders, particularly PSOM, dry eye, and CM, are the result of the jumbled consequences of brachycephalism, while cerebellar infarcts are believed to be due to CM altering blood flow to the brain. But, in no other brachycephalic breed are these hereditary diseases anywhere close to being so prevalent. The accordion effect of breeding cavaliers could explain the uniqueness of these disorders.
All that cavalier owners need to know
about primary secretory otitis media (PSOM)
Primary secretory otitis media (PSOM) has become more frequently diagnosed in cavalier King Charles spaniels. It consists of a highly viscous mucus plug which fills the dog's middle ear and may cause the tympanic membrane to bulge. PSOM has been reported almost exclusively in cavaliers.
Because the pain and other sensations in the head and neck areas, resulting from PSOM, are similar to some symptoms caused by syringomyelia (SM), some examining veterinarians may have mis-diagnosed SM in cavaliers which actually have PSOM and not SM.
The cause of PSOM is unknown. It is suspected to be due to a dysfunction of the middle ear or the Eustachian (auditory) tube: either (a) the increased production of mucus in the middle ear, or (b) decreased drainage of the middle ear through the auditory tube, or (c) both.
The principal symptoms are moderate to severe pain in the head or neck, holding the neck in a guarded position, and tilting the head. Other signs may include scratching at the ears, itchy ears, head tilt, excessive yawning, crying out in pain, ataxia, drooping ear or lip, inability to blink an eye, rapid eyeball movement, facial paralysis or nerve palsy, Vestibular disease, some loss of hearing, seizures, and fatigue. These symptoms, in many cases, are very similar to those of syringomyelia and, to some extent, to those of progressive hereditary deafness. Therefore, the examining veterinarian should take care to consider these other possible causes of the dog's symptomatic behaviors.
PSOM may be detected by veterinary neurology or dermatology specialists from either magnetic resonance imaging (MRI) or a computed tomography (CT) scan. Both require that the dog be under general anesthesia. It also may be observed using an operating microscope with good lighting and at a suitable magnification.
Treatment traditionally has consisted of performing a myringotomy, making a small cut in the eardrum (tympanic membrane), followed by flushing the middle ear to force out the mucus plug. Topical and/or systemic corticosteroids and antibiotics then are administered. The procedure may have to be repeated, in some cases several times, depending upon how the dog responds. An alternative procedure is a ventral bulla osteotomy,which involves making an incision on the under side of the neck behind the jaw bone. The auditory bulla, a hollow bony sheath that encloses parts of the middle ear, then is exposed and is opened.
Some specialist veterinarians have been prescribing N-Acetyl-L-Cysteine (NAC), a mucolytic -- mucus thinning agent or expectorant -- for cavaliers with PSOM, following surgeries.
(This article has been excerpted from "Primary Secretory Otitis Media (PSOM) in the Cavalier King Charles Spaniel" on this website.)
All that cavalier owners need to know
about their dogs' blood platelets
Up to half of all cavalier King Charles spaniels may have both an abnormally low number of blood platelets and oversized platelets. Despite the low platelet counts, the typical cavalier's blood platelets function normally, and the dog does not appear to experience any health problems due to either the size or fewer numbers of its platelets. There are, however, limited exceptions to this typical situation.
An excessively low platelet count normally is a sign which tends to alarm general practice veterinarians, and so it is vitally important that cavalier owners alert their vets about this benign condition in the breed when blood tests are ordered.
No treatment is recommended unless the dog shows other symptoms of a blood-related disorder. Cavaliers should not be treated for immune-mediated thrombocytopenia (IMT) as a precaution. Dog really suffering from IMT must be treated quickly, usually with intravenous doses of immunosuppressive drugs -- steroids, azathioprine, cyclosporine A and others -- to save the dog's life. Such treatments are severe and could do major damage to the healthy cavalier with nothing more than a low platelet count.
Most commercial laboratories use an automated counting system for blood cells, which determine cell types on the basis of their size and volume. Because cavaliers' platelets are so large, automated blood cell counters may not recognize platelets as being platelets and undercount them, thereby inaccurately lowering the platelet count. Researchers have found that CKCS platelet counts using three different automated systems underestimated the actual counts determined manually. Antech Diagnostics, the largest veterinary diagnostic laboratory, has specifically stated on its website that:
"Platelets in this breed should be counted manually, because automated blood cell counters cannot distinguish the large platelets from erythrocytes and therefore underestimate the true platelet count."
An accurate platelet count can be obtained by visually counting the cells. Also, because the large platelets are so fragile, any blood samples should be extracted very carefully. Therefore, all blood samples from cavaliers should be taken in a very careful manner and preferably only from the dog's jugular vein, using a large bore needle, and then should be examined only under a microscope by an experienced clinical pathologist before making a diagnosis of low platelet count.
(This article has been excerpted from "Blood Platelets in Cavaliers" on this website.)
What if the American Kennel Club ceased to exist?
The cavalier’s future after the AKC’s death spiral
The American Kennel Club (AKC) reportedly is withering away. Every year since 1992, its litter and puppy registration numbers have been dropping by as much as double digit percentages. Over the course of the last 21 years*, registrations have declined by over two-thirds, even as the number of dogs in American homes has increased. Observers have predicted that if AKC’s registrations continue to drop at the same rate, it will be out of business by 2025.
* From 1.528,392 in 1992 to 479,404 in 2013.
To continue to survive financially, the AKC has been upping its event fees, such as for conformation shows, obedience, rally, and agility trials, and tracking tests. It even has increased its litter and puppy registration fees, despite the declining registrations. But such counter-intuitive alternative fund-raising initiatives have not stanched its cash crisis. AKC also has cut back on its funding of its programs of kennel inspections, DNA profiling, canine good citizens, search-and-rescue, Canine Health Foundation, legislative issues, etc.
So, what would no AKC mean to the cavalier King Charles spaniel? There are two national CKCS clubs in the United States. One, the American Cavalier King Charles Spaniel Club (ACKCSC), is an official “parent club” for the breed, in the AKC. The other, the Cavalier King Charles Spaniel Club, USA (CKCSC,USA), is independent of the AKC and has been in existence since the 1950s, long before AKC recognition of the cavalier in 1995.
If AKC goes kaput, so too would its CKCS parent club. Except for the occasional “specialty” conformation shows, parent clubs rely totally upon the AKC for direction, litter and puppy registration, rules, judging, and show organization. To survive post-AKC, the parent club would have to learn how to do what the CKCSC,USA has been doing all along for the past 57 years. It would have to re-organize completely, from the ground up, including registering dogs, creating rules, approving judges, organizing its own shows around the country, and finding enough volunteers to do what has been done for them by AKC kennel (all-breed) clubs up to now.
Ironically, after AKC’s demise, the CKCSC,USA may end up being the only show in town for those cavalier breeders who, since 1995, have turned their backs and thumbed their noses at the original cavalier club in the USA.
All that cavalier owners need to know about
natriuretic peptides tests (ANP and BNP)
There has been much research into attempting to diagnose mitral valve disease (MVD), and more particularly, to diagnose the onset of congestive heart failure (CHF) in dogs by measuring "cardiac biomarkers", such as blood plasma concentrations of the natriuretic peptides: atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP).
Natriuretic peptides are hormones manufactured and secreted by areas of the heart. A test of natriuretic peptides measures the quantity of the natriuretic peptides in the dog's blood. Elevated levels of these natriuretic peptides in the blood may be directly related to heart defects, and natriuretic peptides in the blood become elevated only after the heart has to pump harder to compensate for the disorder. In particular, BNP is secreted by the left ventricle in response to heart wall stretching or stress.
Our bottom line on this topic has best been stated by Dr. Jennifer L. Garcia in "The NT-proBNP assay: A portent of heart health." in dvm360:
"For conditions such as mitral valve disease, this test may be of limited value because a diagnosis can be readily made by thorough auscultation and documentation of a heart murmur. In these cases, the assay also has limited utility in determining disease severity; thoracic radiography is preferred."
Translated, she is saying that stethoscopic examinations, combined with periodic x-rays of the heart, are more effective in diagnosing MVD and CHF than any blood tests.
History of natriuretic peptide testing
A 2003 study (conducted by Drs. Kristin A. MacDonald, Mark D. Kittleson, Coralie Munro, and Philip Kass of the University of California at Davis) has shown a positive correlation between BNP and heart disease and CHF in dogs. In that study, BNP increased with the progressively increased severity of mitral valve disease and CHF. For every 10-pg/mL increase in BNP, the 2003 study's dogs' mortality rate increased approximately 44% over the four months of the study. In a 2005 study, Drs. William E. Herndon, Justine A. Lee, Kenneth J. Drobatz, and Matthew J. Ryan concluded that "With further investigation, this new BNP assay may someday provide a widely available noninvasive diagnostic test with rapid turnaround time to help diagnose and/or treat heart disease and congestive heart failure in the dog."
However, in earlier studies (1994 and 1997) conducted by Drs. Jens Häggström, Kjerstin Hansson, Clarence Kvart, and others, the researchers have suggested that BNP levels in cavaliers with mitral regurgitation did not rise as dramatically as in humans, and that N-terminal (NT)-proANP (NT-proANP) may better reflect the severity of mitral regurgitation in cavalier King Charles spaniels than NT-proBNP tests.
Four trademarked names for NT-proBNP tests are Canine CardioCare (Veterinary Diagnostics Institute), Canine VetSign CardioSCREEN (Guildhay Ltd.), Cardiopet proBNP (IDEXX Laboratories), and Antech Cardio-BNP (Antech Diagnostics). There have been studies showing the effectiveness of these types of tests for dogs suffering from asymptomatic occult dilated cardiomyopathy (DCM), which is not the same disorder as MVD and is not known to be a genetic problem for cavalier King Charles spaniels.
Whichever test (NT-proBNP or NT-proANP) is found to be more accurate for detecting MVD, it is believed by some researchers that the test may be useful in assisting examining veterinarians in deciding whether or not detected heart murmurs are innocent or are pathologic in nature. However, in a 2007 study of 54 CKCSs by Drs. Tarnow, Pedersen, Kvart, and others from Denmark and Sweden, they found that "Natriuretic peptides are elevated in cavalier King Charles spaniels with congestive heart failure but not in dogs with clinically inapparent mitral valve disease."
In a May 2008 report by Drs. Mark A. Oyama, Philip R. Fox, John E. Rush, Elizabeth A. Rozanski, and Michael B. Lesser of 119 dogs, they found that "Serum NT-proBNP concentration was significantly higher in dogs with cardiac disease than in control dogs, and a serum NT-proBNP concentration > 445 pmol/L could be used to discriminate dogs with cardiac disease from control dogs with a sensitivity of 83.2% and specificity of 90.0%. In dogs with cardiac disease, serum NT-proBNP concentration was correlated with heart rate, respiratory rate, echocardiographic heart size, and renal function." They concluded that, "For dogs with cardiac disease, serum NT-proBNP concentration could be used to discriminate dogs with and without radiographic evidence of cardiomegaly and dogs with and without congestive heart failure." And that, "Results suggested that serum NT-proBNP concentration may be a useful adjunct clinical test for diagnosing cardiac disease in dogs and assessing the severity of disease in dogs with cardiac disease."
In a May 2009 report from Sweden, the researchers concluded: "Plasma concentrations of the natriuretic peptides measured at re-examination could predict progression in regurgitant jet size."
In a 2012 study of 1,134 dogs, including 37 cavaliers, Stephen J. Ettinger, Giosi Farace, Scott D. Forney, Michelle Frye, and Andrew Beardow concluded that "This biomarker [NT-proBNP] may be a useful tool for staging of cardiac disease and identifying cardiac-related coughing or dyspnea in this species."
In a 2013 study of 36 dogs, none being CKCSs, a team of Japanese researchers concluded: "These results indicated that plasma ANP rose with an increase in the volume overload of the left side of the heart. Plasma ANP discriminated cardiomegaly from non-cardiomegaly caused by asymptomatic MMVD. We conclude, therefore, that plasma ANP concentrations may be a clinically useful tool for early diagnosis of asymptomatic MMVD in dogs."
In an April 2013 report, a team of German veterinary cardiologists studied 352 dogs and found that: "NPs [natriuretic peptides] in canine MMVD are useful to discriminate between asymptomatic dogs and dogs with CHF. Due to a large overlap of NP-concentrations between the groups, NPs do not seem to be useful to differentiate between dogs in stages B1 and B2. Interpretation of NT-proBNP and proANP values should include consideration of sex-specific differences."
Why these blood tests are not necessary to diagnose MVD and CHF
Nevertheless, it appears that veterinary cardiologists and other cardio-specialists should be quite capable of detecting mitral valve prolapse (MVP) murmurs and distinguishing between them and flow murmurs or other innocent varieties of heart murmurs. Since BNP in the blood becomes elevated only after the heart has to pump harder to compensate for the disorder, the question then is: When does the heart start working so hard that BNP levels start to go up? In the cavalier King Charles spaniel's version of heart defects -- mitral valve disease due to deteriorating valve flaps -- there are no immediate external symptoms. It is not yet clear from research studies thus far, as to whether the heart becomes labored enough to produce increased levels of BNP before auscultation is able to detect the murmurs from minimal backflow of blood leaking through the mitral valve flaps. Advocates of BNP testing do represent that that studies of BNP and cardiomyopathy show that BNP is elevated before the onset of signs and murmur. But it does not yet appear that BNP testing is an any earlier warning system for MVD than auscultation.
One possible uniquely valuable use for natriuretic peptides tests is if the dog is approaching congestive heart failure (CHF) without any symptoms. In that case, natriuretic peptides tests, combined with "Left Chambers on Aorta ratio" greater than 4,5, the veterinarian may begin administering ACE inhibitors, pimobendan, and other drugs immediately even though the dog is asymptomatic. See Dr. Gerard Le Bobinnec's proposal in this report to the 2010 WSAVA Congress. See, also, the 2012 report of the PREDICT Cohort Study, which found that measurements of left heart size (using the "left atrial to aortic root dimension ratio [LA:Ao]") and plasma NT-proBNP concentration independently estimate risk of first-onset of CHF in dogs with MVD. It correctly predicted first-onset of CHF in 72.5% of cases out of 82 dogs, which included cavaliers.
Dr. Oyama has stated that natriuretic peptide tests may also be useful to properly diagnose a dog known to suffer from congestive heart failure and also is in respiratory distress. He said that, “When dogs come into veterinary hospitals in respiratory distress, it’s sometimes difficult to know if they are having a respiratory or heart problem. Such a test could speed effective treatment and also help decide if a dog should be referred to a veterinary cardiologist before undergoing more expensive testing.”
(This article has been excerpted from "Mitral Valve Disease and the Cavalier King Charles Spaniel" on this website.)
The cavalier King Charles spaniel is pre-disposed to ...
The list gets longer
In the past two months, we have added two more webpages to CavalierHealth.org – kidney disease and pneumocystis pneumonia. Contrary to some breeders’ claims, we hate to do that; we hate to have to increase our list of genetic disorders to which the cavalier King Charles spaniel is pre-disposed. But when dogs are suffering and dying of genetic diseases and their owners don’t know why, we feel the need to continue their education about the extraordinary list of serious genetic problems in our breed.
Chronic kidney disease and pneumocystis pneumonia are killers. The recent deaths of some CKCSs have prompted us to upload these two new webpages. We urge you all to read about them and become aware of their symptoms. You may save your dogs’ lives by recognizing signs which often elude your veterinarians. One of the unfortunate facts about owning cavaliers is that many vets are totally clueless about some of these serious diseases, mainly because they are either unique to our breed or darn close to it.
The cavaliers’ “pre-disposed” list? Here it is:
Mitral valve disease (MVD)
Chiari-like malformation (CM)
Low blood platelets (idiopathic asymptomatic thrombocytopenia)
Cerebellar infarcts – strokes
Brachycephalic airway obstruction syndrome (BAOS)
Curly coat syndrome
Deafness – progressive hereditary hearing loss
Intervertebral disk disease (IVDD)
Dry eye syndrome
Episodic falling syndrome
Fly catchers syndrome
Primary secretory otitis media (PSOM) – glue ear
Chronic kidney disesase
Masticatory muscle myositis (MMM)
Hip dysplasia (HD)
CKCSC,USA embarks on an offensive “charm offensive”
"Forever Guardians of the Cavalier" is its new spin on a BIG LIE!
The Cavalier King Charles Spaniel Club, USA has noticed its ever-declining membership over the past several years and has determined that the problem is not its fault, but instead has been due to the "economy" and poor public relations. At its 2012 Annual General Meeting, president Bruce Henry noted that membership has dropped from 2,000+ five years ago to the current 1,500 range. He attributed this decline “to the general economy since there is no change in the way our club operates.”
If president Henry wanted to be more pointed about the growing insignificance of the CKCSC,USA, he could have added that over the past ten years, membership has dropped by well over half!
Apparently, the CKCSC,USA president is oblivious to the more likely real reason for the membership drop, which is that “there is no change in the way our club operates.” The way the CKCSC,USA has been operating since the departure of president Anne Eckersley (below right) in 2002 perhaps is the real reason for the lack of interest in joining -- and renewing memberships in -- the “Old Club”. It made a major change for the worse back then, and, as Mr. Henry noted, it has not changed since.
The big change
The 2002 change? When the post-Eckersley presidents and their boards took charge of the CKCSC,USA, they rejected the health-consciousness of the Eckersley-led board of directors (BOD). Recall that in 1998, president Eckersley presided at the International Symposium on Mitral Valve Disease (MVD), where a panel of veterinary cardiologists and geneticist unveiled the MVD Breeding Protocol. Remember that? At the time, in 1998 (CKCSC,USA’s “Year of the Heart!” -- see its logo at left), it was a major announcement, offering cavalier breeders the solution to breeding litter after litter of cavaliers with early-onset MVD. The Eckersley BOD also unanimously endorsed the MVD Breeding Protocol and actually urged its members to follow it! They also created the CKCSC,USA Health Registry, to keep track of cavaliers which did not develop MVD until after their fifth birthday. Remember the CKCSC,USA Health Registry?
But with the retirement of the Eckersley administration, her successors unanimously have dumped the MVD Breeding Protocol. In their narrowed minds, it effectively has been air-brushed away, as if that 1998 MVD Symposium never happened, just like old-fashioned Soviet Union censorship.
Since then, the CKCSC,USA's memberships -- largely non-breeder pet owners -- have plummeted by 50+%, and it has become an indistinguishable step-sister of the AKC’s parent club, the American Cavalier King Charles Spaniel Club. The ACKCSC has been notorious for ignoring the breed’s genetic health problems, and since 2002, the CKCSC,USA has been tagging along right behind. Both clubs deny the existence of the MVD Breeding Protocol and the Syringomyelia Breeding Protocol.
The big lie
So, back to the present: The current CKCSC,USA BOD has unveiled its much-heralded solution to its lousy membership numbers. It is a combination of a new slogan, “Forever Guardians of the Cavalier” (below at right), and a chant of tedious “Watchwords” (which includes a Big Lie):
are Forever Committed to the goodwill of the Cavalier;
We are Forever Historians of the Cavalier – we are the history of the breed, and will always be;
We are Forever Protectors of the Cavalier;
We are Forever Dedicated to the health of the Cavalier;
We are Forever Joyful owners of the Cavalier;
We are Forever in Love with the Cavalier;
and lastly, and most important,
We are Forever Guardians of the Cavalier.”
And so it goes. The Old Club’s solution to the lack of interest in it is to Spin a Big Lie about cavaliers’ health. Maybe this should be its new logo:
AVMA’s House of Nannies aims at homeopathic vets
AVMA is bent upon endorsing veterinary malpractice
Obviously, the AVMA (American Veterinary Medical Association) leadership feels threatened by the complexity and success of homeopathy. So what does it do? It lashes out in ignorance ... again. (It lashed out in August against raw food diets because they were hurting the vets' sales of kibble. See here.) In both instances, AVMA defends its hostility upon the pretext of baseless concerns about health and hygiene. The AVMA is beginning to look like a mass version of the Nanny of New York, Mayor Bloomberg (left).
At its January 5, 2013 meeting, the AVMA’s House of Delegates (read: House of Nannies) probably will pass overwhelmingly this resolution:
"Homeopathy Has Been Identified as an Ineffective Practice and Its Use Is Discouraged
"RESOLVED, that the American Veterinary Medical Association (AVMA) affirms that —
"1. Safety and efficacy of veterinary therapies should be determined by scientific investigation.
"2. When sound and widely accepted scientific evidence demonstrates a given practice as ineffective or that it poses risks greater than its possible benefits, such ineffective or unsafe philosophies and therapies should be discarded.
"3. In keeping with AVMA policy on Complementary and Alternative Veterinary Medicine, AVMA discourages the use of therapies identified as unsafe or ineffective, and encourages the use of the therapies based upon sound, accepted principles of science and veterinary medicine.
"4. Homeopathy has been conclusively demonstrated to be ineffective."
AVMA's premise is a thoughtless lie
Of course, the entire premise of this resolution is a thoughtless lie, as the much more competent American Holistic Veterinary Medical Association has pointed out in its response. Click here to read it.
The AVMA nannies' arrogant adulation of "scientific investigation" is known as "scientism". In his recent article in The New Atlantis, titled "The Folly of Scientism", biologist Austin L. Hughes nails these AVMA hypocrites when he points out:
"Advocates of scientism today claim the sole mantle of rationality, frequently equating science with reason itself. Yet it seems the very antithesis of reason to insist that science can do what it cannot, or even that it has done what it demonstrably has not. ... Scientism claims that science has already resolved questions that are inherently beyond its ability to answer ... Continued insistence on the universal competence of science will serve only to undermine the credibility of science as a whole. The ultimate outcome will be an increase of radical skepticism that questions the ability of science to address even the questions legitimately within its sphere of competence."
AVMA reacts like a hurtin' dog
It is quite ironic that a group of veterinarians whose bag-o-tricks pretty much is limited to antibiotics, steroids, vaccines, indiscriminate neutering, and Science Diet, would condemn homeopathy as "conclusively demonstrated to be ineffective." So, the AVMA leadership is proving once again that its instinctive reaction to successful veterinary care that they do not understand, is to lash out like a hurtin' dog (see at right). When will the AVMA learn that it is not wise to endorse veterinary malpractice? When it forbids vets from using diagnostic and treatment modalities which have been proven to be effective for thousands of years, it is asking to be sued, big time.
Post Script: On January 5, 2013, the AVMA's House of Delegates chose to kick this resolution back for further review. It may raise its ugly head again, at its Spring 2013 meeting. We shall see ...
Dog food companies lie, and allergic dogs may die
Let's say that your dog has a raging skin condition that is driving him crazy with itching and has resulted in gooey infections all over his body. Your veterinary dermatologist suspects a severe allergic reaction to beef and pork, and so he prescribes venison for your dog to eat. You feed your pet a dog food which states clearly on the can that it contains venison and no beef or pork. But, your dog's allergy gets worse instead of better. What's up?
What's up is that dog food companies lie about the ingredients of their products.
In an August 2012 study by ELISA Technologies Inc., manufacturers of ten out of twenty-one tested commercial dog foods falsified the contents of their products by either including ingredients specifically excluded on the label or not including ingredients specifically advertised on the label. For instance:
• A food labeled as containing venison, contained no venison or deer at all, and instead contained beef and pork;
• A food labeled "lamb" contained no lamb and contained pork instead;
• A food labeled "chicken meal" contained pork instead;
• Foods labeled "no gluten" or "grain-free" in fact contained gluten and grain levels four times higher than allowable amounts.
Commercial dog food companies are notorious for switching advertised ingredients, depending upon the varying costs of those ingredients. This August 2012 report clearly substantiates that fact.
When a dog is suspected of having a serious food allergy, veterinary dermatologists typically recommend that the dog be fed an "elimination" diet, by feeding ingredients, usually protein sources, the dog has never had before. For example, if the dog has been fed a typical dry food, usually containing corn, wheat, or other grains, the vet's recommendation is to exclude the corn and grains and feed a particular meat as the protein source. If the allergic dog has been fed beef, the vet might prescribe venison instead.
This study proves that owners of food-allergic dogs cannot rely upon the ingredient lists of dog foods to assure themselves that their dogs are no longer being fed the foods which are causing their allergic reactions. These dog food manufacturers are putting allergic dogs at great risk by falsifying the ingredients described on the packaging, all to save a buck.
Update on Hill's Science Diet junk food
Hill's finally dumps its "superior nutrition" corn and chicken by-products
Earlier this year we blogged "The insidious mind control over clueless veterinarians by Hill's Pet 'Nutrition'", in which we pointed out that many veterinary students have been brainwashed by Hill's about its Science Diet dog food, and that these veterinarians continue their nutritional cluelessness throughout their professional careers.
In that blog entry, we emphasized the horrendous main ingredients in Hill's Science Diet dry food: (a) because its corn and chicken by-products really are totally indefensible as being "superior" to real meat as daily sources of protein for dogs; and (b) because so many veterinarians, including "board certified veterinary nutritionists", have prostituted themselves by actually declaring that corn and by-products are better than real meat.
Well, on September 11, Hill's announced* that it is re-formulating its crappiest dry food, Science Diet, by offering a "quality protein first ingredient" (instead of the current "ground whole grain corn"), and "no chicken by-product". This is the first change of ingredients in Science Diet's 44 year history!
Wow! Without corn and chicken by-products, what will Hill's lapdog veterinary nutritionists and all the other sycophantic veterinarians have to rave about? Will they recant their prior praise for Hills' junk food ingredients of corn and by-products? Will they stop claiming that non-meat chicken by-products are "superior" for dogs than, say, a fresh chicken breast? Will they stop boasting that if corn was good enough for the American Indians, it is good enough for dogs? Has Hill's thrown all of these bootlicking vets under the bus?
Mind you, Hill's did not make this change willingly. Hill's U.S. President Kostas Kontopanos brags in its news release that its "Science Diet is Veterinarians' #1 choice to feed their own pets." (Imagine the scary thought that, for the past 44 years, more veterinarians have chosen Science Diet to feed their own pets than any other pet food. And we have been trusting their judgment to keep our pets healthy!) He goes on:
"We took a food that already delivered precisely balanced nutrition, industry leading quality and great taste and will make it even better by adding the natural ingredients that pet parents want."
So, Hill's grudgingly concedes that, despite Science Diet's "superior nutrition, backed by clinical research", we stupid pet owners no longer are falling for the hype like all of those veterinarians have. Hill's president pleads further: "We also want to be pet parents' #1 choice, with the ingredients you prefer, the uncompromising nutrition that more than 50 precisely balanced nutrients deliver and the quality you can trust."
So, this sea-change after 44 years is not being done to improve the nutritional quality of Science Diet's ingredients. Oh no. Hill's insists that its corn and by-products always have been the best source of pet nutrition there can be. Hill's is doing this solely because picky pet owners are more concerned about "natural ingredients".
Now, don't get too excited about this "new-but-not-necessarily-improved" Science Diet. We don't know yet what the "quality protein first ingredient" will be. And, we also realize that "natural ingredients" means absolutely nothing in the pet food industry. All we know for sure is that Hill's claims that the current first two ingredients, corn and chicken by-products, will be gone from the top of the ingredients list. Is it just a coincidence that corn and chicken prices have skyrocketed recently?
Post Script: It is January 2013 already, Hill's. Where is this new Science Diet? Hill's promised in September 2012 that it would introduce its new version of Science Diet, with "natural ingredients", in December 2012. So, where is it? And, what is it? Hill's still has not even told us what the new ingredients are.
In November 2011, the UK's Advisory Council on the Welfare Issues of Dog Breeding identified its "first eight problems which cause serious health and welfare issues for some dogs" as follows:
• Brachycephalic airway obstruction syndrome
• Limb defects (including hip and elbow dysplasia)
• Ocular disease secondary to conformational problems
• Heart disease with a known or suspected inherited basis
• Skin conditions with a known or suspected inherited basis
• Issues arising from lack of responsible ownership (including problems such as separation-related behavioural issues and obesity)
Do any of these sound familiar to owners of cavalier King Charles spaniels? Well, seven of them certainly are the most serious problems affecting the CKCS. And, two of them -- inherited heart disease and syringomyelia -- are, by far, more severe in the cavalier than in any other breed of dog. Among these eight serious problems, only inherited skin conditions are not commonplace among the cavalier. Otherwise, the UK Advisory Council might just as well have been writing about only one breed -- ours.
So, what are the US cavalier King Charles spaniel clubs doing about these serious problems? Thus far, absolutely nothing. And there really is no reason to expect that they ever will do anything.
Mitral valve disease (MVD) has been identified as a widespread genetic problem in the breed for several decades. Over half of all cavaliers are expected to have MVD by their fifth birthday, and nearly 100% by their tenth year. It is the leading killer of CKCSs. In most breeds, death is more often due to cancer or accidents, but in the cavalier it is MVD. In 1998, a panel of veterinary geneticists and cardiologists recommended to the US cavalier clubs a breeding protocol designed to eliminate early-onset MVD in the breed within as few as three generations. Neither national cavalier club endorses the breeding protocol, and one of those clubs, the AKC's parent club for cavaliers, refuses to acknowledge the breeding protocol's existence.
Similarly, syringomyelia (SM) has been identified as an excruciatingly painful genetic problem in the CKCS for over a decade. It is rampant in the breed; over half of all cavaliers are believed to have SM, and 95% to have Chiari-like malformation, which is part of the cause of SM and its severe pain. Since 2005, veterinary neurologists have designed breeding protocols to rid the breed of SM. However, neither US cavalier club has even acknowledged the existence of any such breeding protocol, much less recommended that it be followed by breeders.
The US cavalier clubs continue to skirt along their merry ways, ignoring any realistic solutions to these severe, breed-wide genetic health problems, and thereby encouraging their breeders to compound the extent and severity of MVD and SM in each and every future generation of cavalier King Charles spaniels.
The insidious mind control over clueless veterinarians
by Hill's Pet "Nutrition"
Ever wonder why so many veterinary clinics have stacks of bags of Science Diet dog food for sale in their waiting rooms? It probably is because so many vet schools do not teach companion animal nutrition to their students. Instead, these many schools delegate to Hill's Pet Nutrition, the maker of Science Diet, the diet and nutrition curriculum taught to their veterinary students.
Dr. Karen Becker, DVM, who authored Dr. Becker's Real Food for Healthy Dogs and Cats, observed recently:
"Most veterinary students don't learn about species-appropriate pet diets in vet school. The only food discussed is processed, commercial pet formulas."
For nearly all vet students, their schools' nutrition classes have consisted of visits by commercial pet food marketeers to talk about their products. Consider this observation by a veterinarian who graduated from the University of Pennsylvania's veterinary school:
"When I was in veterinary school, we received little education in nutrition (and from walking into the average veterinary clinic today, I assume nothing has changed). Precious little was taught on how to keep the pet carnivore healthy for longevity. The small animal nutrition text was published by a major pet food company and given (not sold) to students."
That major pet food company was Hill's. Consider this telling admission in DVM Newsmagazine:
"Hill's provides financial and educational support to nearly every veterinary college in North America, as well as to veterinary students attending those institutions. This commitment to the profession includes Hill's sponsored teaching programs, residencies and faculty programs in veterinary schools and teaching hospitals all over the world. ...
"Hill's has shown its commitment to the partnership with MSU by providing support to many student groups and student activities; covering costs for students to attend the SCAVMA Symposium; providing students with the textbook Small Animal Clinical Nutrition and other various handouts; ... ." DVM Newsmagazine. Aug. 2004;35(8):38.
That veterinary school textbook, "Small Animal Clinical Nutrition", is published by Mark Morris Institute, which is owned by Hill's. Dr. Max Morris was the creator of Science Diet kibble.
Hill's " Feeding Programs" -- like pabulum to vet students
In most USA vet schools, Hill's offers "Feeding Programs", by which it sells its pet foods to students and faculty at majorly reduced cost and donates the sales funds to student groups and scholarships. At each school, one or two students are appointed as "Hill's Contacts" -- not unlike Lenin's useful idiots -- to keep lines of communication open between the unsuspecting students and the pet food conglomerate.
Some vet schools have taken the Hill's bait, hook-line-and-sinker. The University of Florida has a large, permanent display of Hill's Science Diet in the middle of its emergency clinic waiting room. Hill's also is a major benefactor at this vet school, even funding a professorship.
Now, this academic/business relationship would not be so insidious if Hill's Science Diet was a good, nutritive dietary product. But it is not. Here is the list of ingredients in Science Diet adult dry food:
"Ground Whole Grain Corn, Chicken By-Product Meal, Animal Fat (preserved with mixed tocopherols and citric acid), Dried Beet Pulp, Soybean Oil, Dried Egg Product, Flaxseed, Potassium Chloride, Iodized Salt, Choline Chloride, vitamins (L-Ascorbyl-2-Polyphosphate (source of vitamin C), Vitamin E Supplement, Niacin, Thiamine Mononitrate, Vitamin A Supplement, Calcium Pantothenate, Biotin, Vitamin B12 Supplement, Pyridoxine Hydrochloride, Riboflavin, Folic Acid, Vitamin D3 Supplement), Vitamin E Supplement, minerals (Ferrous Sulfate, Zinc Oxide, Copper Sulfate, Manganous Oxide, Calcium Iodate, Sodium Selenite), preserved with Mixed Tocopherols and Citric Acid, Beta-Carotene, Rosemary Extract."
Where's the meat???
Ingredients must be listed on the label in decreasing order by weight. For Hill's Science Diet, the first item is corn, which means that there is more corn in the mix than anything else. Corn is a cheap filler ingredient with little nutritional value. It is not a natural source of food for dogs and is very difficult for them to digest. The second item is chicken by-product meal. Chicken by-products in dog food do not include meat and instead contain cheap, unsavory ingredients ground into the mix, like stomach contents, beaks, feathers, feet, and entrails. But have no fear, because all of it then is cooked to death two separate times, changing the structure of proteins for the worse, and destroying vitamin A, vitamin E, and the B-group vitamins.
No dog should be required to live on this junk. And yet, seemingly intelligent veterinarians tout Science Diet to their patients' owners as "Vets' #1 Choice for their Own Pets".*
* By the way, Hill's Science Diet kibble cat food does not include any meat, either.
Some veterinarians have been so taken by the Hill's mind-numbing indoctrination efforts, that they actually endorse corn and by-products as nutritional ingredients in pet food. Dr. Bridget Edgren, DVM, of All Pets Animal Hospital in Boulder, Colorado, a Colorado State University vet school graduate (where Hill's Feeding Program lures the students) recently authored an article titled "Finding the right food for your pet". Her ignorance about dog nutrition is obvious when she writes:
"Corn ... is a nutritionally superior grain compared to the others because it provides a balance of nutrients not found in other grains. ... Contrary to popular belief, by-products are not hooves, feathers, and beaks, which have no nutritive value. By-products are not harmful and actually have excellent nutritive value."
After all, corn was good enough for the Indians
Dr. Sherry Lynn Sanderson, DVM, PhD, of the University of Georgia's veterinary college and a University of Minnesota vet school graduate (both schools have Hill's Feeding Programs) wrote "Raw Diets: Do They Make You Want To BARF?", in which she fervently defends corn as a main ingredient in dog food. She writes:
"If one considers that corn was a main staple in the diet of Native Americans for many years, it is difficult to understand how critics can claim that corn is a filler used in pet foods."
Sad. Her point? She offers no clue. Chickens eat more corn than the American Indian ever did, but neither humans nor fowl are dogs. And this lady is a board certified veterinary nutritionist!
And, Dr. Sanderson is not unique. Another board certified veterinary nutritionist, Dr. Lisa M. Freeman, DVM, PhD, of Tufts University's Cummings School of Veterinary Medicine (another sucker-school for Hill's Feeding Program), also sings the praises of corn and by-products as the major sources of protein, instead of real meat. She writes in "Answering Owners' Questions About Pet Foods" (as if she actually is trying to be helpful to those owners), this incredible statement:
"Some owners are concerned about using diets that contain any vegetable-based proteins, such as soybean or corn. These are NOT added as fillers and contain important nutrients. There is no reason why 'grain free' foods are better for either dogs or cats. ... Pet food ingredients have strict definitions so meat by-products, for example, are not allowed to contain the non-nutritious animal parts that people sometimes worry about (by-products refer to the non skeletal muscle meat – in other words, the organs)"
Not true, and totally irresponsible. Remember, by definition, "meat by-products" do not include any meat.*
* The AAFCO definition of "poultry by-product meal: Consists of the ground, rendered, clean parts of the carcasses of slaughtered poultry, such as necks, feet, undeveloped eggs, and intestines, exclusive of feathers except in such amounts as might occur unavoidably in good processing practices."
Why this love affair of so many veterinarians with corn and by-products as the major ingredients in dog foods? The answer likely is Hill's indoctrination programs at the earliest stages of their veterinary education. Junk in; junk out.
Logically, what these "nutritionists" claim makes no sense. Humans, who are far less carnivorous that dogs, are not advised to eat highly cooked, dry, and processed foods instead of fresh, whole food-based diets. Why, then, are kibble and other highly-processed non-meat foods more appropriate for pets? To the contrary of all this pro-kibble hype from these "nutritionists", research studies that have not been funded by commercial pet fund manufacturers have reached the opposite -- and more obvious -- conclusion that balanced home-prepared meals are much more healthful for our dogs than commercial diets prepared by pet food conglomerates. For example, in a 2003 Belgium study of 522 dogs*, the researchers found that dogs fed a species-appropriate homemade diet lived 32 months longer on average than dogs fed commercially available dog foods.
* Relations Between the Domestic Dogs’ Well-Being and Life Expectancy. Lippert, G., & Sapy, B. Prince Laurent Foundation Price, 2003.
Post Script: Has the AVMA now legitimized veterinary nutrition malpractice? On August 3, 2012*, the American Veterinary Medical Assn. (AVMA) voted overwhelmingly to condemn the feeding of home-prepared raw food to dogs and cats. Not surprisingly, the AVMA's meeting was heavily funded by Hill's and by Purina, another producer of junk dog food. So, these vets apparently have learned nothing beyond what the commercial pet food manufacturers indoctrinated them about in vet school, and continue to wallow in their self-imposed ignorance. The question now is: Has the AVMA legitimized veterinary nutrition malpractice?
* According to the AVMA website, in the four months preceding this AVMA vote, over 60 commercial brands of dog and cat food were recalled, nearly all for "possible Salmonella contamination". Despite these massive recalls of kibble and canned pet foods, AVMA chose to condemn only pet owners for feeding healthful raw food diets to their dogs and cats. Pet owners have been feeding raw diets to their dogs and cats for decades, yet to date, not one documented case of raw pet food causing illness in humans has been reported.
Congratulations to Her Majesty, lover of cavaliers!
The Diamond Jubilee of Her Majesty, Queen Elizabeth II! This is a once in several lifetimes' event for the peoples of the United Kingdom and the Commonwealth realms. For the first time in 115 years, their monarch has served 60 years, and only for the second time in the history of the monarchy.
The ties of the cavalier King Charles spaniel to Britain are many and obvious. The breed's name owes itself to one of its kings. But for the prompt and willing response of UK breeders of the English toy spaniel to the challenge of an American, Roswell Eldridge, in 1926 (the same year the Queen was born), there would be no CKCS breed. Through World War II, those British breeders rescued and salvaged the fledgling breed.
And, thanks to Her Majesty for her total dedication to her life-long job of serving as her realm's sovereign. At age 86 years, she seems indefatigable in dutifully offering herself this weekend in ceremony after ceremony, rain or shine, hours on end, all with grace and dignity. She truly is an amazing person, "a living flag"!
And while she may be a backyard breeder of a lengthy royal line of inbred corgis, the photo above attests that she also loves cavalier King Charles spaniels! May God save the Queen and the cavalier King Charles spaniel!
When ignorance (stupidity?) guides cavalier PSOM research, and the federal government funds it
Dr. Charles Bluestone doesn’t even know what “PSOM” stands for
What do you get when a medical researcher who thinks chimpanzees are in his own pedigree and that the cavalier King Charles spaniel “has been bred over 300 years to have a short snout”, decides to solve the mystery of what he calls “persistent secretory otitis media” in our breed? Answer: You get Charles D. Bluestone, M.D., professor of otolaryngology at the University of Pittsburgh School of Medicine (UPMC).
Yes, this man is convinced that his ancestors were chimpanzees, despite the lack of any evidence to prove it.* He apparently has blind faith in such unproven theories, which is not a good thing for a research scientist. And yes, he obviously knows nothing factual about the cavalier King Charles spaniel, beyond being able to identify one in a photograph.
* His alleged “evidence”? He irrelevantly and erroneously asserts: “Chimpanzees share an astounding 98.4% of their genetic code with us.” Actually, using Dr. Bluestone’s intellectually shallow means of DNA comparisons, the similarity is more like below 70%, under the most optimal alignment conditions. The 30+% difference represents almost 35 million single nucleotide changes and 5 million insertions or deletions. By his same simplistic standard, the lowly house mouse shares more of our genetic code -- 99% -- than does the chimpanzee. The notion of man's alleged descent from chimpanzees has long been rejected by knowledgeable evolutionists and creationists, alike. (See, e.g.: "The common chimp [Pan troglodytes] and human Y chromosomes are 'horrendously different from each other', says David Page of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts." The fickle Y chromosome, Nature, Jan. 2010;463:149.) Why Dr. Bluestone bothers to bring the topic up in a report about PSOM is beyond comprehension. Click here for some more interesting reading about Dr. Bluestone's credibility.
He doesn’t even know the name of the disease he claims to be researching. He repeatedly has called PSOM “persistent secretory otitis media” instead of its real name, “primary secretory otitis media”. Scientists really ought to know the name of what they are researching.
But, with the full weight of federal funding behind him and his co-conspirator, UPMC’s J. Douglas Swarts, Ph.D., he is determined to prove that 300 years of breeding the cavalier for its “short snout” altered its palate muscles to keep its Eustachian tube from operating correctly, thereby causing “persistent secretory otitis media” in “up to 40%”, or “50%”, or “greater than 50%” (pick one) of the breed. Never mind that the modern-day cavalier was created less than 85 years ago and has been bred to have a longer snout – not a shorter one – and that the percentage of cavaliers with PSOM has not been determined.*
* If you want to learn more about PSOM, click here.
When does ignorance morph into stupidity?
Dr. Bluestone's lack of knowledge about the cavalier King Charles spaniel goes way beyond sloppy research. He is so wrong about this breed in so many ways that it is impossible to determine whether he is monumentally ignorant or just flat stupid. Where is his intellectual curiosity? Has he not researched the breed’s founding in the years following Roswell Eldridge’s challenge in 1926? Has he not learned that the cavalier’s longer muzzle sprung from the shorter muzzle of the King Charles spaniel? Does he not even care to learn the actual name of the disorder he has decided to research?
(Specimens from the collections of the Albert Heim Foundation, Museum of Natural History, Bern.)
Note in the comparison of the breeds’ skulls above: the King Charles spaniel skull is at the left, and the skull of the cavalier King Charles spaniel is at the right.
How does federal funding fit into this mess? Leave it to the National Institutes of Health (NIH)* to have wasted our tax dollars on this “research”: Human evolutionary history: Consequences for the pathogenesis of otitis media, published in Otolaryngology -- Head & Neck Surgery in December 2010.
* Federal NIH funding fits Dr. Bluestone's modus operandi: "Bluestone submitted numerous grant applications to the NIH throughout the 1970s and 1980s and ultimately was awarded approximately $17.4 million. At the same time, Bluestone began receiving funding from various pharmaceutical companies to test the effectiveness of their antibiotics in treating otitis media. Collectively, this industry funding totaled approximately $3.4 million. ... Cantekin claims that as early as 1976, he raised with Bluestone his failure to list his industry funding on his NIH grant applications, but Bluestone allegedly brushed him off, saying that he was not going to tell the 'federal feather merchants' because it was 'none of their business' and would 'muddy up the waters'." Click here for source.
What next for Dr. Bluestone?
Dr. Bluestone stated in his 2010 article that “The underlying pathogenesis of the Cavalier’s ME disease is currently under investigation in our laboratory.” He re-affirmed this disquieting news in his 2011 video, when he redundantly said “It’s a current research project which we are undergoing now.” Most recently, in February 2012, he stated:
“Another ongoing research project involves a potential animal model, Cavalier King Charles Spaniel, which has a greater than 50% incidence of chronic otitis media effusion.* Research being conducted with his colleagues in this animal involves histopathology of the middle-ear cleft in cadavers, and Eustachian tube function tests in live animals, conducted at the Ohio State University School of Veterinary Medicine in Columbus Ohio. ”
* It seems he keeps increasing the percentage of incidence of PSOM in the breed, each time he makes a public comment, and this time, he has re-named the disorder “chronic otitis media effusion.” So, apparently his new acronym for PSOM would be “COME”!
We can only pray that some wild hair will distract him from his focus on the cavalier King Charles spaniel. Otherwise, we will have to endure more of his ignorance, hopefully not on our tax dime.
Don't be fooled by cavalier breeders who brag about CHIC
The American Kennel Club* (AKC) sponsors the Canine Health Information Center, also known as CHIC, with the stated mission "To provide a source of health information for owners, breeders, and scientists, that will assist in breeding healthy dogs." Unfortunately, for the cavalier King Charles spaniel, CHIC not only does not work; it actually encourages bad breeding practices and allows bad CKCS breeders to hide behind the CHIC "Good Housekeeping" seal (see right).
*And its partners, the Canine Health Foundation (CHF) and the Orthopedic Foundation for Animals (OFA).
The two major genetic diseases affecting the cavalier King Charles spaniel are mitral valve disease (MVD) and syringomyelia (SM). Contrary to its "mission", CHIC provides absolutely no useful MVD or SM "health information ... that will assist in breeding healthy" cavaliers.
MVD is the leading killer of cavaliers. Statistics have repeatedly shown that over half of all cavaliers are expected to have MVD by their fifth birthday and nearly 100% by age ten years. SM is a spinal disorder which can cause excruciating pain. Statistics show that up to 25% of cavaliers may have SM by their first birthday and up to 70% by age 6 or older.
One would think that if AKC's CHIC program really wanted to "assist in breeding healthy" cavaliers, CHIC would recommend that breeders follow the breeding protocols* designed to reduce MVD and SM in future generations of cavalier puppies. Well, CHIC does nothing of the sort.
Test for MVD? Yes ... but pass that test? Not necessarily!
As for MVD, all CHIC requires is that the breeding stock be examined by a veterinary cardiologist. It does not require that the results of the examination show no mitral valve disease. A cavalier of any age can be examined, flunk the exam, and still qualify for a CHIC certificate and be bred! See for yourself, from the CHIC policies webpage:
Syringomyelia? Never heard of it!
As for SM, CHIC has no requirements at all! As far as CHIC is concerned, syringomyelia is not a problem in the breed, and any cavalier may be bred without testing for it, much less found not to have it.
So, if a cavalier breeder brags to you about her dog having a CHIC certificate, tell her you know exactly what a CHIC certificate means, and most importantly, what it does not mean.
Pedigree Dogs Exposed: The Sequel, or The End?
Most all cavalier breeders still refuse to get the message
Pedigree Dogs Exposed was a televised investigatory documentary about the British purebred dog scene. It was first broadcast in the United Kingdom in 2008 and then on PBS in the United States in 2009. Since then it has been available on YouTube.
The program focused on a handful of dog breeds, but it had an enormous impact on the cavalier King Charles spaniel (CKCS) because it included video clips of cavaliers writhing in agonizing pain from syringomyelia (SM). (See photo below.) So, for many cavalier owners it was particularly eye-opening because, for the first time, many who viewed it were able to recognize similar symptoms of SM in their own pet cavaliers.
The program produced howls of protest from many corners of purebred dogdom, including over here in the US. The chairman of the American Kennel Club, Ron Menaker, referred to it as "sensationalist fiction and tabloid journalism masquerading as a documentary." But, he's an ignoramus. As far as the CKCS is concerned, every second of that program was factually accurate and needed to be publicized.
"From creation to ruination in less than 100 years"
Earlier this week, its sequel, Pedigree Dogs Exposed -- Three Years On, was broadcast in the UK. It, too, now is available periodically on YouTube. The cavalier remained a prime topic in this sequel, and the conclusion to be drawn from it is that, with early-onset mitral valve disease (MVD) -- nearly 100% affected by age 10 years -- as well as syringomyelia -- over 70% affected -- it is time for pet buyers to seriously avoid getting cavaliers. As the program's commentator put it, "From creation to ruination in less than 100 years." The rationale is that if the breeders persist in refusing to follow the MVD breeding protocol and SM breeding protocol, so as to avoid producing future generations of only terminally ill cavaliers, then this breed should come to an end.
What has been the response of many cavalier breeders, to this sequel? Pretty much the same as to the 2008 broadcast: hostile condemnation. So, we are likely to see no progress on the breeding front. For the most part, the only people who "get" the truth are the pet buyers.
The likelihood of finding a cavalier puppy in the USA that either won't develop a heart murmur before its fifth birthday or won't have Chiari-like malformation and syringomyelia, is pretty much nill. Many US cavalier breeders have known about the MVD breeding protocol since 1998 and the SM breeding protocol since 2005, and yet most all of them have ignored both protocols.
For the rest of the US breeders, well they just don't even know about these real breeding protocols. In the US, there are two national breed clubs, one in the AKC and one out of it. Both of them refuse to recommend that their members follow either protocol. In fact, both of them recently have concocted their own phony MVD breeding protocols which no panel of cardiologists has ever approved, and neither club has even acknowledged the existence of the SM breeding protocol.
So, with breed clubs like those two, the CKCS appears to be on an unstoppable downward slide. The end result in the US probably will be generation after generation of sickly cavaliers, with high price tags and even higher veterinary and medicine bills. Surely that cannot go on very long. And then we will have none.
Will the next SM breeding protocol be
BAD FOR THE BREED?
Breeding under age 2.5 years would increase early-onset MVD
The cavalier King Charles spaniel has TWO severe genetic health disorders, NOT JUST ONE! While syringomyelia (SM) is very widespread in the breed, so is mitral valve disease (MVD), and it is MVD – not SM – that is the cavaliers’ leading killer!
While the next SM Breeding Protocol, scheduled to be released in 2012 by the British Veterinary Association and the Kennel Club (BVA/KC), still is a work-in-progress, a preliminary draft of it (see below) would permit the breeding of cavaliers as young as 12 months old! If so, this certainly would violate the MVD Breeding Protocol, which sets the MINIMUM AGE for breeding cavaliers at 2.5 years of age.*
* A September 2010 statistical report has shown that anything less than following the MVD Breeding Protocol has not worked.
Have the new BVA/KC's SM protocol drafters forgotten about MVD? Are they giving CKCS breeders a deadly choice? Is the SM protocol really going to recommend that breeders ignore the MVD Breeding Protocol and thereby produce future generations of many more cavaliers which will die early, painful deaths from congestive heart failure?
It has been five years since the International Syringomyelia Conference issued its “Revised CKCS MRI Screening and Breeding Recommendations” in November 2006. The introduction to those breeding recommendations, also called the SM Breeding Protocol, stated:
“These breeding recommendations are made using current information and in response to CKCS breeder request for guidelines. It has yet to be proven if this guide is appropriate. The aim of these recommendations is to reduce the incidence of symptomatic syringomyelia (SM) in the breed, not to create litters of puppies guaranteed not to have SM as the chance of producing an affected dog cannot be predicted without knowing the inheritance.”
The general principle of the 2006 guidelines is that dogs graded “Code A” are more desirable to use than those graded “Code B”, and so on, but that dogs with a higher letter code may still be used in some limited circumstances.
Significantly, the protocol was predictively accurate. Statistics reported in October 2010 showed that:
• 75.9% of the offspring of matings of a Code A sire to a Code A dam were SM-clear.
• 41.9% of the offspring were SM-clear if only one parent was Code A.
• 0% of the offspring were SM-clear if neither parent was Code A.
Statistics reported a year later, October 2011, were similarly on target:
• 70% of the offspring of matings of a Code A sire to a Code A dam were SM-clear.
• 23% of the offspring were SM-clear if only one parent was Code A.
• 8% of the offspring were SM-clear if neither parent was Code A.
Still, much more has been learned about SM in the cavalier since the “current information” available to the International Syringomyelia Conference in 2006.
A June 2011 UK study of 555 cavaliers (Parker Report) showed that:
• 25% of 12 month old asymptomatic CKCSs had SM.
• 70% of asymptomatic CKCSs six years and older had SM.
These figures do not include SM-affected cavaliers which displayed symptoms, so, as the researchers concluded, “The true prevalence of syringomyelia in the general CKCS population is expected to be higher.” They also concluded that, based upon their statistics, the minimum age of the SM Breeding Protocol ought to be raised from 2.5 years to 3.0 years, although they recognized that “many breeders would consider 36 months unduly old.”*
*There is irony for you! The fact is that most cavalier breeders consider 2.0 years unduly old for initial matings.
In an October 2011 UK study (Knowler Report), the researchers go even farther. First, they concur with the Parker Report that “the optimum age for this early MRI screening is 36 months.” Then, they recommend that, if only one of the breeding pair is SM-clear, it be “five years or older”.
This is a matter of veterinary ethics!
So, with those two recent reports on the table urging raising the minimum breeding age to three or even five years, how can the BVA/KC possibly – even ethically – decrease that age from 2.5 years to one year?
The clear answer is that they should not! If the final, approved version of the new BVA/KC SM Breeding Protocol allows breeding any cavalier under the age of 2.5 years, then it will undercut the MVD Breeding Protocol, and it will be encouraging rampant early-onset MVD in the breed!
At the very least, the final version of the BVA/KC guidelines chart should change Age from "1-3" to "<3".
What do the two USA CKCS clubs have against
healthy cavalier King Charles spaniels?
The syringomyelia (SM) breeding protocol works! (See the October 2011 statistical report.) And, anything less than the mitral valve (MVD) breeding protocol has not worked! (See the September 2010 statistical report.)
BUT ... STILL ... neither of the USA cavalier King Charles spaniel clubs will recommend that their members follow either of these breeding guidelines.
Why don't these two breed clubs, the American Cavalier King Charles Spaniel Club (ACKCSC), and the Cavalier King Charles Spaniel Club, USA (CKCSC,USA), oppose SM and early-onset MVD in future generations of CKCSs?
Why don't they endorse the MVD and SM breeding guidelines?
Ask their presidents. Call and email them.
The president of the ACKCSC is Patricia Kanan, telephone 805-688-7830, email firstname.lastname@example.org
The president of the CKCSC,USA is Anne Eckersley, telephone 203- 616-5443, email ChadwickCavaliers@comcast.net
A neurologist answers our August 13 questions:
"Okay syringomyelia researchers:
What now? Where do we go from here?"
Lo and behold! For a moment there, I thought we might have had a definitive answer to the query: "So, where do we go from here ...? Yo, researchers, do you have any suggestions?" in our August 13 editorial.
In the September 10, 2011 issue of the Veterinary Record, UK veterinary neurologist Rita Gonçalves wrote an editorial titled, "Understanding Chiari-like malformation: where are we now?"
"Ah ha", I thought! What wisdom does she have to impart? Well, not much, actually. After a brief but thorough and concise review of CM research in the cavalier King Charles spaniel, up through mid-2011, along with comparisons to the research of human Chiari malformation, Dr. Gonçalves reaches this painfully disappointing but quite obvious conclusion:
"Chiari-like malformation has for a decade now been widely identified in the CKCS population but despite its high prevalence, little is still known about its pathogenesis. Further studies are necessary to increase our understanding of this condition in order to allow the development of new treatment options and improve the welfare of the CKCS affected."
So, the answer essentially is that we need more money to continue the research, so that we can close in on the mysteries of the causes and solutions to CM and SM in our precious breed.
Plucking the MVD genes:
The first shoe has dropped!
The headline of the September 2011 Journal of Heredity article says it all: "Identification of 2 Loci associated with development of myxomatous mitral valve disease in cavalier King Charles spaniels." Translation? It means that the first step towards finding a DNA test for early-onset MVD genes has been taken. The first shoe has dropped.
Soon there should be a second shoe heard hitting the floor, when the researchers announce they've identified the actual genes themselves. In their report, they state:
"We will initiate studies of the most promising candidate genes in the 2 candidate regions which hopefully will lead us to the mutations affecting the development of mitral valve disease."
And then the thud of a third shoe (yes, we are talking about a triped here) will be felt when the researchers offer the DNA test to determine which cavaliers do or do not carry the offending genes.
That will be when the shoes hit the fan! For it has been well over a dozen years since the MVD breeding protocol was offered to cavalier breeders in the USA as the means of eliminating early-onset MVD in the breed. Since that announcement in 1998, nearly all of those "reputable", "responsible" cavalier breeders have declined, claiming that they would prefer to wait until the MVD genes are identified. Instead of trying to reduce MVD in their breeding stock, they chose to hide behind that excuse, and they continued to produce generation after generation of cavaliers with worse and worse early-onset MVD.
But now, those breeders' big bluff is about to be called. Soon enough, they will have what they claimed they've been waiting for. They claimed that they would not risk following the MVD breeding protocol because they feared that it would eliminate too much of their breeding stock. If they thought the MVD breeding protocol would have that much of an effect, just imagine what the DNA test will do to their bloodlines! It may wipe out entire kennels of breeding cavaliers!
So, it looks like they're going to have to come up with a new excuse for ignoring the DNA test. Start thinking hard now, you "reputable", "responsible" breeders. You don't have much time left!
Will the CSF-space gap predict
future syringomyelia in cavaliers?
In a recent research study of cavalier King Charles spaniels with Chiari-like malformation (CM) and some with both CM and syringomyelia (SM), the researchers reported:
"When [cerebrospinal fluid] CSF space between the cerebellum and brainstem was compared in CKCS with and without SM, there was a significant increase in CSF space in CKCS with CM alone compared to those with CM/SM when head position was flexed. In their cine MR imaging study of CSF flow dynamics in CKCS with CM or CM/SM, Cerda-Gonzalez and others (2009a) found that turbulent CSF flow and jets are associated with SM presence and severity and CSF flow velocity at C2/3 is inversely related to the presence of SM. The reduced CSF space in CM/SM dogs reported in this study could explain this jet like CSF flow in dogs with CM/SM compared to those with CM alone."
Translation? We THINK it means that there is more space for cerebrospinal fluid (CSF) between the cerebellum and the brainstem of cavaliers with just CM than there is of cavaliers with both CM and SM.
Now, one of the current issues about CKCSs is that those younger ones with only CM still may develop SM as they age. Another recent study found that most cavaliers do not develop SM until after their third birthday and as late as age 6 years. Most all cavalier breeders believe that it is unreasonable to have to wait until their breeding stock is over 3 years old before being bred for the first time.
It would be a very valuable piece of information for any breeding program to be able to predict if a young cavalier (say, at age 18 or 24 months) will or will not ever develop syringomyelia.
This study may lead to the answer to the question: Can an MRI at an early age, showing the amount of CSF space between the cerebellum and the brainstem, predict whether the cavalier will or will not end up with SM?
Okay, syringomyelia researchers:
What now? Where do we go from here?
HERE IS THE SITUATION: In June, a team of veterinary neurologists issued a devastating report. They examined the MRI scans of 555 cavalier King Charles spaniels, and found that at age 12 months, 25% had syringomyelia (SM), and by age six years, 70% had SM. And, all 555 of these were cavaliers which reportedly had no symptoms of SM.
THINK OF IT: Not only did 25% of these cavaliers already have SM by their first birthday, but in the five years between age 1 and age 6, 45% of the rest of the cavaliers acquired SM.
Previously, these neurologists thought that most dogs afflicted with SM would start to show symptoms before age 3 years. When the International Syringomyelia Conference issued its revised CKCS MRI screening and breeding recommendations in 2006, the panel of researchers stated:
“The age cut off at 2.5 years has been decided so as to tie in with MVD recommendations and because most dogs with symptomatic SM will show signs before 3 years of age.”
That cut off age meant that cavaliers at least 2.5 years old without SM would be classified as Code “A” and could be mated with any other cavaliers over 2.5 years, even if they had asymptomatic SM.
Now, we find, most cavaliers do not even contract SM until after they are 3 years old, much less also become symptomatic.
The authors of the June 2011 report, J. E. Parker, S. P. Knowler, C. Rusbridge, E. Noorman, and N. D. Jeffery, carefully worded the serious impact of these findings upon the current SM breeding protocol:
“The evidence for a lower prevalence in younger animals is more reliable ... and this effect lasts until dogs are at least three years of age. This finding has important implications for the design of a screening test procedure and may conflict with the current recommendations that the optimum age for screening should be 30 months. These data would imply that it is probable that dogs aged up to three years may yet have reduced odds for the diagnosis of syringomyelia. However, there is a need for the dogs to be screened when they are reasonably young so that breeders can decide at an early stage whether their animals are suitable for breeding; many breeders would consider 36 months unduly old.”
GET IT? This means that more cavaliers develop SM after age 2.5 years than before that age. So, the current SM breeding protocol is ineffective. But, they also observe that breeders would not consider waiting until their MRI-clear cavaliers are 3 years old (“unduly old”). Thus the dilemma in which we CKCS fanciers find ourselves.
WHAT TO DO? WHAT TO DO? Well, the researchers don’t give us much hope. They go on:
“The high lifetime prevalence of syringomyelia raises concerns for the welfare of the CKCS breed and also suggests that eliminating the genetic risk factors for the disease by selective breeding may be difficult, because the heritability has previously been shown to be complex ... and the prevalence of the determinant genes within the population is therefore likely to be high. The true prevalence of syringomyelia in the general CKCS population is expected to be higher than that found in this sample population because symptomatic dogs were specifically excluded.”
RAISES CONCERNS!!! To say the least! MAY BE DIFFICULT!!! What an understatement! We now know that SM is far more widespread in the breed than anyone, even the experts, ever thought. We now know that the 2.5 year cut off in the SM breeding protocol is way too early, but that many breeders would not stand for extending that age by even another six months.
(Actually, the dirty little secret is that nearly all US cavalier breeders always have been ignoring the current SM breeding protocol. Neither of the two CKCS national clubs in the US will even acknowledge that the breeding protocol exists, much less recommend that breeders follow it.)
So, where do we go from here, cavalier fanciers? Yo, researchers, do you have any suggestions?
AKC's chairman Ron Menaker condemns
"Pedigree Dogs Exposed"
Then reinserts his head firmly back underground
Is this any way to lead the American Kennel Club through the genetic morass it is facing? On July 19, the chairman of the board of the American Kennel Club, Ron Menaker, signed a petition to the UK's Parliament to prevent the British Broadcasting Company from broadcasting a sequel to "Pedigree Dogs Exposed" (PDE), the 2008 BBC documentary which has turned the British purebred dog world upside-down.
Chairman Menaker did not stop at just adding his name to the petition to Parliament. He also wrote:
"Responsible dog owners, the dog loving public and responsible dog breeders should not be subjected to another piece of sensationalist fiction and tabloid journalism masquerading as a documentary. Any investigation of dogs, breeding or health matters should be balanced and fair. If the BBC insists on repeating this exercise in media sensationalism, why not present the truth about the progress that has been made as a result of responsible dog breeding and scientific research projects funded by organizations that truly care about dogs. For the BBC's next installment, how about 'Jemima Harrison Exposed'?"
Thus, the AKC chairman wants UK's Parliament to both ban the BBC from broadcasting its upcoming PDE-2, and to force the BBC to present an exposé of PDE's producer, Jemima Harrison. Putting aside all of the anti-Freedoms of Speech and Press and censorship aspects of AKC Chairman Menaker's comments, it is jaw-dropping that the highest ranking officer of the American Kennel Club would wage so public and vicious an attack against PDE and its producer, just as that same producer is putting together the sequel which Mr. Menaker so desperately seems to want to prevent.
Hullo, Mr. Menaker? Can you spell "Good Public Relations"?
One of the reasons PDE has had such a dramatic impact upon the British pedigree dog world since 2008 is that the UK Kennel Club and its breed clubs, including the UK's cavalier King Charles spaniel club, refused to substantively cooperate during its production. CKCS club members literally turned their backs on PDE's cameraman. But even those UK clubs had enough savvy to not publicly and personally lash out at Ms. Harrison, its producer.
On the one hand, AKC Chairman Menaker attacks PDE and it’s producer for not being "balanced and fair", and yet on the other hand, instead of offering information to help make PDE-2 more balanced and fair, he wants the British government to ban it! And investigate its producer, to boot! His head-in-the-sand approach is not going to work for the AKC, and if Chairman Menaker is not careful, soon Ms. Harrison may cross the pond to produce PDE-3, and re-pay him for his courtesies.
How the syringomyelia breeding protocol
could lead to the Popular Sire Syndrome
Many "D" bitches mated with the same "A"
genetic crisis for the CKCS
For corner-cutting breeders of cavalier King Charles spaniels, trying to follow the syringomyelia (SM) breeding protocol could lead to a uprising of the dreaded Popular Sire Syndrome*.
*A Popular Sire has been defined in canine research papers as having produced more than 100 offspring.
The current SM breeding protocol, introduced to the cavalier King Charles spaniel community in 2006 by the International Syringomyelia Conference, only requires that one of a breeding pair of cavaliers not have syringomyelia. The other cavalier of that pair may either have syringomyelia but without any symptoms – according to its magnetic resonance imaging (MRI) scan – or it may not even have been MRI scanned at all.
Specifically, the protocol provides that a dog classified as an "A" must be over 2.5 years of age and that SM is "absent or less than 2mm central canal dilatation in the C2-C4 region only". A "D" cavalier is one which is over 2.5 years and diagnosed by MRI to have "asymptomatic" SM, meaning that the dog has the disease but does not act like it does. That is one way a cavalier may be classified as a "D". The other way is to be over 2.5 years but to not be MRI scanned at all. So, as long as the dog is over 2.5 years and does not behave like it is suffering from SM, it is a "D" dog. This is known as a "default D" dog.
Most cavalier breeders have more female breeding stock than males. Having too many – in some cases even just one – intact males around can cause more problems than the males are worth. So, most cavalier breeders who do not rely much upon line breeding, will hire other breeders’ studs for mating, rather than keep the dogs in their own households with all those bitches around.
When a financially-challenged CKCS breeder with, say, a half dozen bitches as her breeding stock, considers the SM breeding protocol, she finds that MRI scanning can be quite costly. One thorough scan for just one bitch can cost thousands of dollars, when the ancillary procedures are taken into account, such as blood tests, anesthesia, radiologist and neurologist fees, transportation, etc. Multiply that cost by the number of bitches in the breeder’s kennel, and then maybe double that figure, since more than one MRI scan could be necessary during the breeding years for each bitch. Dealing with just this one protocol for this one genetic disorder could wipe out any hopes of the breeder breaking even on the litters all of her bitches could be hoped to produce.
An apparent solution to this breeder’s dilemma is the option under the SM protocol to not scan her breeding stock at all. If they don’t have symptoms of SM, then she can call all of them "D"s, hence the term, "default D". And if she can find a sire which has been MRI scanned and classified an "A", she could use that sire on all of her "default D"s and still satisfy the SM protocol.
But what about using that one "A" sire on so many "D" bitches? And what about all the other cavalier breeders who decide to take the same approach and also use that "A" male on all of their "D" bitches?
That would be a classic case of Popular Sire Syndrome (PSS). Yes, the current SM breeding protocol encourages corner-cutting breeders, with "default D" bitches, to use the same limited pool of sires, called "Popular Sires", in this case "popular" because they are among a very limited number of "A" dogs.
The PSS is believed to be one of the main causes for the spread of genetic disorders in any breed. As a result, geneticists have urged all breeders to avoid using the same dog for mating all or most of their own breeding stock, and also to avoid using the same sires that several other breeders have been using. Even the owners of the sires themselves have been urged to limit the usage of their dogs by breeders.
Cavalier breeders should not take the short-cut of calling their unscanned bitches "D" (for default), and then breeding them to the same "A" male, to satisfy the SM breeding protocol. But, if past history is a guide, many of corner-cutting cavalier breeders will do just that, and the CKCS community will face another genetic crisis soon enough, thanks to another round of the Popular Sire Syndrome.
CKCSC,USA's board admits Its ignorance
but not its stupidity!
After repeated denials, the CKCSC,USA's current board of directors finally admitted that its 1998 predecessor board really did endorse the real MVD Breeding Protocol. In the official minutes of the board's October 14, 2010 meeting, it says:
"In response to numerous inquiries and comments regarding the guidelines adopted by the CKCSC-USA, David Frederick clarified that guidelines are not medical protocols. The protocol suggested by a cardiology symposium held in conjunction with the 1997 [really was in 1998] National Specialty specified 2.5 years as the minimum age for first time breeding of dogs and bitches. This protocol was endorsed by an earlier Board." (Emphasis added, of course.)
So, there you have it. The current CKCSC,USA board admits that it was wrong when it claimed that its April 2010 breeding recommendations were "historic" and that "none had existed before"*. Unfortunately, what it did not do at its October 2010 meeting is re-instate the real, one-and-only MVD Breeding Protocol, which this current board un-ceremoniously dumped at its April 2010 meeting. Read "CKCSC,USA Dumps MVD Breeding Protocol" for those details.
The current CKCSC,USA board still endorses only a worthless breeding guideline which no panels of cardiologists or geneticists researchers have ever recommended, and which, they have told us, has not worked and would not work! Stupidity and callous disregard for the hearts of future generations of cavaliers still reign at the Cavalier King Charles Spaniel Club, USA!
*Interestingly, one of the current board members was also on the 1998 board which unanimously endorsed the real MVD protocol. Notwithstanding her inexplicable memory lapse, she now can say that she voted for it before she voted against it!
Beware the pimobendan/Vetmedin "EPIC clinical trial":
There is no upside
If your cavalier is in it, PULL OUT!
There comes a time when owners of cavalier King Charles spaniels must say “NO!” to participating in a pharmaceutical company’s study of its proprietary brand wonder drug. The on-going “EPIC Clinical Trial” of pimobendan is a prime example. EPIC is being sponsored by its developer, Boehringer Ingelheim GmbH, a German pharmaceutical company, which markets the drug under the registered brand name “Vetmedin”.
Background of pimobendan
Cavalier King Charles spaniels suffering from mitral valve disease (MVD) and in the late stage of congestive heart failure (CHF), often are prescribed pimobendan. This drug has been shown to improve the quality of life for dogs suffering from CHF due to MVD. It can be very effective at increasing the strength of the heart muscle contractions, thereby improving the heart’s efficiency to function as a pump, and increasing the blood flow to major organs. It even has been shown, in some studies, to actually reduce the amount of backflow of blood through the mitral valve and reverse the enlargement of the heart chambers.
But, there also can be negative aspects to pimobendan. It can have life-threatening (or worse) side-effects when prescribed for asymptomatic dogs or to dogs which, even though they have enlarged hearts and are in CHF, also still have strong heart muscles and good contractility. For those dogs, pimobendan has over-increased their hearts’ pumping ability and contractility to the extent that their mitral valves’ major chordae tendineae have been overworked and, in some cases, have actually ruptured, causing immediate death. (Click here for summary of three disturbing research reports about the inappropriate administration of pimobendan to dogs not in CHF, and a dire warning from Vetmedin's manufacturer itself.)
The U.S. Food and Drug Administration’s (FDA) 2007 report approving the use of pimobendan for dogs also contained the warning that the drug not be prescribed by dogs which are not in congestive heart failure. On each container of Vetmedin is the warning that “Vetmedin should not be given in cases ... where an augmentation of cardiac output is inappropriate for functional or anatomical reasons. Warnings: Only for use in dogs with clinical evidence of heart failure.” (Click here to read more about pimobendan and its downsides.)
The bad news EPIC trial
Pimobendan’s manufacturer’s EPIC Clinical Trial has no upside for cavaliers. The trial’s criteria are that cavaliers with some heart enlargement due to MVD but which do not have any clinical signs and are not in CHF, are to be given twice-daily doses of either pimobendan or a worthless placebo and nothing else. This daily medication (or placebo) is intended to go on until the dog develops heart failure.
We already know, from the extensive studies relied upon by the FDA in its approval report, that pimobendan should not be prescribed to dogs if they are not in CHF. Even the EPIC Trial's own website contains this pointed reason to not prescribe pimobendan at such an early stage. It states:
"In the recently published ACVIM Consensus Statement, there is no treatment recommendation for dogs in this stage of heart disease."
We also know that treating a progressive disorder like MVD with only a worthless placebo -- and nothing but a worthless placebo -- until heart failure results, can be an extremely risky protocol for any cavalier. It would be irresponsible of the cavalier’s owner and its cardiologist.
So, much like Hobson’s choice, you can allow your cavalier to risk pre-mature death due to being given pimobendan when it could do more harm than good, or you can allow your cavalier to not be treated with anything at all until it develops heart failure.
Just say NO!
Occasionally, or perhaps even more often than that, pharmaceutical companies’ motivations to sell their products tend to outweigh the ethical prudence they should display to not encourage inappropriate marketing. We are not suggesting that this manufacturer’s current EPIC Clinical Trial is such a marketing ploy. But knowing what we do know about the lethal dangers of prescribing pimobendan to cavaliers too early in the progression of their MVD, or to cavaliers even in congestive heart failure but still with strong contractility, this is a potentially terribly flawed study, and cavalier owners should not allow their dogs to participate in it.
In "Comparative adverse cardiac effects of pimobendan and benazepril monotherapy in dogs with mild degenerative mitral valve disease: a prospective, controlled, blinded, and randomized study", published in 2007 in the Journal of Veterinary Internal Medicine, the researchers found that "PIMO has adver se cardiac functional and morphologic effects in dogs with asymptomatic MVD."
In "Increased Mitral Valve Regurgitation and Myocardial Hypertrophy in Two Dogs With Long-Term Pimobendan Therapy", published in 2005 in Cardiovascular Toxicology, the researchers concluded "This is the first report to describe an increase in mitral regurgitation under clinical conditions in dogs treated with pimobendan. We also suggest that pimobendan may induce ventricular hypertrophy."
In Cardiac Care for Pets' (CVCA) "Pimobendan– A Silver Bullet?", published in May 2009, the cardiology department stated: "In a small study performed by CVCA, it was determined that after two to three weeks of Pimobendan therapy about 75% of dogs had an increased frequency of ventricular arrhythmias documented on 24 hour ambulatory ECG monitoring."
In the U.S. Food and Drug Administration’s (FDA) 2007 report approving the use of pimobendan for dogs, it stated this conclusion in a four week toxicity study of pimobendan administered to 30 previously healthy lab Beagles: "Conclusions: Pimobendan administered IV daily to healthy Beagles caused dose dependent increases in heart rate, mitral valve myxomatous thickening, left ventricular outflow tract endocardial thickening, and ventricular muscle ischemic lesions (multifocal subendocardial necrosis and scarring). The cardiac pathology seen in these dogs is typical of positive inotropic drug toxicity in normal dog hearts, and is related to the physiologic effect of the drug on contractility and exaggerated hemodynamic response."
On Vetmedin's website, it has this warning: "The safety of VETMEDIN has not been established in dogs with asymptomatic heart disease."
Chiari-like malformation HAS been re-defined!
Our January 28, 2011 editorial, "Maybe Cavaliers Don’t Even Have Chiari-Like Malformation (CM)!", pointed out that, in view of recent research reports, either cavalier King Charles spaniels do not have CM ("decreased caudal fossa volume") or CM needs to be re-defined to fit within these current research findings.
Well, apparently CM has been re-defined! On the website of syringomyelia researcher Dr. Clare Rusbridge, CM now is defined as "a condition characterized by a mismatch in size between the brain (too big) and the skull (too small). There is not enough room for the brain and the back part (cerebellum and medulla) is pushed out the foramen magnum." The foramen magnum is a hole in the back of the skull -- in the occipital bone -- leading to the spinal cord. Dr. Rusbridge goes on to explain that the cavalier appears to have a brain more appropriate for a bigger dog.
This new definition of Chiari-like malformation pretty much neutralizes the point of our January 28 editorial, so in the inimitable words of Saturday Night Live’s Gilda Radner’s character, Emily Litella, "Never mind!"
Maybe cavaliers don't even have
Chiari-like malformation (CM)!
It may be time to let Chiari-like malformation (CM) off the hook! For many moons, CM has been tagged as the "usual suspect" in the blame-game for a cause of syringomyelia (SM) in the cavalier King Charles spaniel (CKCS). But based upon recent studies, it looks like cavaliers do not even have CM!
CM is defined as, "decreased caudal fossa volume with caudal descent of the cerebellum, and often the brainstem, into or though the foramen magnum." The caudal fossa is the cavity within the hind portion of the skull, also known as the occipital bone. The occipital bone contains the foramen magnum, which is the hole at the base of the skull.
The implication has been that the smaller caudal fossa volume within the occipital bone would force the cerebellum (the hindbrain) to squeeze through that hole, the foramen magnum, causing excessive pressure on the cerebrospinal fluid (CSF) and resulting in the production of a syrinx. The conclusion was that it was the smaller size of the hind-skull that was to blame for that squeeze play and the consequent syrinxes.
However, three veterinary research journal articles published in 2009 and 2010 point to evidence that cavaliers’ hind-skull volumes are not different from other small breeds, particularly those with short muzzles, and that the percentage of the volume of the caudal fossa to the volume of the total cranial cavity did not differ significantly between CKCSs with and without SM.
Instead, the oversized cerebellum may be the culprit. These studies also found that the volume of hindbrain was significantly greater for young -- 2-years and younger -- cavaliers with SM than older dogs -- 5 years and older -- without SM. They also found that increased hindbrain volume in CKCSs with SM, compared to that of the hind-skull, was directly correlated with the size of the dogs’ syrinxes.
If the 2009 and 2010 studies are on the right track, then we may have to either re-define "Chiari-like malformation" or use another term to describe the disorder, since the "malformation" may not be of the skull, but of the brain. A re-definition could be "increased cerebellar parenchyma volume with caudal descent of the cerebellum, and often the brainstem, into or though the foramen magnum." But then, would that really be "Chiari-like", or just some other type of malformation?
So, indeed, the SM cavalier’s brain may be too large for its skull!
CKCSC,USA's board reinstates a third of
the REAL MVD breeding protocol
In our October 7 Editorial, we called upon the CKCSC,USA's board of directors to reinstate the REAL mitral valve disease breeding protocol at their October meeting. Well, apparently they did a third of that. Recall, if you will, that at their April 2010 meeting, they dumped the real protocol, which their predecessors had unanimously approved in May 1998 when the protocol was introduced. See our September 7 Editorial ("CKCSC,USA Dumps MVD Breeding Protocol") politely pointing out their act of virtual insanity.
In April, the current board replaced the REAL protocol with an odious, worthless version, in which they stated: "The CKCSC,USA recommends that prior to breeding any Cavalier, the dog have a clear rating at two years of age from an auscultation by a board certified veterinary cardiologist."
In the face of an onslaught of justifiable criticism, the board met in October and tweaked their bogus breeding recommendation thusly:
"The CKCSC,USA recommends that prior to breeding any Cavalier, the dog should have a heart clearance from an auscultation by a board certified veterinary cardiologist that is consistent with prevailing cardiology protocols; however, the CKCSC,USA recommends a minimum of a cardiology clearance at age 2.5 years by a board certified cardiologist."
Say what??? I suppose we should be grateful for whatever crumbs the board chooses to throw our way, but really!!! This October revision is only a miniscule improvement over their April abomination, and the bottom line is that, according to the researchers, it is still worthless. After all, whatever the CKCSC,USA board "recommends" is toothless at best. No breeders are bound by it, so why doesn't the board go all the way and actually reinstate the REAL MVD protocol that the Club stood by for the past twelve years until this board came along?
Why not add the other two-thirds of the REAL protocol?
• Do not breed any Cavalier under the age of 5 years, unless its parents' hearts were free of MVD murmurs by age 5 years.
• Do not breed any Cavalier who is diagnosed with an MVD murmur under the age of 5 years.
Come On, CKCSC,USA Board: MAN UP!!! Show the world that your Club really does take early-onset MVD seriously, instead of showing your incredible pride and your heinous contempt for future generations of Cavalier King Charles spaniels.
To CKCSC,USA's board:
Reinstate the REAL MVD breeding protocol!
Dear CKCSC,USA board of directors: Your next board meeting on October 14 is your chance to redeem yourselves. Reinstate the REAL MVD Breeding Protocol!
The Club’s 1998 board wisely endorsed the REAL protocol which the international research panel of heart specialists and geneticist drew up and urged all cavalier King Charles spaniel breeders to follow, at a minimum! They told us at the Club’s MVD Symposium in May 1998 that we could eliminate early-onset MVD in just a few generations if enough breeders faithfully followed it. Since then, we know that only a handful of cavalier breeders ever paid any attention to it, so twelve years after 1998, there has been no progress in ridding the breed of young cavaliers with bad hearts, suffering and dying all too soon. But that was no excuse for you to dump the REAL protocol at your April 2010 meeting!
In April, you had your chance to re-new the endorsement and urge all club members to follow the REAL protocol. Instead, you replaced it with a worthless recommendation to breed cavaliers "clear at 24 months", which no cardiologist or geneticist researcher has ever recommended. In fact, they told us in 1998 that breeding "clear-to-clear" has not worked and would not work!
You have ignored the research experts’ conclusions that, at a minimum:
(A) All four parents of the breeding pair be MVD-clear as of their 5th birthday;
(B) The breeding pair be at least 30 months old and MVD-clear at the time of breeding; and
(C) No cavalier be bred if diagnosed with an MVD murmur before its fifth birthday.
Just last month, Sweden’s Dr. Clarence Kvart reported that the Swedish CKCS club’s "clear at 24 months" protocol has not reduced the percentage of cavaliers having MVD, and as a result, the Swedish club is considering making the REAL protocol mandatory!
Whatever your purpose in rejecting the REAL protocol, now is your opportunity to redeem yourselves. You owe it to the future generations of cavaliers. Remember, the next edition of Pedigreed Dogs Exposed is focusing on you!
How self-absorbed can the CKCSC,USA board be?
Now, after the editorial CKCSC,USA dumps MVD breeding protocol first appeared on September 7, the CKCSC,USA has added to its website an introduction to the announcement of the board's April 29, 2010 decision to reject its 1998 endorsement of the MVD breeding protocol. The introduction falsely states:
"The Board took a historic step and established minimal recommendations for conducting health tests ... where none had existed before."
This is a very odd attempt to revise the club's history. The club's 1998 endorsement of the MVD breeding protocol was indeed "historic". The only thing which is historic about the board's April 2010 decision is that it has replaced the MVD breeding protocol with a worthless "clear at 24 months" recommendation, which the research experts told the club back in 1998 would not work.
In the face of the laser now shining brightly and critically upon the cavalier King Charles spaniel, beginning with the broadcast of Pedigree Dogs Exposed, one would expect the CKCSC,USA's board to take a giant step forward and, at the very least, re-new its recommendation of the MVD breeding protocol, if not make it mandatory for registering litters. Instead, the board in April of this year has pretended that it never had recommended the protocol at all, and then replaced it with nonsense. Why does the board now deny that it approved the MVD breeding protocol in 1998?
Taking a giant step backwards from its May 1998 decision endorsing the MVD breeding protocol, the board of directors of the Cavalier King Charles Spaniel Club, USA rejected that protocol at its April 2010 meeting. Instead, its board approved a watered down, proven worthless "recommended guideline", calling for the breeding pair to have MVD-murmur-clear hearts at only 24 months.
It has been twelve years since the CKCSC,USA sponsored the "International Symposium on Chronic Cardiac Valve Disease (CVD) in the Cavalier King Charles Spaniel" in Atlanta, Georgia in May 1998. The club invited a panel of veterinary cardiologists from the USA and the UK -- Drs. Andrew Beardow, James Buchanan, Virginia Luis Fuentes, and Bruce Keene -- and the renowned canine geneticist, Lennart Swenson from Sweden. Before a packed theater of club members, the panel reported on the severity of the disease and its pervasiveness throughout the breed. They stated these conclusions:
• MVD is the leading cause of death in Cavaliers;
• It is a hereditary, genetic disorder;
• There has been no statistical improvement in Cavaliers' mitral valves in the eleven years since the first studies; and
• The disease can be decreased and the age of onset delayed by following guidelines of only breeding Cavaliers who are over the age of 2.5 years, have hearts free from MVD murmurs, and have parents whose hearts were MVD murmur-free at age 5 years. No Cavaliers should be bred which have murmurs before age 5 years.
The panelists then introduced:
That same weekend in May 1998, the CKCSC,USA's board endorsed the protocol and then sent a verbatim transcript of the symposium to all club members, with this statement:
"In this 'Year of the Heart' in which the CKCSC,USA is instituting a number of programs geared toward the study and control of chronic cardiac valve disease, this symposium was organized to bring together international experts to present data and provide guidelines for breeders.
"We urge our members to follow their recommendations, and hope that we will attain our goal of bringing the prevalence, the age of onset, and the severity of the disease to the levels seen in other breeds of dogs."
The Club also mailed to its members annually, beginning in 1998, a Health Registry booklet, which included this set of MVD breeding guidelines:
Even with these strong endorsements, only a handful of cavalier breeders have faithfully followed the MVD breeding protocol. As evidence of that lack of participation, in March 2009, eleven years after the protocol was introduced, cardiologist Simon Swift stated: "In the UK and the USA, about ½ of all cavaliers [still] have a murmur by the time they are 5 years old."
Purebred breed clubs -- of which indeed the CKCSC,USA is one -- are obliged to educate breed owners on the nuances of the breed and oversee the breed’s health and welfare. The leadership of breed clubs owe a fiduciary duty, not to the club's breeders, but to the breed, to assure that the dogs are protected from irresponsible breeding practices and from the creation of future litters of genetically damaged puppies. Since most all cavalier breeders in the club have failed to faithfully follow the MVD breeding protocol these past twelve years, the responsible thing for its board to do, to protect the breed, would be to re-affirm the importance that its breeders comply with the protocol.
But now we find, twelve years after endorsing the MVD breeding protocol, that instead of doing that responsible thing, the CKCSC,USA board has dumped it and instead has contrived this totally bogus guideline which has been proven to be a failure:
"The CKCSC,USA recommends that prior to breeding any Cavalier, the dog have 1) a clear rating at two years of age from an auscultation by a board certified veterinary cardiologist; ..."
This new worthless guideline ignores the research experts' conclusions that: (A) All four parents of the breeding pair be MVD-clear as of their 5th birthday; (B) The breeding pair be at least 30 months old and MVD-clear at the time of breeding; and (C) No cavalier be bred if diagnosed with an MVD murmur before its fifth birthday.
Sadly, the Club's board has effectively thumbed its collective nose at the heart-health of all future generations of CKCSC,USA cavalier King Charles spaniels.