If you’re a type 1 Diabetic, do you stop being diabetic if you cut sugar out of your diet? If you have a genetic predisposition to alcoholism or drug addiction, do you prevent having alcoholic children if you abstain from drinking? If you’re allergic to peanuts do you cure the allergy by not eating peanuts?
NO.
You can prevent, limit, or forestall manifestation of a disease path with nurture, but this doesn’t mean that the disease path itself originates in nurture or behavior, and managing it in this generation does nothing to solving it in the population as a whole, especially going forward.
If your collie is MDR1, you don’t solve the disease simply by NOT giving them MDR1 drugs. It’s still there. The weakness will be passed on.
This is not a profound idea, but it’s a concept that I see abused regularly, even by people who claim genetic literacy.
Example 1: Uric Acid disease in Dalmatians
All traditional Dalmatians are homozygous for the disease gene causing Uric Acid disease. All of them have two copies. There’s no diversity on that one gene in the breed.
And yet all Dalmatians don’t suffer the problems the same. Does this mean the disease is not genetic? No. Does this mean that the best path to limiting the disease is a nurture strategy versus a genetic strategy? No.
The renal disease of the sort Dalmatians get is fleetingly rare outside of Dalmatians. Other breeds can safely process purines in their food and don’t produce excess uric acid which leads to kidney stones. We can give Dalmatians a special diet which tries to avoid the disease much like denying a genetic-alcoholic booze or avoiding peanuts for someone with the allergy.
Before the High Uric Acid gene was identified, you could even run an analysis on the disease expression across generations showing that its “heritability” was some X percent where X is less than 100. Meaning that if both parents had kidney stones, not all of their children necessarily would.
Idiots use this number to say that “it has a genetic component but is not fully genetic.” This is stupid, especially when we artificially limit our view to a population that is all essentially the same genetically.
“Not all Dalmatians get High Uric Acid disease! Therefore it’s food and we can manage food so we don’t have to change our gene pool!”
This ignores that of all the cases of HUA disease almost every single one comes from a dog with two copies of the bad gene. You can certainly alter nurture in an unaffected dog and get them to express the disease, you could overdose them massively on uric acid, overwhelming even their normal ability to process it. Sure.
But this no more makes the disease nurture than genetically homozygous Dalmatians not getting it frees it from being genetic.
Genes aren’t assured destiny. Expression is variable. Penetrance is not absolute. So what? This doesn’t change one thing about the strategies that must be employed to improve health in dogs. And yet all too often people who DON’T WANT to outcross use this uncertainty as some justification.
“I can manage my dog’s food and get somewhat better results, so I won’t dare consider outcrossing to introduce a healthy allele and eventually breed out this problematic allele. That’d be totally uncalled for!”
The logical solution is to zap that gene and not require an entire breed to be fed a special diet to avoid disease expression.
Example 2: Hip Dysplasia is caused by kibble?
Carol Beuchat has an article about Hip Dysplasia in dogs that points to kibble as the culprit, specifically too much of it.
The results of a study show a delay and a decrease in expression of HD in dogs feed less, who are presumably less fat, which presumably puts less stress on the hip joint, which would lead to less disease expression.
This is no more profound than not feeding peanuts to an allergic, preventing an alcoholic from drinking, and stripping the Dalmatian diet of the compounds they are unable to process normally.
It’s nice advice to people and it will certainly lead to less pain in dogs, but it’s no cure. It speaks nothing to the actual cause of the disease. Putting less stress on a weakened joint doesn’t cure the joint, it just doesn’t accelerate the disease as fast.
And yet Carol can’t help but say dumb things.
It seems clear that it has some genetic component (it is thought to be polygenic) but there are clearly environmental (i.e., non-genetic) influences as well.
This is boldly meaningless. Almost every single disease can be said to be both genetic and environmental. But not in equal measure, which is usually the next stupid thing said. It’s both, therefore it’s both equally and also therefore I don’t have to do anything about one because I can or can not control the other!
I can control the environment, therefore I don’t need to address the genetics. Or I cannot prevent X in the environment therefore it’s going to happen anyway at some rate and damn you if you remind me that genetics could drastically lower the rate no matter what the environment presents.
There has been some modest success in reducing its incidence in some breeds by screening programs, but for the most part it remains an intractable problem and the focus of many research programs.
Translation: Breeders have done next to nothing useful in combating HD in their breeds because they refuse to employ the most potent tools, like outcrossing and accelerated breeding and culling (which is how HD was bred out of many sight hound breeds). What breeders have done is said, heck, we’ll not stop our drinking but we agree to call a cab when we’re blotto and we’ll go to the hospital when we get alcohol poisoning. This decreases a few deaths here and there, so woo hoo. It does not, much like trying to breed out HD from within a closed pool with high saturation of the genes that cause it, remove the genes very fast.
In Dalmatians, it would be IMPOSSIBLE to breed out HUA disease because it was 100% saturated. It was FIXED in the gene pool.
So “breeding away” from the dogs that were diagnosed would do nothing, much like it did… it did nothing for all the years people tried to breed away from it from within the pool. Only the outcross made breeding away from it possible.
With HD we don’t have the candidate genes, BUT WE KNOW THAT HD IS PROFOUNDLY GENETIC!
How can I say that? Because it is almost entirely absent in several sight hound breeds. You can feed THOSE dogs whatever you want, limiting their kibble will not make the disease stats go down, doubling it will not make the dogs profoundly dysplastic. You can’t turn a Greyhound into a Lab by feeding it like one, you can not make it dysplastic with the normal environment which produces profoundly dysplastic Labs.
So if the Dysplasia is SECONDARY to the gene pool, talking about kibble is a diversion from reality. Greyhound breeders don’t have to feed their dogs special diets for HUA or HD. Because genetics.
Genetics trumps environment, even here.
Consequently, I was quite surprised to run across a paper (1) published in 2006 about a study that was able to substantially reduce in incidence and severity of hip dysplasia in Labradors – not by locating particular genes or implementing strategically-designed breeding programs – but by reducing food consumption.
And guess what, any and all benefits of denying calories to the Labs would immediately stop producing a reduction in HD expression in any and all future generations where such a diet was not maintained.
This is management. Not treatment. Not prevention. Not cure.
Great news, though. It is something that can immediately be done to stop current dogs from suffering. But Beuchat doesn’t run a wellness blog. She runs a breeding blog and diet is not a breeding decision. Diet is not a population genetics matter. It’s not genetic counseling strategy.
It’s a patch on a faulty tire.
In each litter, puppies were paired and one assigned to the control group and one to the treatment group. The control group was provided food ad libitum (unrestricted) starting at 8 weeks, and each puppy in the treatment group was fed 25% less than the amount consumed by its pair in the control group. Their weight was monitored and hips x-rayed at regular intervals throughout the lifetimes of the dogs.
Picture
Dogs that were fed less had dramatically lower incidence of hip dysplasia. How dramatic? Have a look at these graphs (modified from Smith et al’s paper).Dogs allowed to eat as much as they wanted showed evidence of hip dysplasia at younger ages than dogs fed less, and the difference between the groups got worse as they got older. By 6 years of age, 50% of dogs in the unlimited food group had evidence of osteoarthritis, compared with only 10% of dogs in the restricted food group. More than 50% of the dogs in the restricted food group still had radiographically normal hips at 12 years old; in the other group, 90% were arthritic. Dogs fed 25% less food than their pair in the control group weighed about 25% less throughout their lives. Heavier dogs had worse hips.
You want to know what’s missing here to make any statement about genetics? Another two control groups of Greyhound puppies fed in the exact same manner.
When none of those dogs would develop HD, you wouldn’t be fooled into saying such things like “some genetic component.”
If somebody was to submit a grant proposal to test a treatment that promised to reduce the incidence of hip dysplasia in dogs – not by 10%, or even 25%, but 50% – I should hope it would receive very serious consideration for funding. And what about the Canine Health Foundation and also the Orthopedic Foundation for Animals (OFA), which owes its founding to concern about the high incidence and crippling effects of hip dysplasia in dogs? A browse of the information on their websites about the disease makes no mention of this study or the potential benefits of lifelong food limitation.
Feeding Dalmatians a low purine diet (compounds that metabolize into uric acid) is a palliative. And frankly promoting it does more harm than good. It might help current dogs to not suffer, but it gives aid and comfort to the enemy: breeders who resolutely will refuse to do what is right for all future generations of Dalmatians by removing the disease entirely.
Feeding Labs less is a palliative. You can prevent wear on the joints and delay the disease, but the outcomes even with the low-calorie Labs were not spectacular. Their hips still went bad. Over 70% of them eventually went dysplastic. It bought them time though, more than half the more food Labs had HD by 6, the less food labs didn’t pass 50% until 12. Yay. But so what?
What is more likely: Getting the majority of Lab owners to restrict their dog’s diets or producing more sound dogs that will not get HD no matter how they’re fed, especially out of the normal given that we damn well know that the vast majority of any dog breed owners aren’t paying attention to studies?
Greyhound owners don’t need compliance from their owners.
“Less Food” – such a simple (and cost-effective!) way to substantially reduce the suffering of dogs, reduce veterinary bills for treatment, x-rays, and pain relief, and increase the amount of time the family dog can continue to lead an active life. Millions of dollars are spent every year looking for sources and cures of disease in dogs so that we can offer them better lives. Maybe we should direct some of this funding to an informational public service campaign to get this simple information to breeders and pet owners, and perhaps also some clear recommendations on dog food bags, maybe even brochures in veterinary offices.
Well meaning but stupid. Let’s divert resources from study which could solve the problem for EVERY future generation of dogs into advertising which will be an endless pit that needs to be filled every generation, forever, until someone actually manages a cure that doesn’t require owners to know and comply to some special diet.
I mentioned up top that there was also most certainly some genetic component to development of hip dysplasia, and that’s certainly worth talking about because there might be some surprises there as well.
Some? Again with the nonsense. All you need to remember is that HD was PURGED from a breed by genetic selection. Diet and environment be damned, it didn’t matter and the problem was eliminated.
Do you want an HD and HUA free breed or do you want a fussy food case that requires compliance to a so-so plan that might spare your dog some suffering, or not, but will do nothing to all the dogs in the future who you saddle with the same bad predispositions because “management” sounds more palatable to breed purists than doing something that’s actually an imposition like culling and outcrossing and preserving diversity while purging disease which requires strategies that aren’t nearly so easy as just going along with the corrupt current culture.
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Anton
Christopher
Lawrence Dillard
Lech
Stephanie
Essere
“Dumb”? “Stupid”? Did Carol Beuchat kill your cat or something?
It is absolutely legitimate to highlight the Purina study – and nowhere in that piece is Carol saying there’s no need to untangle the genetics. DJD is painful and limiting and the fact that diet alone can be so effective is of course worthy of dissemination.
Labradors are the dogs I grew up with. I’ve seen any number of them seize up as they limp painfully into old age- and it has, sadly, often been made worse by older relatives over-feeding them. A delay of up to *six years* in the lean-fed dogs is half a lifetime for a typical Lab – not to be minimised or down-played.
I use the Purina study evidence all the time with my rescue’s adopters in an effort to stop them overfeeding their dogs – to some effect at least.
Not at all. It’s not personal, it’s a fair assessment of what she wrote and how she wrote it.
Much like the UC Davis press release, I ran across this piece when it was being used by English Shepherd breeders as a reason they didn’t have to breed smart about hip because it was kibble! Kibble will set you free!
If you had a PhD write a piece that said the LUA Dal project was bunko because the problem could be solved with Science Diet, you’d call it out.
Carol’s piece is lazy and actually stupid because it gives aid and comfort to the enemy, specifically breeders who will now say “it’s not genetic, or at least not much, so we don’t have to change our ways. Blame the kibble.”
If Carol didn’t write a stupid piece, I wouldn’t call it stupid. As it is, it’s a totally fair assessment.
Or should we wait until the Pug people claim that the problem with them is kibble. They’re rampant for HD. You think cutting their kibble is the answer?
I don’t think so.
Write a stupid essay, get a “stupid” response.
I know this is months old, but I didn’t see it until today, so that’s my excuse.
I don’t agree that “dumb” is a fair assessment of Beuchat’s article. Limiting their dogs’ food intake is a step practically every owner can take to immediately and dramatically improve their dogs’ quality of life and longevity. In my opinion, this gives the article value as a tool for both owners and breeders.
The fact that certain breeders have lazily misinterpreted it to serve their own agenda doesn’t necessarily make it “stupid,” although it is irresponsible on the part of the breed club to disseminate it in such a way. Where in the article did Beuchat discourage research into long-term genetic and selective breeding-based solutions to hip dysplasia? Looking through her other blog posts, it seems like she has written quite a bit about the benefits of genetic diversity in breeding programs.
You claim that the absence of hip dysplasia in sighthounds proves that it is a genetic problem, but it also supports a correlation between hip dysplasia and weight. Breeds of dog that are heavier relative to their size (such as pugs), like the heavier labs in the study, tend to have higher incidences of hip dysplasia than more lightly-built breeds. A greyhound weighs half as much as a mastiff of the same height.
Of course, that doesn’t mean there is no genetic component to the disease, but it does raise doubts about your assertion that the cause is “profoundly genetic.” Your claim that hip dysplasia was eliminated from sighthounds by artificial selection was news to me – I would love to see the sources on that if you still have them.
You have a valid point regarding the complacency of many breeders on the issue, but it’s hard to take you seriously when your reaction to a factually correct, thoughtfully written article is to insult the author and belittle her viewpoints simply because they don’t explicitly support your preexisting beliefs about the cause of canine hip dysplasia.
> Carol saying there’s no need to untangle the genetics. DJD is painful and limiting and the fact that diet alone can be so effective is of course worthy of dissemination.
Except people are using her poorly worded and ill thought out piece (she’s fundamentally wrong, let’s not forget, the SINE QUA NON is genetic, not kibble) are using it for specifically the purpose to claim that no, they don’t need to figure out the genetics, kibble is easier.
If you’re not going to take “we can feed them purine free food” as a reason to not outcross the Dalmatians, you shouldn’t accept the careless interpretation Beuchat pulled on the Purina study.
> A delay of up to *six years* in the lean-fed dogs
And here’s where we actually need to look at the study and methodology. There’s actually no good indication that the kibble change has produced a profound difference in the hips. The study didn’t track these dogs with X-rays showing their laxity over time or their DJD over time.
At best we can say with a poorly small sample size and no control for genetics, that fat dogs get diagnosed sooner.
Which is on its face a no-brainer. Dog A and B can be in the same amount of pain from their DJD but if dog A is obese the owner is more likely to notice than if the dog is not. Dogs mask pain.
But Carol has ZERO business even invoking genetics in relation to the Purina study which doesn’t in any way speak to the issue.
“It’s kibble, not genetics” is the take away and that is asinine to allow from someone who claims to promote the actual effective solutions to the issue.
It’s an incorrect omission entirely against interest. And thus STUPID.
And your rescue adopters are irrelevant. Of course we should tell people to not have fat dogs. This is not controversial, nor is it poorly understood. Compliance is poor, perhaps, but “edumacation” on the issue is not actually the problem.
Your rescue dogs are NOT breeding stock and they are not factoring in to opening stud books and outcrossing. This idiotic slant on the Purina study IS being used as supposed fodder against actual successful breeding methods.
Allowing that: dumb.
And let us not forget that off loading genetic stewardship responsibility on to FOOD is a major (and poor) argument that breed purists LOVE to use. They continue to produce genetic monsters and then the second they get called out for producing them, “well it’s the food, I can’t help what my puppy buyers feed!”
And the popularity of blaming food and “der toxins in the water!” and all the other conspiracy theory level bullshit. You must certainly know this, no? You must see it on your blog. It’s not us, the Fancy, causing trouble, global warming is killing the dogs! DER FOOOD IST BADZ! You must feed this brand that gives me a kickback!! Oh, your dog has fits, well you must not have tickled its toes enough as a puppy.
All that bullshit is finding comfort in the idiotically poorly worded post by Beuchat that has no business pushing all the wack-a-doodle dog whistles (it’s the food! It’s the food!) and in any way belittling the genetic component.
The genetic component is the only one that matters. It’s the only cure. It’s the only way out. It’s the only way to actually STOP suffering instead of delaying it a bit.
Totally agree Chris…Genetic Diversity and using the new breeding technology is the key to eliminating genetic weaknesses in our pure breeds. It is just a ‘cop out” to those protecting old breeding protocol that developed these health issues in my opinion. https://www.betterbred.com/why-genetic-diversity/
Other studies indicate “”Other studies
indicate we are only dealing with two to four genes.”
To add further optimism, Brewer points out that there are reliable tests available that offer some help with…”
http://www.thelabradorclub.com/uploads/file/hip_dysplasia.pdf
“CLINICAL IMPLICATIONS:
This report gives practitioners documented proof that genetic selection will work to improve hip quality. Dog breeders must be advised to be patient, however, to allow enough generations to elapse to make meaningful genetic change.”
Resource:
http://www.ncbi.nlm.nih.gov/pubmed/9154200
“Or, maybe we’re talking about three genes—two that are responsible for CHD and one that is less involved,”
Brewer says. “That, too, would be a different testing method, because it would mean we would have to run two tests.
Obviously, we will develop a test based upon whatever genetic data we have indicating which gene or genes produce
the most significant amount of risk for CHD.”
Agree seeing people over feed. Witnessing the lack of mobility and heavy breathing of their dog is a sad expression of loving them. Just as sad to see their dog’s paws spread out due to lack of paying attention to those toenails with lack of exercise. However, good nutrition begins when puppies are weaned. Actually begins in the womb and mother not getting bacteria infections for example.
The problem that x-rays are limited just as in human medicine. Forty years…
http://www.offa.org/history.html
http://www.offa.org/hd_grades.html
Do you not find it interesting the expansion of disease testing for developmental HD by this same registry? http://www.offa.org/dnatesting/dm.html
Just as I have request of two new clients of German Shepard want a new puppy of another breed with parent testing for this disease.
Christopher, you have a point. I listen to a great deal of this from breeders too. Almost everything is genetic.
As an aside my 10yr old Lapphund has developed renal failure. I have turned her blood work around by diet. I have not (sadly) undone the 75% of her kidney tissue that has gone forever. Nor have I changed the age of onset of disease. That is her genetic predisposition.
I share frustration with all the dog food glitz that implies you can keep your dog healty by feeding some all natural, grain free blend enhanced with this and that and containing some exotic ingredients (also costing an extra $10+ for a big bag). However, I don’t think the Purina study should be discounted. Fat dogs do have more health problems. As for the equivalent study with greyhounds. . . .sure, it would be wonderful to have. BUT long term feeding trials of any sort (the Purina study went for 10 years) are almost unheard of. Eukanuba did another 10 year feeding study on Labbies . . . with no control group and no scientific documentation. I’ve looked and can find no others. I wish it were easy to find better evidence. But long term feeding trials are expensive and there’s little to motivate anyone to conduct them.
Hell’s bells. If food QUANTITY were not a problem, medical science would not be so concerned about human obesity. It is extremely well established that carrying a lot of extra weight is hard on the body and adversely affects rates of diabetes (type 2), heart disease, and cancer . . . as well as being hard on joints.
As Labrador breeder (now retired) I protest. The Labrador community is not in denial of genetics as a component in HD (or elbow problems). Scoring of breeding stock is almost universal among registered Labrador breeders, and discriminating buyers look for low scores and evidence of low scores in the bloodlines. Ok, I know you prefer PennHip. But you claim the OFA-using breeders are in denial of genetics. The BC community may be in denial, but the gun dog community isn’t.
My old girl (Labrador) is 11 years 11 mo. She runs 5k a day with me and shows no sign of arthritis. She scored out at 2:1 hips and 0:0 elbows. I keep her lean and well exercised. I bred her five times, always to studs with excellent hip and elbow scores . . . resulting in 48 pups. Still got a couple pups who have had HD or ED. One of them had to be euthed because, by one year, all four limbs were bad enough to require surgery. The other is pretty comfortable after drastically reducing her weight and keeping her on NSAI’s.
Because the genetics of hip and elbow problems is complex, breeding can’t resolve problems easily or completely. Diet, particularly avoiding over-feeding, CAN greatly affect the way that genetic problems manifest themselves. My guess is that exercise is also important in how badly the propensity to HD is experessed, but there is pathetically little study of this.
You are restating what Christopher wrote. No less and no more.
Christopher’s writing needs restating. My restatement is minus words like ‘stupid’. There are many axes being ground here. IMO ‘feed less’ and ‘breed smarter’ are both useful and important messages. No need to make them warring camps.
As far as I can deduce, there is only one axe being ground: that all ×600 dog dideased , and as examples HD andHUA, are genetic. The old Purina study only proved that less food is better than too much. That is also true with humans. But less food does not change genes. It may influence their expression. Period.
Dorothea Penizek I totally agree diet is not the answer to responsible breeding ethics although believe in feeding something better than Purina. Avoiding commercial dog foods that use synthetic proteins, and ingredients of “the disease dead and the dying” I have been following the Poodle leaders on a replacement for old breeding protocol knowledge and their findings are fascinating.
Stupid is fully justified. I’d go further, it’s sabotage to the entire effort of promoting breeding strategies that will actually result in generational change.
The fact that her work is already being used as a weapon by the breed purity establishment on NOT CHANGING A THING about how they breed is already proof that the damage has been done. You’re misguided if you think I’m making them warring camps, Beuchat already undermined a major issue that calls for outcrossing (HD) and makes it seem like a weapon for the “blame anything but our breeding culture” camp who is already fond of claiming anything other than rampant inbreeding and closed stud books are to blame for everything.
As I proved the thyroid function as a breeder found what I called the fat gene now has some genetic studies and findings. My question for decades was why between litter mate study…from birth to death one or two offspring would have what I named the “Fat Gene”. They all ate the same food and amount. One almost to thin ..while other litter mate fat. We had for the fat ones …Green Bean Diet.
“In addition to proteins in tissues and body fluids, gene expression profiles or circulating metabolites suitable biomarkers might include genetic variants. Genetic analysis of common forms of obesity has revealed associations with a range of individual genes, each of modest effect, but although individually these markers have modest predictive value, typically conferring a relative risk of 1.2–1.5, they might be much more informative when used in combination? Despite replicated associations, no systematic analysis of the utility of these key genes, and their protein products as biomarkers for obesity-related health risk, has yet been carried out. The challenge will be to understand how the data can be combined, incorporating new information from proteomics and metabonomics, to define a minimal effective set of biomarkers for risk prediction. These types of articles are just more of the propaganda to convince one that the tool most important to a respectable breeder is Diversity. Everything else is just smoke and mirrors in my opinion to protect the historical fantasy of pure breed club.
http://jn.nutrition.org/content/136/7/1940S.full
Off topic. The duscussion is ot about what causes fat but about hip dysplasia.
Dorothea Penizek to really understand what causes the mammal body to create fat , diseases such as hip dysplasia one must likewise address the biology of genes. Example: Point mutations are the most common type of gene mutation. Also called a base-pair substitution, this type of mutation changes a single nucleotide base pair. Point mutations can be categorized into three types:
Silent Mutation: Although a change in the DNA sequence occurs, this type of mutation does not change the protein that is to be produced. This is because multiple genetic codons can encode for the same amino acid.Amino acids are coded for by three nucleotide sets called codons. For example, the amino acid arginine is coded for by several DNA codons including CGT, CGC, CGA, and CGG (A = adenine, T = thymine, G = guanine and C = cytosine). If the DNA sequence CGC is changed to CGA, the amino acid arginine will still be produced.
Missense Mutation: This type of mutation alters the nucleotide sequence so that a different amino acid is produced. This change alters the resulting protein. The change may not have much effect on the protein, may be beneficial to protein function, or may be dangerous. Using previous example, if the codon for arginine CGC is changed to GGC, the amino acid glycine will be produced instead of arginine. This topic of biology and genes could be too heavy for the average breeder?
Jennifer Robinson, I read no axes being ground here. I join Christopher with the frustration of poor educational material being provided to the public. The truth about HD is problematic to responsible breeders. Only through usage of modern technology breeding protocols …not excuses can once again Pure Breed Canines due to popular sires (matador breeding) cleanse and get out of the bottleneck of ultimate extinction breeding such diseases. We should be aware that Carol’s site is a commercial endeavor. Just as we must recognize OFA’s were a knee jerk solutions decades ago.
You don’t get it. There’s no problem with the “fat dogs are bad” message. But it’s EASILY the #1 message in dogs. This is not a mystery. Fat shaming fat dogs is perhaps the most popular facebook past time of dog people. The message is not rare, it’s not under appreciated. We CERTAINLY don’t need to spend money on an ad campaign, taking it away from scientific research, to tell people to SLIM DOWN YOUR DOGS.
Throwing the ONLY means to actually make progress against HD under the bus in the process? Is evil. Stupid and evil.
I do get it Christopher when first began OFA there were less than 2,000 Collies ever evaluated when tens of thousands had been bred. Year was 2000 when the “powers to be” confronted me at a National Breed Club Show. “Why are you doing hip evaluation…Collies don’t have hip problems. My answer, “How do you know if you do not test?” When I achieved all OFA good and excellent Collies but had them come up crippled at eight years old …What good was the screening as a breeder of OFA?
Yup. And? We ALL know this. We know it in humans, we know it in dogs, and the lecture has reached saturation. There are no fat people out there who are mystified that being fat is unhealthy. Still not changing the rates of obesity.
The ANSWER there, is the same as the answer elsewhere… until there’s treatment that takes behavior OUT of the equation, the issue will not change. It’s like bitching at alcoholics that they should just put down the brown bag. GOOD LUCK WITH THAT.
Beuchat’s idiotic article is both factually wrong, dangerously misleading, and being used by establishment-thinking breeders to justify NOT changing the status quo. Putting a “thinner dogs are better” mask on it does not change any of that.
I agree because the Pure Breed Clubs want to keep their Great Champions and the Pillars of the Breed foundation breeding homage in tack. The article was despicable and reprehensible to the progress of saving our pure breeds from disease and some from Extinction.
And yet how many of them have done any sort of outcross to a sight hound breed to bring in better hip genes?
They ARE in denial if they think they can purge bad hips breeding only within their closed gene pool. For all we know the genes are already fixed or near-fixed in that breed and trying to breed to the few dogs that themselves have decent hips DESPITE their genes, is not going to produce profound results. And it will certainly create even more of a genetic bottleneck.
Scoring stock is necessary, it’s NOT SUFFICIENT.
Bullshit. Explain why there’s virtually no HD in Greyhounds. They are a LARGE BREED DOG. Almost all their peers of that size and larger have horrible rates of the disease. Tell me why they don’t have it when they as a rule have their hips stressed greatly?
Why? Because BREEDING DID RESOLVE THAT PROBLEM COMPLETELY.
So be honest. Breeding within a closed gene pool, further reducing and concentrating the inbred stock, chasing after the few decent hips in any give breed, is NOT going to resolve the problem. And the only reason we’re NOT talking about the sure-fire-cure is because it sounds like too much trouble and violates the religion of dog culture creating breeds-as-species that SHALL NOT BE MIXED!
Which is PERFECTLY reasonable if you’re a Vet giving your client advice on an already-bred dog and how to manage their disease. This is not breeding advice. This is not population health advice. It’s patient management. Beuchat is actively selling herself as an expert to BREEDERS and population genetics, population structure, population health issues. And the way she wrote this article and the specific words in it (I quoted a bunch of them) are dangerously counter productive, wrong on their face, and an almost unforgivable level of misrepresenting science and genetics to people who are WANT to find any support to maintain the status quo.
For me it reveals a major lack of understanding on her part. Stupid is hardly unjustified. It’s worse.
Christopher I totally agree with your point of view once again. HD is a complex genetic disease. It is not a simple one gene mutation that causes the expression of the disease. Similar to all the most current genetic markers on DM and DMS. These recent new genetic markers only reveal “risk factor” of developing disease. I refer your readers to your posting on three Genetic Mode of Inheritance. Your readers need to understand how the immune system is genetically inherited not by the accepted knowledge of the shuffle of genes but in a group of genes. I might have made it over simplified but best for those who have not studied as I have done. I understand to some degree the biological approach of Carol as mammals. However it is protein and such issues of synthetic protein of GMO certainly would have impact on mammal’s inability to properly be able to use the synthetic protein. Recent research is uncovering the negative health issues on even human children.
Examples: https://ghr.nlm.nih.gov/gene/SOD1
“Now understand The Orthopedic Foundation for Animals has a DNA saliva test to screen for the mutated gene that has been seen in dogs with degenerative myelopathy. Now that a test is available the disease can be bred out of breeds with a high preponderance. The test is only recommended for predisposed breeds, but can be performed on DNA from any dog on samples collected through swabbing the inside of the animal’s cheek with a sterile cotton swab or through venipuncture.”
“The test determines whether the mutated copy of SOD1 is present in the DNA sample submitted. It must be interpreted with caution by a veterinary clinician in combination with the animal’s clinical signs and other lab test results.”
The results reported are:
Normal / Normal (N/N, or ‘clear’): The dog does not have the mutation and is extremely unlikely to develop degenerative myelopathy. There have been cases in which dogs that tested clear were found to have DM upon necropsy. This information was given to Dr Keller from the OFA. Dr Coates performed necropsy. It is important to note the OFA statement on their website that states “Recent evidence suggest that there are other causes of DM in some breeds”.
Normal / Abnormal (N/A or ‘carrier’): The dog has one mutated copy of the gene (is heterozygous) and is a carrier but will not have degenerative myelopathy though there has now been some cases of heterozygous carriers developing DM.[3] It will be possible for it to pass the mutation to offspring. A thorough examination of the dog’s pedigree and DNA testing should be undertaken prior to breeding a dog with this result.
Abnormal / Abnormal (A/A or ‘At Risk’): The dog has two copies (is homozygous) for the mutation and is at risk for degenerative myelopathy.
Hmmm… Philosophically I think it is relevant to consider this in an evolutionary context. Although I don’t really disagree Christopher, it does occur to me that this “disease” may be considered to be a failure to evolve to cope with the abundant food supply for domestic dogs now. Could it have been there all along? Could it? Is it now only manifested due to these changes in environment? I’m not arguing against your proposed remedy, only trying to point out that inability to cope with changes in the environment perhaps needs a fuller consideration than to label it a disease.
Sure, it’s a fair point. Same with humans and obesity. We and our dogs are not evolved compared to the major changes in the type, quantity, calorie count, etc. of our food. But this doesn’t mean Type 2 diabetes, obesity, etc. are not diseases. Even if they are caused by our bodies being at odds with our current culture.
You and I are humans who are already bred. Our genes are fixed. We don’t yet have the ability to edit our genes on the fly. So we can ONLY look at how to avoid the disease paths with behavior. It’s our only option. But as DOG BREEDERS our responsibility AND power is to change the genetic profile for future generations of dogs.
We know things like the faster a puppy grows up the more likely it is to have HD (except Greyhounds … they are a larger breed that grows up fast like most other large breeds). So is the answer growing up fast? Is the answer being larger? It’s true in all those other breeds. But all those other breeds are also not built for speed. Breeding for speed has purged HD from Greyhounds. HD is very limited in other speed bred sighthounds, but we do see it in those same breeds that have no longer been bred to a speed standard but instead a pretty show ring side gait standard. It’s not inconceivable that speed requires both tight hips and tight ligaments, etc. and that swooshy side gait selects for the opposite.
So pretending that it’s just size or rate of growth forgets that most other large dogs are not a random sampling… many large dogs do the same thing… be large and menacing or be large and lazy or just be large.
Greyhounds and other sighthounds are large AND fast. And fast was good enough to overcome the disease path that has been tied to being large. And what of Pugs and such. They are small. They still have rampant horrible hips. They do not grow quickly. They probably are obese vs. body frame size.
Anyway… it’s a disease because it causes pain and suffering and we don’t have a reason at this point in evolutionary history to believe that there’s some benefit to it or a benefit that outweighs the damage done.
Just like in humans… being able to extract more fat from food per bite of the same food might have been a major advantage to our ancestors 100,000 years ago or more. People who are now obese on a modern diet likely survived famine in the past. Yay. But on a practical manner, it will be easier to end obesity related problems by short circuiting our biology than it will be to change our culture to return to wandering humans eating low calorie foods like our ancestors.
Christopher you bring a very good point…What is the most practical method to address mutation in genes causing disease involves many topics One topic that Vets and Animal Rescue programs will rise out of their chairs likely and scream: mandatory spay/neuter however, for me worth the backlash due to health risks associated with it.
Studies reveal that early spay and neutering raises the risk factor of cancer in our canines. https://niceorg.wordpress.com/2009/02/04/early-spay-and-neuter-causes-cancer/
Spay and neutering before the growth plates close rises the risk factor of HD. Controversy based on an exaggerated point of view. However let us consider the other functions of hormone removal for example
Hormones do lots of thing besides
sexual development. They regulate growth, muscle, moods, brain- cognitive, feelings..hormones
most significantly plays a roll in bone growth and density this study says 70% more likely to get
HD if spayed before 5.5 months of age! Both estrogen and testosterone build bone.. A puppy
spayed young will grow taller, generally will have a narrower chest and lighter bone and a
smaller more narrow head of their un-neutered counter parts…. We also can consider the behavior problems. The biology is a critical point to consider as breeders and we have voided all guarantees if our pets genetically tested in our contracts are spayed and neutered too early.
There is nothing philosophical in my opinion about outdated breeding protocol and closed registry to block genetic diversity by the Kennel clubs.
It’s news to me that Carol Beuchat emphasises environment over genetics as a solution to inbreeding disorders…..
Could I be missing something here?
Yup. She does not want to offend her purebred fanatics.
Yes, Dorothea got the same opinion from reading Beuchal to get them to enroll in her classes. However, understanding the biology of gene mutation that causes malfunction of proteins would be considered keynote in development of disease.
In my reading, science doesn’t back your claims. According to veterinary literature, HD is only moderately heritable. See eg., http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0039620 http://www.ncbi.nlm.nih.gov/pubmed/21737322 also lit review in krontveit’s thesis cited below. The analogy to Dalmations with HUA doesn’t hold. HUA is a condition with known cause in a single gene and can be prevented easily by outcross/backcross. The causes of Type 1 diabetes are poorly understood . . . .but the role of diet and exercise in Type 2 diabetes is decisive.
There seems to be a consensus that massive dogs with massive bone structure are more prone to HD. see, eg., http://cal.vet.upenn.edu/projects/saortho/chapter_83/83mast.htm or look at data in offa.org. Sight hounds are less affected. Out crossing to a sight hound should work IFF you follow the outcross by selecting for sight hound skeletal architecture. Thanks, no. I don’t want a Labrador that’s built like a greyhound.
Furthermore, greyhounds may not be as immune as you claim. OFA data from dogs born 2011-2015 show as many greyhounds with HD as with ‘excellent’ outcomes. Granted, it was a small sample. For the same years, Labbies had three times as many excellents as dysplasic.
Would be good to have better data.
Krontveit didn’t study greyhounds, but found 10% incidence of HD in Irish wolfhounds, plus he found that the effect of chronic HD on wolfhound survival was much worse than it’s effect on survival in Labradors.
http://www.knickerbockers.se/upload/Krontveit_PhD_thesis_2012.pdf
As for the relative efficacy of outcrossing vs. selective breeding within the breed, it’s going to vary. Some breeds have much larger effective population sizes than others. Outcrossing is far more important for small breeds descended from a bottleneck situation or created from a small number of individuals, eg., Dalmatians. I think both GSD’s and Labbies could make great improvements by sticking within their breeds (though I wouldn’t turn up my nose at aflattie cross Lab).
Good comment, Jen, but let me elucidate where I think you misunderstand my points and genetic terminology.
The heritability calculation does not say what you think it says. To wit, this quote from wikipedia (albeit a less desirable source, but one which we can both easily access) should explain:
https://en.wikipedia.org/wiki/Heritability
So I don’t think heritability means what you think it means.
More so, it is merely a measure made under assumptions. We can easily game it, and let me show you how.
If there is a disease path that has a sine-qua-non (without which it does not occur) gene, say MDR1, our estimates for heritability can be easily gamed by altering the environment and the sample we are studying. If our sample has MDR1 dogs, collies, and non-MDR1 dogs, we could say that oh dear, MDR1 shows up only in this population, across the other common environment. Therefore it must be highly heritable.
But if our sample is only MDR1 dogs, and we have not identified that it is the drugs that cause the issue yet, we would say, oh dear, the disease appears random. It does not travel in families, but heck it looks like certain cities in the country have higher rates. Low heritability, must be environment.
If our sample only includes MDR1 dogs and we don’t know this, we assume they are a random sample of all dogs, we might even say that it is entirely environment once we see the disease pattern clustering around dogs living in cities where the drug is commonly used. We might even say “that drug is a toxin” and the disease path is entirely environmental.
All humans lack the ability to safely digest arsenic. We call arsenic a toxin. We don’t classify people as having arsenic susceptibility disease. We could though, if we found a gene that allowed humans to safely consume arsenic.
So for MDR1, no matter what any study says about its heritability, the sine-qua-nature of the gene-to-disease means that we can, as breeders, remove that gene from our populations and obliterate the disease expression. We could also destroy all the drugs and eliminate the disease expression. But as a practical matter, it’s a better argument that the drugs are better to keep around and use and the gene is not, so do away with the gene and keep the drugs makes more sense.
Talking about kibble and HD is rather like giving breeders the excuse that they can just NOT treat their dogs with MDR1 and not have to worry about it. Sure, it’s a half-assed partial approach to the problem, but it is not in any way a good approach for POPULATION considerations and BREEDING ethics and supporting the status quo of more inbreeding, more closed gene pools, more diversity loss, etc.
Of course feed your dogs less. That’s not controversial, it’s not even NEW or important in light of HD. The dog community and Vets have been screaming about dog obesity for a long time.
We want to make REALLY good progress against HD, we remember that it’s not a disease of behavior. It does not originate in obesity. It is genetic. We solve the genetics and the behavior becomes much less relevant, much like solving MDR1 means producing dogs that can have any of the medications.
Christoper agree why we will see Poodle/ Lab crosses Doodles that look exactly like a Poodle. I would like to discuss a breed many might not know very much. However, most know about: The Irish Red and White Setter. Here in America we bred for the Red until recently when AKC brought them into the registry.
The solid red setter first appeared in Ireland in the 19th century. Its earliest ancestors primarily were red and white. While its precise ancestry is the subject of debate, some speculate that the Irish Setter descends from crosses of Irish Water Spaniels and Irish Terriers. According to other experts, it is more likely that the breed’s progenitors were English Setters crossed with Irish Water Spaniels, Springer Spaniels and Pointers, with some Gordon Setter blood thrown into the mix.
“The average life expectancy for the better know Red Setter American Irish Setter is 11 to 14 years. Breed health concerns may include arthritis, bloat (gastric dilatation and volvulus), canine leukocyte adhesion deficiency, entropion, eversion of the cartilage of the nictitating membrane, corneal ulceration, epilepsy, hip dysplasia, hypertrophic osteodystrophy, hypothyroidism, insulinoma, Irish Setter hypochondroplasia, congenital idiopathic megaesophagus, melanoma, vascular ring anomaly, osteosarcoma, patent ductus arteriosus, progressive retinal atrophy and von Willebrand disease.”
The breed was developed to locate birds with its keen sense of smell and, once the prey was discovered, to hold its position (instead of chasing the birds) to avoid entering the line of fire. The first Irish Setters were imported to America in the 1800s to work as gundogs on game, particularly ruffed grouse, quail, prairie chickens, woodcock, partridge, pheasant, wild duck and teal. A legendary setter named Elcho, imported from Ireland to the United States in 1875, was one of the first of his breed to be a phenomenal success in both the show ring and the field. However, most sportsmen did not continue breeding and refining the Irish Setter for public field trial competitions. The Llewellin Setter and the Pointer eventually cornered the market in that sport, although the Irish Setter remains a competent hunting companion and high-class shooting dog, pointer and retriever in its own right.
http://www.exclusives-irws.be/history.htm
Please note the issues of HD
http://www.dogbreedhealth.com/irish-red-and-white-setter/
Clearly Kibble could be factored into the HD issues but inbreeding protocol and gene pool bottleneck outweighs this defensive masterminding.
And are massive dogs with massive bone structure a product of kibble or GENETICS? Hrm?
And what does that say of Pugs? They are neither massive nor have massive bone structure. They are one of the worst HD breeds. And I assume you won’t make the argument that by some magic power all Pug owners are feeding their dogs differently than all other breeds.
Nor those Greyhounds. Are Greyhound owners magically controlled to not feed their dogs the same as Lab owners and Border Collie owners and German Shepherd owners?
Structure is genetic. And what if it is structure? You might not want a sight hound structure in your Lab, but then you are inherently saying that you prefer Labs as they are now, with their current structure, AND all the HD suffering thatcomes with it, versus making Labs look a bit different and removing that problem. I’d call that a moral and ethical issue right there.
It’s one that is made all the time by qualzucht fetish breeders. I WANT my Pug just the way it is. I WANT my Dalmatian just the way it is. I WANT my Chinese Crested just the way it is. I WANT my Dane just the way it is.
Your point is valid in most breeds with a larger gene pool. However, a popular sire could put even the Labs in the same position and has from friends in the breed. New findings especially with the progress Poodle Breeders reveal that genetic differences occur within the same litter. In other words, genetic diversity can be found within the same sire and dam breeding is now being discovered by breeders that are testing for Genetic Diversity. I agree would be great if we had better data but improved Breeder friendly education Example:
Dr Carol Beuchat is a vertebrate biologist.
http://www.instituteofcaninebiology.org/carol-beuchat-phd.html
I would have believed Beuchat would have included such important information breeder friendly such as this:
https://www.brightstorm.com/math/biology/molecular-biology/genetic-mutation/
I don’t totally disagree the search for external factor that may prevent disease such as HD and diabetics but the search for genetic and biological factors created by mutation in cells must continue to be address for responsible breeding of pure breeds. This topic of biology is deep and totally understand how difficult with all new discoveries with new technology. . Many diseases run in families without any genetic cause because of shared habits such as food choices, exercise, sun exposure, smoking, exposure to environmental chemicals, etc. While the risk of hip disease is slightly increased when one child or parent has the disease, not just canines. Should be factored into the equation. The answers are complex and no one is handing out the solution on a silver platter.
https://www.brightstorm.com/math/biology/molecular-biology/genetic-mutation/
Hahahahaha. Hahahaha. Hahahah. Oh dear, did you really go there? In the “OFA data from dogs born 2011-2015” there is only ONE SINGLE Greyhound that was found to have HD! One dog. Because only 7 dogs were tested over those 5 years. Hahahaha. Ok, so yeah, do I even need to respond to this? OFA is not a random sample. It’s not large numbers. It’s not blind. It’s not anything close to useful for assessing what the incidence of anything is in any of the breeds.
How many dogs in breeds where MDR1 has never been diagnosed have EVER been tested for MDR1? When people don’t see the problem happening organically, why would they waste money on tests which are likely to never tell them anything?
With a sample size so small, just 7 recent dogs even submitted for testing, and the already strong bias against testing for hips at all in breeds that are deemed very low risk (fewer than 3% of most sight hounds show HD even in the problematic OFA numbers), there’s actually a really good chance that the one dog that spiked HD could have been entirely environmental. For instance, if nearly no one in your breeding culture, Greyhounds, is OFA’ing their hips anymore … and you get this one puppy that seems to have a strange gait. You submit it for x-rays to see what’s going on and boom, one hip is dysplastic. Could that not be the puppy that was squished against the side of the whelping box? The one that fell down a step and began an injury related remodeling of the hip? Etc.?
This is not to wish-fulfillment away the one blip of a Greyhound that has HD, it’s to point out the issue with testing and statistics. The more rare a disease, even with a test that has a very high success rate, it’s still the case that if the disease is more rare than the failure rate of the test, that when we test a huge number of people… there will be so many that come back positive. But the majority of those who fail the test, are still not affected by the disease! This is why most important and rare tests get done at least twice, when false positives and negatives greatly outnumber the expected true positives or true negatives.
You are mistaking kennel club classifications with animals that have actually been breed for speed. Irish Wolfhounds are a recreation. And to point out the issue with OFA, less than 5% of all IWHs tested had HD and in the 2011-2015, it’s only 0.6% that have HD. I have no doubt that a study has better numbers, however, than OFA.
But why are you bringing up Irish Wolfhounds at all? Are you implying that IWH breeders and owners are worse kibble dispensers than Greyhound owners?
Nothing I’m putting out there requires that Irish Wolfhounds have purged their gene base to the same success as Greyhounds (Italian Greyhounds, Whippet, Saluki, Borzoi, etc.). We don’t even need to limit our success stories to sight hound members, but in general other sorts of dogs that have very low HD come from groups that don’t have such wide-sweeping success.
But there are plenty of breeds of rather different structure that have low to fleeting HD.
And as for the notion that you need your lab to look like a Greyhound. Nonsense. I don’t think most Lab owners now even appreciate dogs that look like Labs, at least labs 20, 40, 60, 100 years ago.
Meh. I don’t really agree. Effective population size can be easily inflated by simply having a very popular breed. That says nothing about the effective number of alleles available for any given trait. Which is what matters here. It doesn’t matter at all if Labradors have genes with a dozen evenly distributed alleles if for the gene loci that are important for HD they have very little diversity or very little representation in the breed of the good allele.
Meh. Science is decided by evidence, not opinions. Do you have any evidence that the genetic factors contributing to HD are so homogeneous in the Labrador population that outcrossing is necessary to improve hip outcomes. Doubtful. The genetic basis for HD has yet to be specified, and evidence tends to suggest that HD, itself, is diverse. (see https://www.dovepress.com/diagnosis-prevention-and-management-of-canine-hip-dysplasia-a-review-peer-reviewed-fulltext-article-VMRR ).
btw, Labradors have a reputation for HD, but statistically they are #90 out of 177 breeds in the OFA’s ranking . . . ie. they’re in the bottom half … excellent scores are much more common than dysplasic scores, and dogs born 2011-2015 show improvement over averages from 1974 to 2015. Yes, OFA data has reporting biases . . . but the Finnish data, which, because it’s a more of a census than a sample, should be relatively unbiased. In the Finnish data 57% of Labs scored after 2011 have grade A hips . . . only 19% having grade C, D, or E. See http://jalostus.kennelliitto.fi/frmTerveystilastot.aspx?R=122&Lang=en
Some segments of the pedigree dog community ARE changing outcomes through better breeding. See: http://www.kennelliitto.fi/en/news/frequency-of-canine-hip-and-elbow-dysplasia-decreasing-in-finland . . . which shows significant improvement in hip scores for most breeds through selective breeding (including the BC and the Lab). . . There is also slippage in a few breeds.
I haven’t heard much argument that diet is of primary importance, except as a means of reducing the extent that a predisposition to HD is expressed.. Carol Beuchat chose her title badly. so? Her article says nothing about genetics . . . nor does it pretend to be advice to breeders.
btw. It’s not ALL genetics. Injury can also wreck havoc on hips. Unilateral HD is pretty common in dogs that suffered early traumatic injury to the hindquarters.
It’s rather simple, really. We don’t know about genetically GOOD dogs to breed to within Labs. We do know genetically good dogs to breed to in general: Greyhounds. Knowing, what we do, about how quickly you can return to form with back crosses, you’d make greater strides breeding to a breed that is ALREADY GENETICALLY PURGED versus … what… “guess and check” within Labs where if it’s multifactorial and they’re already one of the worst breeds, you’re likely to have a bad time as it is pinging or carrying the bad alleles.
You are mistaken to think that we need a gene test to breed away from anything. Not the case.
And so what? The genetic basis for most of the things breeders look for has not been specified. And diversity doesn’t make it any less of a genetic problem to solve. It’s worth nothing just how many of the other trends (the stabs in the dark) that the paper you linked to mentions are BUCKED by Greyhounds. They grow up fast, they ossify earlier. Other large breeds do the same, they get CHD. They have a marked ration between length of body and height. And yet the paper says this is supposedly a CHD marker.
Greyhounds are the answer because they are proof made flesh. They’ve been selectively bred and purged CHD. Everything else is pussy footing looking for excuses to not do much, maintain the status quo. Etc.
I have a question: when you say that Greyhounds have been “purged” of HD, do you mean racing or show Greyhounds? Afaik CHD is not a problem in sighthounds, at least not in the progeny of desert bred Salukis which participate in open field coursing in CA.
Racing. The sighthounds bred for speed have negligible rates of HD.
If you ask people like Jess Ruffner about show bred sighthounds, you’re bound to get an analysis which says that show gait breeding is sufficiently different than racing gait and that the former is more likely to come with loose ligaments and swoopy inefficient but “flashy” movement … and an uptick in HD as well.
I am familiar with Jess Ruffner.
My guru re sighthounds is Dr. John Burchard. I have been openfield coursing several times and have spoken to the sighthound coursing folk. Selection for performance and not for show. Difference in angulation as well as other phenotypical traits.
Great. Iggies score even better than greyhounds for HD. Why don’t we all outcross to iggies. Oops! The breed is not recommended for families for children because they have fragile bone structure and they are fracture-prone. Another form of torture breeding?
Border collies are only one step better than Labradors for average hip scores. Are you wiling to cross breed to a racing greyhound to reduce the probability of bad hips? I’ll bet the result will not do well with frisbee sports. You might get the BC traits back after a few generations . . . if you are lucky . . . but in the process you might lose the advantage re. HD.
Racing greys are, in general, docile, fast, inclined to chase (no problem, I don’t like cats and am happy for my dogs to kill vermin) and stupid. They often suffer injury because they run into things when running fast. I like greys, but I would never want to own one. Nor do I want a greyhound cross. I can find Labrador studs with a multi-gen history (including siblings and progeny) of low hip scores, and strong evidence of working ability as hunting dogs or assistance dogs. Breeding programs that select for low hip scores don’t produce perfect outcomes. But they do show gradual improvement. That’s good enough for me. Especially as many Labs whose scores are not so good only show hip problems in old age, and those are easily managed with keeping the dog trim and exercised, plus non steroidal anti inflamitories if the pain gets bad. I’m 67 and carry a few extra pounds. Sometimes my hips hurt and I may eventually need a hip replacement. My 12 yr old dog may slow down and be happier with some medication. BFD.
The source you cite on the Finnish data says (in her summary . . . I haven’t had time to read the whole thing.) “Estimates of heritabilities in the studied breeds indicated that there is sufficient genetic variation for successful selection of breeding dogs according to their dysplasia status.”
The routine and often brutal culling of racing greyhounds has interesting ramifications. However, breeders should have multiple objectives. Using a racing grey stud would putting hips above all other objectives.
I’m sorry Dublin suffers from HD, and I hope the stem cell therapy works. But unless you’re willing to do a greyhound outcross program and carry it to F3 and beyond, why put the onus on others? Science may eventually pin down the genetic and non genetic causes of the various forms of HD and provide specific guidance about how to manage breeding programs. Until then, I’m quite happy to see breeders doing hip and elbow testing within their breeds (btw. elbow problems can be every bit as bad as hip problems), preferring lines with good scores, and steering away from lines with bad scores. And, of course, keeping their dogs slim and fat-shaming puppy-buyers to do the same.
Sure, there are problems, like the Dalmatian UA mutation case, where outcross makes sense. You have not convinced me that HD is one of those problems.
p.s. too much information on the table here . . . hard to digest it all properly.
You should talk with Katariina Mäki about the Finnish data and the heritability of CHD and what has happened in Finland. She not only did her dissertation on it, she contacted me about this article in support and I discovered that she LEFT Carol Beuchat’s “Institute” over the very article I criticized due to Carol’s gross misrepresentation of the science and the understandings about CHD.
Here’s some commentary from Katariina Mäki:
Here’s a test for you. Read this:
If we have Dalmatians, and we only look at Dalmatians, would not our “heritability” calculation be skewed? No matter what the number we produced said, if all Dals have the same gene for the disease, then pretty much all the variation we see would be environmental. Perhaps some other factor that might be genetic, like another gene that could temper the severity or whatever. Maybe. Or more likely, differences in diagnosis… dogs with the disease not getting diagnosed in the timeframe we’re looking at or the nature of their diet putting less strain on their malfunctioning digestion, etc.
If there’s no variation in the genes, how can heritability really be calculated in a matter that is informative? Are we not then really calculating something more akin to penetrance? That given the same genotype what are the odds that the phenotype matches? Add in expressivity too, what if the expression of the phenotype is variable (say moderate HD to severe) given the same genes.
http://www.ncbi.nlm.nih.gov/books/NBK22090/
Those two factors can greatly change a calculation of heritability and yet not in any way suggest that the issue is anything other than sine qua non on the genetic level.
Notice that last bit. “The high heritability of the disease makes it possible for breeders to effectively select against the disease.” combined with “The prevalence of the disease was 34% (24.99-43.70%) among male Dalmatians in our survey.” You might take those two bits of information and claim “well, it’s only in a third of the population and it’s highly genetic, so we can assuredly breed it out within our population, no need for an outcross.”
AND THAT WOULD BE TOTALLY WRONG.
This is because you’d be confusing phenotype (diagnosed with the disease) with genotype (predisposed toward the disease). The genotype is actually FIXED within the population. Breeding around it would do nothing to change the frequency of that gene. Mistaking the diagnosis for the physical reality (heck, you can show that almost every single Dalmatian produces the uric acid in high numbers, if you call THAT the disease and not just the stone formation leading to intervention… then almost all the males AND females would be classified as having the disease).
Having variable penetrance and expressivity does not in any way negate that certain diseases can be best combated with genetic answers.
” The main reason why people have not achieved genetic improvement in HD is that there has not been any systematic selection against it.” … written in 2002.” Really? Have a look at
Monitoring Hip and Elbow Dysplasia Achieved Modest Genetic Improvement of 74 Dog Breeds over 40 Years in USA
Yali Hou ,
Yachun Wang ,
Xuemei Lu ,
Xu Zhang,
Qian Zhao,
Rory J. Todhunter ,
Zhiwu Zhang
Published: October 4, 2013
http://dx.doi.org/10.1371/journal.pone.0076390
See especially Table 2. There has been significant improvement in many of the breeds they consider. No outcrossing to greyhounds.
Cathy Bittorf: You have described mutations. How does that relate to Christopher’s statements?
He said quite clearly that CHD was genetic.
Have I missed something?
Dorothea it seems that the topic is complex but does involve biology and how these disease conditions related to biological changes. You likely have not read the article by Carol Beuchat PHD…”Locating the genes for hip dysplasia in dogs (Psssst! Look in the kibble bag)”
7/6/2012
Genes are the basic units of inheritance and are made up of chemicals called DNA. Genes provide instructions for cells to make proteins that carry out all body functions and form our physical characteristics. Each gene is present in 2 copies. One copy is inherited from sire and 1 copy is inherited from sire. . Genetic conditions are caused by a change (or mutation) in 1 or more genes passed from generation to generation. For example: Most genetic heart conditions are inherited in an autosomal dominant pattern. Autosomal means that both male and female men and are equally affected. Dominant means that although there are 2 copies of each gene, a mutation in just 1 copy is enough to cause disease. Therefore, an autosomal dominant condition has 1 normal copy of the gene and 1 copy with a mutation. The chance of passing the abnormal copy of the gene to offspring is 1 in 2, or 50%. By the same token, each offspring has a 50% chance of inheriting the normal copy of the gene and having no risk of developing the condition. On average, half of the members of a litter with an autosomal dominant heart condition or HD will develop the disease.
Christopher your statement :”This is because you’d be confusing phenotype (diagnosed with the disease) with genotype (predisposed toward the disease). The genotype is actually FIXED within the population. Breeding around it would do nothing to change the frequency of that gene. Mistaking the diagnosis for the physical reality (heck, you can show that almost every single Dalmatian produces the uric acid in high numbers, if you call THAT the disease and not just the stone formation leading to intervention… then almost all the males AND females would be classified as having the disease).”
This applies so perfectly with any mutation such as the one found in Rough/Smooth Collies with CEA around the world with over 80 percent of the breed that only through genetic testing can this be brought under control. CEA not just rcd2 causes Collies to be blind. No adjustments of diet will eradicate this genetic mutation from the breed.
Having variable penetrance and expressivity does not in any way negate that certain diseases can be best combated with genetic answers.”
Ummmm…….
Perhaps I have missed something or am too ignorant to understand it, but is that not precisely what Christopher is stating???
No way would I characterize you too ignorant to understand. The very title of this Blog is about diet being the answer to genetic mutations trenched into the gene pool of varies breed registries of varies breeds. http://learn.genetics.utah.edu/content/epigenetics/nutrition/
You see Carol’s article plays heavy on theory that genes can be changed through nutrition. http://advances.nutrition.org/content/1/1/8.full
I can share those who are supporting this theory and tell you it does not work very well in the next generation. It will be only a temporary solution for present generation from my studies to lack of genetic diversity and doubling up on recessive mutations.
I’m going to let Christopher answer this, Kathy Bittorf.
Bottom line we would have expected from PhD of Institute of Biology Blog to have utilize all current biological information .Rather than studies from a commercial dog food company making millions selling this propaganda. Take it Christopher.
There is now a general view of transcriptional regulation that can account for most observations that geneticists have made in the past century with studies in this newer field of genetics. However, there are still some phenomena that beg for explanation. An important set of phenomena, termed epigenetic inheritance, seem to be due to heritable alterations in which the DNA sequence itself is unchanged. Indeed, it is likely that these phenomena constitute another, poorly understood level of gene control. Epigenetic inheritance activity state of a gene depends on its genealogical history are para mutation and parental imprinting. https://en.wikipedia.org/wiki/Paramutation
Kathy Bittorf: that is nothing new. Please reread your postings,particularly the one about inheriting alleles.
Some of your sentences are a bit odd. Is English your first language?
BTW as I read it, CB is not saying that kibble causes epigenetic changes in gene expression
The Purina study shows mechanical facts: a joint which carries less weight has less damage. That does not mean that the genetic basis of CHD is changed, nor its expression.
Exactly, agree nothing is stated in the article on epigenetics or the biological changes of mutated genes. The blog’s title please Dorothea.
Pet MD just published an article with yet another insane level of denial. The piece is about “9 Breeds with the Highest rate of Cancer.”
#8 is Bernese Mountain Dogs, for which they quote an average lifespan of 6 to 9 years, but it goes on to say, sidetracking onto another breed..
“While we don’t know why certain cancers are common among breeds, Coates said some environmental factors may be important. ‘For example, exposure to chemicals applied to lawns is associated with an increase risk of bladder cancer in Scottish Terriers,’ she explained. ”
From http://www.petmd.com/dog/slideshows/general-health/dog-breeds-highest-cancer-rate?utm_source=Facebook&utm_medium=SocialMedia&utm_campaign=petMD_9DogBreedswiththeHighestCancerRate_06222016
We don’t know? That seems silly in a piece that talks about BREEDS with a lot of cancer problems. Why on earth would being a Scottish Terrier or ANY breed in particular be of significance? Why, should any BREED have a higher incidence of cancer? Their particular gene pool and its uber-tightness!!!! It’s already spelled out. Okay maybe you can say you mean, you don’t know the incredible details of what genes cause what. With regards to finding solutions for lessening the rates of cancers, does the typical breeder really HAVE to? Not necessarily.
The diplomatic approach to the writing is no doubt to prevent the wrath of defensive breeders. And I get that many want to soften the walls some breeders sit behind so that they will eventually come out and listen. But it’s a very slow process, and I don’t blame some for not having the patience to handle things that way in a world where we sometimes treat adults as if none of them should ever learn to deal with hurt feelings or hard news and facts. Heck, every one of us is going to get bad news from a doctor some day..pancreatic cancer etc, …surely hearing about breeding your dogs too tightly should be something we can deal with by comparison.
Urban CC: Well said!
I first learned of epigenetics back in the 90s. It’s not a new topic. It IS however, a great example of that old saying “The devil is in the details.”
Allow yourself to get mired in the information regarding spontaneous mutations, environmentally caused mutations, etc, and you allow the excuse-train to chug on for people who either fear, or simply don’t want to, work towards genetic diversity using simple methods they absolutely CAN control in breeding.
Most environmental factors cannot be controlled. In developmental biology, “environment” also often includes the biochemical fluctuations in the womb during fetal development. Biochemistry is incredibly complex.
Diet, exercise and weight are among the few environmental issues you CAN control! So are mate choices. I think most breeders would do best to stick with those.
Epigenetics writing is mostly a fad by blank state people who want to push nurture over nature. There have been no wonderful breakthroughs, nothing you can use to make better dogs so far.
The major take-away is this: you can’t activate or suppress a gene you don’t have in the first place. Breeding decisions still trump epigenetics.
Simply put and easily understandable !
My findings have been believing epigenetics or nutrition as the cause and cure is denial that modern breeding protocol must be adopted.
My family has this kind of disease that runs out in our family from our grandparents.
Ivan Jordon recently posted..best-juicing.com – Rika’s Juicepicker
Ivan totally agree. Likewise in continuing study agree with Christopher little value in Epigenetics other than to advance into the biology and genetics of proteins.
Proteins are large, complex molecules that play many critical roles in the body. They do most of the work in cells and are required for the structure, function, and regulation of the body’s tissues and organs. Why I do agree that synthetic proteins ..made made engineered proteins GMO are dangerous to all mammals human and canine. Currently only factor can agree has anything to do with Kibble except the quality of proteins it would seem.
proteins do all of the heavy lifting in your body: digestion, circulation, immunity, communication between cells, motion-all are made possible by one or more of the estimated 100,000 different proteins that your body makes.
But the genes in your DNA don’t make protein directly. Instead, special proteins called enzymes read and copy the DNA code. The segment of DNA to be transcribed gets “unzipped” by an enzyme, which uses the DNA as a template to build a single-stranded molecule of RNA. Like DNA, RNA is a long strand of nucleotides.
It can be confusing, but remember: DNA is used to make RNA, then RNA is used to make proteins-and proteins run the show.
Proteins are made up of hundreds or thousands of smaller units called amino acids, which are attached to one another in long chains. There are 20 different types of amino acids that can be combined to make a protein. The sequence of amino acids determines each protein’s unique 3-dimensional structure and its specific function.
Proteins can be described according to their large range of functions in the body.
I found this interesting link for some diversity in this discussion.
.http://hipdysplasia.org/developmental-dysplasia-of-the-hip/causes-of-ddh/
I love this article so much. Carols research and statements annoy the hell out of me because of that one person and her stupid articles it’s making it impossible for me to try get anyone of the breeders in my breed to start xraying as they share that article and claim it as evidence that HD is not genetic. My puppy arrived in my care at 13 weeks old severely dysplasic already showing every symptom for HD there is. And all the breed club and breeders still refuse to X-ray because it’s not genetic and blame puppy buyers environmental factors. Like seriously I miraculously caused severe HD in both my puppies hips in a month feeding him top quality food ,minimally excercising him, keeping him slim through food intake, reducing jumping, whole house carpeted , no stairs.