3 minutes a day in a centrifuge was part of the failed biosensor "super dog" program.

Dog culture is lazy and unoriginal, and profoundly stagnant. The desire for easy answers, simplistic how-tos and formulas for success is rampant. Just do this one simple thing! 

Breeders eschew complexity, uncertainty, and experimentation. They fear change and embrace unproven tradition on face value.  We do it this way because we’ve always done it this way.

Reason gives way to mimicry, and that is the true mark of conformation: not in the dogs keeping to a written standard but in breeders kowtowing to the unwritten rites and rituals to fit in.

One cherished ritual that can be found proudly advertised on numerous breeder websites (usually after the “Our Boys” and “Our Girls” links) as a sign of their reputable status and deep commitment to superior dogs is the adoption of the “Bio-Sensor” program as the one true path™ to dog raising.

In only 15-25 seconds a day for only 14 days in a dog’s life you will realize “life long lasting effects:” “improve performance,” “respond maximally,” “attain sexual maturity sooner,” “resist cancer and infectious disease,” “withstand terminal starvation,” achieve “psychological superiority,” “stronger heart beats,” “stronger adrenal glands,” and “improved cardio vascular performance!”

That’s less than 6 total minutes of work to make a super dog!  AMAZING!

The brains over at the sci-ence blog have come up with a handy chart to recognize quackery, the relevant parts of which I’ve reproduced here.  Their instructions:

“If you come upon a treatment or product that seems too good to be true, consult this handy guide to finding pseudoscience, scams, and quack medicine. Remember, it only takes one match to be considered suspect! Be safe, and be skeptical!”

This widely tauted “Bio Sensor” a.k.a “Super Dog” a.k.a “Early Neurological Stimulation” program has many warning signs of quack science.

Let’s start with who is peddling this pseudoscience:  Dr. Carmen a.k.a Carmelo Battaglia, Board of Directors of the American Kennel Club.

Dr. Carmen L. Battaglia, of Roswell, Georgia, owns and breeds German Shepherd Dogs and is Delegate and Past President of the German Shepherd Dog Club of America. Carmen has chaired the Committee for the Future and Business/Planning Committee and as a former AKC Director, served as Board liaison for the Health, Parent Club, HEC and By-Laws Delegates committees. He has published articles on breeding and legislation as well as several award-winning books. He also serves as an AKC expert witness in dog legislation cases and has written county dog legislation which resulted in the model that is used in several states. Carmen possesses a Doctorate from Florida State University and has been Assistant Dean at Emory University and Regional Administrator at the US Department of Education. He is also the President of Atlanta Student Aid (financial aid consulting Firm) as well as the past president/owner of three post secondary schools which were located in two states.

You’ll remember Dr. Battaglia from his resurrection of Lloyd Brackett and his infamous “Brackett’s Formula.”  Dr. Battaglia gives lectures on cruise ships to up-and-coming brown-nosers in the AKC hierarchy who want to buy the secret knowledge and pay the right gate keepers to fast track show success.  He’s the closest thing the AKC community has to a celebrity doctor.

But don’t get too comfortable with the idea that he’s a medical doctor, he isn’t.  He’s a Ph.D. doctor, which he readily advertises at the end of his publications:

Carmen L Battaglia holds a Ph.D. and Masters Degree from Florida State University. As an AKC judge, researcher and writer, he has been a leader in promotion of breeding better dogs and has written many articles and several books.

Dr. Battaglia is also a popular TV and radio talk show speaker. His seminars on breeding dogs, selecting sires and choosing puppies have been well received by the breed clubs all over the country. Those interested in learning more about his seminars should contact him directly.

Visit his website at http://www.breedingbetterdogs.com

What he doesn’t advertise anywhere that I’ve found despite an extensive search is what subjects his degrees are in.  So I contacted the Curriculum Publications Coordinator at Florida State University and found out the unpublished truth:  B.A. Psychology 1958, M.S. Social Welfare 1960, PhD Joint Doctoral Program in Criminology Corrections and Sociology 1968.

So by way of education, Dr. Battaglia is more equipped to run a prison than a breeding program.  His dissertation was titled “Deviant behavior of parolees and the decision-making process of parole supervisors.”

The next indicator that “Bio-Sensor” is quack science is because it’s being SOLD as a how-to guide to success without having been vetted in any way by scientists in peer reviewed publications resulting from studies done according to the scientific method.

Dr. Battaglia sells his program along with breeding and puppy selection advice as part of his self-help for dog breeding commercial venture.  You can buy books, videos, DVDs, and subscribe to his newsletter and attend his lectures.

In accordance with yet another quackery red flag, Dr. Battaglia is pitching program that offers medical benefits but he (nor anyone else) has no peer-reviewed journal articles on his protocol. And it’s not for lack of trying.  If you visit his website you will find a link to request his so far unpublished journal article.  When you do so, you will be e-mailed a copy of an extended version of his Bio-Sensor article spruced up to look like an actual experiment with “Methods and Materials” and everything.

It appears from the file that Dr. Battaglia has attempted to get this article published since at least 2007, but he will warn you that the article is still under intense review and thus you can not share it.

This wouldn’t be the first time that the “Bio Sensor” program has been used to sell a self-help program, however, as Dr. Battaglia collaborated with Stanley Coren–king of marketing shoddy dog science to pet owners in book form–who included the information in his book Why Does My Dog Act That Way?

Battaglia and Coren’s considerable influence on the dog fancy combined with Battaglia offering the super simplified how-to instructions for achiving super dog success for free on his website as a teaser for his suite of videos, books, and lectures the “Early Neurological Stimulation” program has saturated the hobby pet breeder culture.  Breeder testimonials and reprints of the method are everywhere.

Diligently following Dr. Battaglia’s advice, there are breeders out there inbreeding their lines and producing singleton puppies who none-the-less credit Brackett’s Formula and the amazing Bio-Sensor program for giving them a super puppy abounding with exceptional qualities.

Apparently I’m part of a silent minority who have even questioned this program’s merits and the academic bona fides of the man who peddles it from coast to coast, as I’ve found no online criticism of the methods and not even one other soul who questioned what Dr. Battaglia’s field of study was until I sent out feelers over a year ago.

But it’s clear to me that Bio-Sensor is being marketed just like quack science is marketed, by people who have a vested financial interest in selling easy answers and quick fixes to gullible pet breeders who spend fortunes trying to rectify their ignorance with short cuts and feel-good nonsense.

In a quadrumvirate of quackery, Battaglia also uses his “Breeding Better Dogs” website to sell Japanese (think Eastern medicine) magic magnetic shoe inserts and magic magnetic dog beds that are “combined with magnetic technology, another ancient principle” and “enhance the body’s energy flow to allow healing and proper metabolism.”  This is a man perfectly willing to market quack science as a miracle product for profit.

So far I’ve shown that Bio-Sensor looks like a duck, and in a future post I’ll show you how it quacks like a duck as well.

The breed is believed to be the creation of one man, Heinrich Essig, who was a dog dealer and traveling salesman; his claimed formula was Landseer Newfoundland x Saint Bernard, followed by more Saint Bernards and a Pyrenean Mountain Dog with the goal being a large white dog that was fashionable at the time.  After Essig’s death in 1889 his nephew had the inspiration to promote the breed as a lion-like mascot for the town of Leonberg and established the final conformation of the dogs as having a lion-like rough coat with reddish-brown coloration, a black mask and black sable accents.  Like most breeds, the origin mythology is poorly documented and stud books were not kept in earnest on the breed for several decades after its establishment.

As a German breed, the Leonberger was severely affected by both World Wars: only 5 known breeding dogs survived the first war and only 8 pedigreed dogs emerged from the second.  Two severe bottlenecks like this are not conducive to preserve genetic diversity within a closed population.

That is why I was surprised to find that the 5 Leonbergers which were DNA tested as part of a study analyzing the genetic composition of Alaskan Sled Dogs showed that they had excess heterozyosity compared to Hardy-Weinberg equilibrium. Of 141 breeds tested over 96 genetic marker sites, there were only 9 purebred breeds found to be surplus heterozygous and most of those are only marginally so.

Note, this is not a measure of gross diversity in the breed, it’s a measure of which way the breed is being pushed genetically, either toward more conformity and homozygosity or toward more diversity and heterozygosity.

Genetic rescue requires a push toward heterozygosity before reaching a new equilibrium with the new alleles.

Inbred or Outcrossed? Bars that extend to the left indicate excess heterozygosity compared to the Hardy-Weinberg equilibrium (red line), suggesting active selection for allele diversity (i.e. outcrossing). The Leonberger is one of the most heterozygous breeds tested.

Here is the actual data represented in the chart.  The purposely out-crossed hybrid sled dogs were found to be 20% more diverse than equilibrium and the Leonberger was second only to the Puli with over 10% excess heterozyosity.

I’ve only found one documented outcross on the Leonberger books: In 1954 a Leonberger stud Arko von Leonberg with a COI of 20% was bred to a Newfoundland dam Grisette von Bruckberg and one female from that litter, Alma von Rossbach, would cement herself into the Leonberger gene pool.

More recently European kennel clubs have registered Leonbergers with full breeding rights certificates “titre initial” (as opposed to a 3 generation provisional appendix registration “registre initial”) which are given after a number of criteria are met; typically an evaluation against the breed standard or significant show success, health testing, and perhaps even temperament evaluations.  These dogs are believed to be pure-blooded Leonbergers instead of hybrid dogs which would normally take 3 generations to be admitted into the gene pool with full breeding rights and purebred status in registries that allow new blood.  Sometimes they come with full pedigree and while the kennel club would void the known pedigree and perhaps calculate the COI of offspring as 0%, it’s not clear that either the registre initial or titre initial schemes are a source of new Leonberger blood.

Another possible source of Leonberger diversity lies in the history of Germany and the East after the wars.  The Leonberger isn’t just a dog of the West and so it existed on both sides of the Iron Curtain.  It is unknown and undocumented what sorts of possible crosses came into the breed during the Cold War before the reunification of Germany and the resumption of normal trade across Europe.

The last and least verifiable source of unexpected diversity would be intentional and unintentional pedigree fraud or error.  It’s possible that some breeders when faced with a line that was not producing what they wanted or suffering from inbred disease or infertility decided to outcross, or an accidental litter proved sufficiently virtuous to register and the breeder either could not or did not choose to disclose this.

There’s also the possibility that I simply haven’t accounted for some factors which would have preserved heterozygosity in Leonbergers and that the bottlenecks did not have the expected effects on the gene pool.  Certainly more questions than answers, but what an intriguing mystery it is.

Inbred lab mice are so healthy you only have to keep them in a sterile bubble and wear biohazard getup just to watch them.

The Pure Blood Brigade™ (licensed for use from Jess Ruffner) will sometimes invoke laboratory mice as the go-to example of a perfectly healthy inbred population. Here’s a quote from NSDTR-apologist and accomplice to Dr. Claire Wade, Dr. Danika Bannasch:

I don’t know if you are familiar with inbred mice.  There are 100s of laboratory strains that are completely inbred- ie homozygous at every locus.  They breed prolifically and are healthy.  They are not living in the wild but neither are domestic dogs.

To verify the health of laboratory mice I went to Jackson Laboratory–the “most important supplier of lab animals to science“–and viewed their “Breeding Strategies for Maintaining Colonies of Laboratory Mice.”  The manual claims that the breeding strategies that are used to create inbred lab mice are:

“safe, reliable, economical, efficient, and ensure that the mouse strains produced are genetically well-defined.”

Notice that they don’t claim that the mouse strains produce healthy mice that live long and have good temperaments, they are just genetically well-defined (highly homozygous).  Here are snippets which hint at the deep underlying dysfunction that is found in inbred lab mice:

• Reproductive life span. Typically, laboratory mice can breed for about seven to eight months, producing four or more litters (Table 1). However, some strains produce only one or two litters, usually because strain-specific characteristics or mutant phenotype affect their fertility. AKR/J mice (000648) develop leukemia, and breeders must generally be replaced when they are about six months old. C3H/HeJ mice may stop breeding early because they have a high frequency of ovarian cysts and tumors. NOD/ShiLtJ (001976) females may develop diabetes when they are 12 weeks old, but their reproductive lives can be extended with foot pad injections of Freund’s Adjuvant.

• Fertility. Fertility of inbred strains varies. For example, whereas nearly all breeding pairs of C3HeB/FeJ (000658) mice are fertile, less than half of C57L/J (000668) breeder pairs are fertile.

Wild mice breed for up to 24 months. Laboratory mice can breed for only 7-8 months.

Wild mice can have 5-10 litters per year, so 10-20 litters over their two year reproductive lifespan. These lab mice have 1-6 litters, the most popular strains average 3-4 litters.

Average wild mouse litter size is 10-12 pups. The mean litter size of the top 12 most popular lab strains are: 5.4, 5.2, 4.5, 5.0, 5.6, 4.0, 4.7, 7.3, 7.7, 5.8, 6.4, 4.9; so about 5 pups.

• Birth defects in the pups. C57BL/6J (000664) mice tend to have more pups with hydrocephaly than do other strains. A/J (000646) mice tend to have relatively more pups with cleft palates, the incidence of which can be influenced by the uterine environment.

• Hybrid vigor. Hybrid mice tend to have more, larger, and healthier litters than inbred strains.

• Strain-specific behaviors. The aggressive behaviors of some strains and the poor mothering instincts of others affect breeding performance and pup survival. For example, SJL/J (000686) males are aggressive and attack their mates and offspring; NZB/BlNJ (000684) females are poor mothers.

Here we have pretty much the death knell for using lab mice as an excuse to inbreed dogs.  Aggressive behaviors and poor mothering are deal breakers for almost any decent dog breeder.  Birth defects in many breeds are at epidemic levels, and yet many breeders are so jaded they consider it normal. We should not consider it normal and those of us in healthy breeds should steel our spines against becoming such moral sellouts.

Oh, and hybrid vigor is real. We can reverse this.

Don't let outcross breeders tell you otherwise, small litter sizes are actually a bonus! Who needs those extra offspring, they are just a hassle.

• Mutations and transgene effects. Some mutations are embryonic lethal; some cause infertility or reduced fertility; some affect mammary gland function. For example the Tg(SOD1*G93A)1Gur transgene (also found in several strains) induces neurodegeneration. The severity of such effects depends on strain background.

If you’ve been reading this blog for any amount of time you should be well aware of the embryonic lethal mutations that are prevalent in certain breeds of dog.  Many of these have been identified because they associate with a marked phenotype change of interest such as merle or bobtail. How many more exist that do not have a visible phenotype?

• Feed. Some strains of mice have bad teeth, no teeth, or other phenotypes that affect their ability to eat grain pellets. These mice need special foods, such as ground or dampened grain.

Does this remind you of the poor dentition we see in several toy breeds and especially hairless dogs?

Females of some strains are poor mothers (e.g., NZB/BlNJ, 000684) or cannot nurse, and a few mutations, such as toxic milk (Atp7btx) and lethal milk (Slc30a4lm), render the mother’s milk harmful to her pups.

I wonder if those toxic and lethal milk mothers were intentionally bred to have harmful milk or if those are just known side effects of strains used for other kids of research.

Some strains are so screwed up they are only viable by transplanting the ovaries of the inbred mice into healthier females:

Some strains are best maintained by ovarian transplantation. Homozygous B6C3Fe a/a-Csf1op/J (000231) females fail to lactate, and homozygotes of both genders are extremely fragile. Therefore, we transplant ovaries from a homozygous (op/op) female into a recipient female of a histocompatible strain. To quickly expand the colony, the donor ovaries may be quartered and each quarter ovary transplanted into a ovariectomized recipient female. We also maintain B6.V-Lepob/J mice (000632) by ovarian transplantation because, though the females produce functional gametes, they cannot sustain a productive pregnancy. Additionally, we maintain colonies of B6CBA-Tg(HDexon1)62Gpb/1J (002810), B6CBA-Tg(HDexon1)62Gpb/2J (004601), and B6CBA-Tg(HDexon1)62Gpb/3J,(006494) by ovarian transplantation to extend the breeding lifespans of the females. Although these females produce viable oocytes for a long time, they develop a progressive neurological disease that renders them physically incapable of mating or sustaining a pregnancy.

Fantastically healthy, no?

Don't worry, not all inbred lab mice are satanic albino demons, some are really cute! And that makes everything ok.

But all is not lost, the manual provides some advice on how to maintain an outbred colony to turn to if your inbred strain crashes and burns.

Maintaining Outbred Stocks

The genomic diversity of individual outbred mice contrasts directly with the genetic identity among individual mice of an inbred strain. To maintain genetic diversity in an outbred colony, matings between related individuals should be avoided; however, some inbreeding may be inevitable over time in any relatively small, closed outbred colony.

Therefore, the following should be considered when establishing an outbred colony:

• Use numerous, genetically diverse founder mice

• Use a defined breeding scheme that is designed to minimize inbreeding: Several different outbred breeding program have been described (see Berry & Linder, 2007)

• While random breeding — using a random number table or computer program to select breeders — can be used, random breeding will result in occasional matings between closely related individuals

• Keep the colony at a minimum size of approximately 25 breeder males per generation

So if you’re interested in breeding dogs that burn out young, are riddled with disease, have nasty temperament issues, have trouble conceiving, develop horrible diseases young, etc., then believe that you too can develop an inbred strain and it’ll all turn out just dandy, just like those inbred lab mice.  Just be sure to buy yourself a nice dog bubble and some bio-hazard gear to wear around your dog while you keep it in a perfectly sterile environment after burying a truck load of its siblings and ancestors who died in the process of making your inbred little mess.

The wolves of Isle Royale Michigan

Sweeping comparisons between wild animals and domesticated pets are dangerous given the unique and often mutually exclusive conditions in which those two groups often find themselves.  Wild animals must hunt for their food, compete for resources, suffer predation, lack medical intervention, self-select their mates, and exist in numbers based upon a complex interaction between their own merits and the conditions in their environment. Pet dogs are fed from a bowl daily, compete only for our affection and attention, are largely free of predation, have ready access to modern veterinary techniques and treatments, have their mates chosen for them–sometimes from dogs long dead or on other continents, and exist in numbers based upon human concerns and rarely on their own merits or the environmental carrying capacity.  Their selection is very much unnatural. But there are very few scientific studies of domesticated pets versus numerous investigations into wild populations, so dog lovers would be remiss in not learning lessons from our pets’ wild cousins.  One particularly interesting ongoing scientific inquiry is the study of the wolf and moose populations on Isle Royale Michigan.

Wolves colonized Isle Royale, a wilderness island in Lake Superior, North America, in 1949 or 1950. The population is isolated from mainland wolves by a channel of frigid water, 24 km wide. In many, but not all years, this channel freezes for several days or weeks. Although an occasional ice bridge makes immigration possible, the analysis of mitochondrial DNA and the Y chromosome suggests that the population was originally founded by only one female and two males.

This makes Isle Royale analogous to a small dog breed based on a few founders or even a single kennel that rarely brings in any new blood.  Nova Scotia Duck Tolling Retrievers, Leonbergers, Cavalier King Charles Spaniels, Vallhunds, and many other breeds were founded by only a few sires and dams and have had very little influx of blood since and there are quite a few old time breeders who would only occasionally bring in a sire from outside their own moderately sized kennels. As with the above breeds, the mostly-closed gene pool on Isle Royale became steadily inbred over time.

By the late 1990s, the population’s estimated inbreeding coefficient had risen to 81%. Fifty-eight per cent of Isle Royale wolves showed congenital bone deformities compared with only 1 per cent in two outbred wolf populations. Some of these deformities could reduce individual fitness, particularly components of fitness associated with predation and reproduction.

So the first lesson to be learned from the Isle Royale Wolves is that isolation leads to inbreeding and inbreeding is detrimental.  In dogs, closed registries and kennel blindness are a form of isolation and in both cases we see rising inbreeding followed by increased expression of otherwise rare diseases.

Some of the most studied wolf packs in the world are in serious jeopardy. Researchers report that the occurrence of debilitating bone deformities in wolves marooned on Isle Royale, an isolated island in Lake Superior north of Michigan, has risen sharply over the past five decades due to inbreeding.

Diseased wolf vertebra due to inbreeding of Isle Royale wolves.

A genetic defect now common in the Isle’s wolves causes bones in the spine, the vertebrae, to grow gnarled and crooked. Also found in domestic dogs – close wolf relatives – the bone malformations  can pinch nerves in the spinal cord, causing pain that makes it tough to walk and can lead to paralysis of the back legs and tail in severe cases, according to research published in February’s issue of Biological Conservation. Back in the 1960s, about a quarter of Isle Royale’s wolves appeared to have the anatomical abnormality, but now the percentage of afflicted wolves has risen to nearly 60 percent of the population. “In normal, healthy wolf populations without inbreeding, you are only supposed to see this kind of defect in about one out of a hundred animals,” says paper coauthor John Vucetich, an assistant professor of wildlife biology at Michigan Technological University (MTU) in Houghton. The deformity, discovered during autopsies of recovered, dead wolves, has grown so rampant, Vucetich says, “we haven’t found a normal wolf in the past decade.”

- Scientific American

The second lesson to learn from the Isle Royale Wolves is that hybrid vigor is real and powerful and that inbreeding depression is real and powerful.

We used molecular techniques to document the consequences of a male wolf (Canis lupus) that immigrated, on its own, across Lake Superior ice to the small, inbred wolf population in Isle Royale National Park. The immigrant’s fitness so exceeded that of native wolves that within 2.5 generations, he was related to every individual in the population and his ancestry constituted 56 per cent of the population, resulting in a selective sweep of the total genome. In other words, all the male ancestry (50% of the total ancestry) descended from this immigrant, plus 6 per cent owing to the success of some of his inbred offspring. The immigration event occurred in an environment where space was limiting (i.e. packs occupied all available territories) and during a time when environmental conditions had deteriorated (i.e. wolves’ prey declined).

This event is an excellent example of what one outcross might do for a small breed and especially a single kennel. The immigrant wolf’s offspring were true hybrids, a mix of the formerly isolated pool and fresh blood; versus having an outside pack supplant the locals in toto, as one might expect in a contiguous geography that was not isolated like the Isle.

We have here an analogous situation that fits existing human patterns of behavior regarding dog breeds and strains that have virtual barriers instead of physical ones.

The astounding aspect of this immigrant on Isle Royale is just how potent his genetics were to effect change on the island.  None of the existing males could even compete with him and he became the sole sire.  His initial success is likely caused by the inbreeding depression in the inbred Isle wolves.

The high fitness of this immigrant wolf was also associated with distinctive behaviour and physical appearance. First, he was physically larger than most Isle Royale wolves. As alpha male of the Middle Pack, his high fitness was also reflected by his dominance over other ISRO packs. Specifically, he exhibited strong territorial behaviour that completely displaced West Pack, driving that pack to extinction by 1999.

This immigrant wasn’t necessarily a super-wolf, he was in all probability a young male that was driven out of his birth pack’s territory for being non-competitive with that pack’s alpha male. His success on Isle Royale shows just how compromised the inbred population had become.

The inbred Wolves of Isle Royale, genetically refreshed by the genes of a new sire.

It’s an open question if and how much the influx of new genes has changed the bone deformities which had come to define Isle wolves.  Surprisingly, before the results of the bone study were published, Isle Royale was used as an example of a wild population that was thriving and unharmed by inbreeding and isolation.  This is why I’m cautious of anyone who argues from ignorance regarding their ability to inbreed and avoid disease.  This is the third lesson: don’t assume that inbreeding can exist in high levels without detriment and don’t cite wild populations if no one has ever done a detailed health study to document the true health of the population.

The new results offer the first evidence of the wolves’ closed population leading to a decline in natural fitness. This is important, Vucetich says, because for years some policy makers and conservationists have pointed to the apparent health of the Isle Royale wolf packs as an indication that small animal populations can maintain proper genetic diversity. “Isle Royale is not this robust place that some people thought it was,” says Vucetich.

Now, not all the lessons are positive ones.  Given the isolation of the island, the complete genetic sweep of the immigrant male, and the small population size the rates of inbreeding swiftly ticked back up.  The smaller the population size and the greater degree of inbreeding done following new blood, the shorter time you’re going to reap the benefits of that new genetic material.  Outcrossing can forgive a myriad of sins, but it needs to be used in measure to the problem.  On Isle Royale, this new wolf didn’t simply add to the sires on the island, he supplanted them and then bred with his children, creating more inbreeding instead of extending the benefits of outcrossing.

This isn’t an advisable strategy for refreshing a dog breed, essentially going from one popular sire to another.  Diversity in breeding males should be maintained over each generation and proceeding to breed father to daughter–and similar–after a single outcross will swiftly return the gene pool to inbred status. The other issue that researchers have is that to complete a “genetic rescue” one must be able to document the benefit on a population level, an this is often done with the most crude methods, namely demography (head counting).  An increase in population size was not observed here, although there was a precipitous drop in the wolves’ main food source, Moose, during this time and the wolf numbers did not suffer either.

Genetic rescue, in which the introduction of one or more unrelated individuals into an inbred population results in the reduction of detrimental genetic effects and an increase in one or more vital rates, is a potentially important management tool for mitigating adverse effects of inbreeding. … The immigration event occurred in an environment where space was limiting (i.e. packs occupied all available territories) and during a time when environmental conditions had deteriorated (i.e. wolves’ prey declined). These conditions probably explain why the immigration event did not obviously improve the population’s demography (e.g. increased population numbers or growth rate). Our results show that the beneficial effects of gene flow may be substantial and quickly manifest, short-lived under some circumstances, and how the demographic benefits of genetic rescue might be masked by environmental conditions.

This is not a problem with outcrossing at all, rather it’s a problem of the limitations of the crude science of demography. Head counting might speak to quantity, but it is wholly lacking in useful information about quality.

Demography is likewise a poor tool to employ when analyzing domesticated dog health.  The numbers of dogs within breeds has little to do with their vitality and much more to do with fashion and the whims of a handful of breeders.  No one would claim that a Pug is popular due to competitive natural gifts of robust health and fitness, rather they are much like the inbred wolves on Isle Royale, they are artificially supported by beneficial conditions, easy access to food, and a blunting of natural pressures against their survival; in the wolves’ case it’s the benefits of living on an island, in the case of the Pug it’s being coddled by owners and breeders willing to spend a pretty penny on their upkeep.

In open and competitive environments, population numbers can serve to estimate vitality when better data has not been taken, but it seems that on Isle Royale, the wolves have a sheltered niche as the apex predators with ample food supply.  The Moose can’t migrate away and there is little in the way of competition for the wolves.  In such conditions, even sickly inbred wolves can reach a carrying capacity at about the same numbers as more robust wolves can.  It’s possible that more wolves could have thrived had the main food source not plummeted, or it could be that even at the lowest levels the moose populations were not small enough to be a significant factor in the head count of the wolves.

Without a marked improvement in population size on the island and without documentation of the rates of disease and bone deformities improving with the influx of the immigrant wolf, the technical definition of a “genetic rescue” has not been met with the current state of knowledge about the Isle Royale wolves.

Doctors Wade and Cattanach don't want you to buy this puppy. They'd rather have you buy one without an anus or a functioning immune system.

In a previous post I spoke about new research making Dr. Bruce Cattanach’s old understanding of the Bobtail Gene obsolete and reopening the debate about the ethics of this gene which he had previously (more than 15 years ago) declared problem free. But Dr. Cattanach decided to weigh in on the current debate over the Toller x Aussie outcross and his position is disappointing and uninformed.

Bruce Cattanach said…

I am somewhat amazed at the positive responses to this cross. I have had 20 years of vitriol against my Corgi x Boxer cross for every reason imaginable, but I kept it going as I felt that to give up – and so failing – I would damage the leverage it gave to the concept of breed crossing for health reasons. So the seemingly easy acceptance of the Toller cross is perplexing even if done for a different reason.

I really don’t know what to make of this statement, as it sort of reads like sour grapes. It’s unfortunate that Dr. Cattanach has gotten “vitriol” against his work, but he’s clearly learned enough to handle just criticisms. My analysis against his outcross comes after decades of new evidence and his unwillingness to acknowledge new findings. I don’t consider it vitriol.

It’s strange that Dr. Cattanach is seemingly jealous about the positive vibes the dog world has for the Toller cross litter. If I had to estimate why one has been received with more praise I can think of two immediate causes. One, Dr. Cattanach’s work paved the way and quelled many fears, so this new cross is benefiting from Cattanach’s work. It’s a pity he’s not more supportive. Two, this cross was done for much more noble reasons. As I’ve already documented, Dr. Cattanach inserted a problematic gene into a breed to avoid a docking ban. While it’s an interesting effort for the political reasons and documenting how easily breed type could be restored, the motives are decidedly shallow and superficial.

Does Dr. Cattanach really expect the world to beat a path to his door when he built a WORSE mouse trap?

However I had great difficulty achieving what I did with just the one gene to be transferred. It really needed more than one individual to succeed fully. I am therefore quite sceptical about this Toller effort to increase the diversity across the whole genome.

Dr. Cattanach has really moved the goal posts to an unjust distance in coming out against this one cross. He is holding this one cross to the standard of “increase the diversity across the whole genome.”

That’s unfair. No one claimed that doing one outcross could accomplish this goal! How about we evaluate a single outcross in a rational manner and judge its power to effect change commensurate with what we should expect from a single breeding. A single outcross can not save an entire breed, but it can certainly bring in much needed diversity and vitality to a single breeding program, a whole kennel and all the dogs that are bred to that line for several generations.

Any breeder who is disappointed with the options within their breed can accomplish this style of outcrossing themselves. And many more breeders will need to do this before we can claim that Tollers as a breed are refreshed.  The LUA Dalmatian project was only one out-cross and the entire breed is not yet free from uric acid problems, nor will it be for many generations to come. But you have to start somewhere and if we want fundamental change in our breeds, we’re going to have to accept that breeders will out-cross for a slew of reasons and that this isn’t that scary of a prospect.  It might just mean that we have to go back to objectively evaluating the dogs we see right before us instead of being overly obsessed with their hidden and mostly irrelevant pedigrees.  If we limit “allowable” out-crosses to combat single recessive diseases that are 100% saturated in our breed pool then we will never see the day when our breeds are getting healthier rather than the current reality where they are getting worse.

I think this needs to be done at a scale only possible at KC level with several crosses perhaps involving several breeds, and then there would be the yet trickier part of keeping the diversity while somehow getting back to breed type. That numbers of people might independently attempt this is frightening; it could result in no more than a mongrel mix-up.

I agree with Cattanach, this does “need to be done at a KC level” and of course I’m in support of using “several breeds” with “several crosses.” This is all true, but it’s not a just criticism of what this one breeder has begun to do. It really should be reserved as a criticism for the Toller breed club and for double-speak geneticists like Claire Wade who put their name on papers which advocate genetic diversity and proactive health measures but then declare zero reason to out-cross in their own breeds and attack those who do.

What good does Dr. Cattanach do by bashing this beginning step? He didn’t bring his out-cross program to the world after just one breeding, the dogs weren’t even retroactively registered with the KC until he had back-crossed several generations. So if there is some amount of “sausage making” with out-crossing, where the intermediate results aren’t indicative of the final product, isn’t it a bit rash to just criticize this nascent effort?

Is this out-cross so detrimental that it needs to be cut off at the knees by someone with Cattanach’s clout? I think he does great harm to anyone who would choose to out-cross for any reason by being so negative.

Jemima said…
Bruce’s position and enthusiasm managed to get the project sanctioned by the Kennel Club and the acceptance of it has paved an important way. Of course, the KC’s endorsement of the project was because of the impending threat of the docking ban; which the anti-dockers would argue is not the most worthy of motives.

His stance here even brings into question my previous view that his out-cross program was a good example of how one can work within the registry/breed club to accomplish something like this. In retrospect, Jemima makes a good point, that it’s perhaps much easier to get a conformation club to go along with an out-cross for conformation reasons when they are being threatened with a BIG BAD BAN on docking tails from those EVIL AR folks. Perhaps Dr. Cattanach’s efforts aren’t that informative to the rest of us who would support an outcross that you can’t see in the breed ring, one that is done for health reasons, for vitality, for genetic diversity, for longevity, for temperament, instead of one that allows you to keep some little irrelevant but highly valued feature like an earset or a particular length of tail.

If Dr. Cattanach paved a trail for future breeders, no one has yet to walk down that path in the 20 years since his out-cross and we’ll soon celebrate the 40th anniversary of the commencement of the LUA Dalmatian out-cross.  The first and last men to walk on the moon completed their missions in the years and days before the LUA Dalmatian cross and man has not set foot on the moon since; nor has man endeavored to out-cross a breed for health reasons.  One requires billions of dollars and the greatest minds the world has to offer in an attempt to overcome nearly insurmountable odds.  The other requires two dogs and a little patch of grass.  Why must we create political obstacles which make an out-cross more rare than a man walking on the moon?

If superficial out-crosses are the first step, how are we ever going to get to the next phase if the heroes of Step One decide to handicap future efforts like Cattanach is doing here? There hasn’t been another example of an out-cross in the KC since Cattanach did it, so the theory that he greased the wheels for those that followed hasn’t produced any results.  If we want results, we should try a new strategy, 20 years between out-crosses is long enough.

I am sceptical for another reason too. It almost seems that the Toller cross was done to resolve the high level of inbreeding but if there is no consequent problem of the inbreeding, to my view, the need for the cross does not exist. Is the breed impaired by the inbreeding? Frequencies of certain defects have been presented but I have seen nothing on the distribution across the breed (is the whole breed at risk?) and any indication of the inheritances. Everything seems based on a ‘belief’ that there will be problems even if there are none as yet. If there are indeed problems now or clearly looming, yes, go ahead or at least experiment and see what difficulties there are. But let this be done in an organised controlled way and on a scale commensurate with that needed.

Did Bruce just criticize someone about the NEED to out-cross? Really? Perhaps he can review my Toller articles and comment. Recall that Cattanach argued from ignorance before, claiming that there were no side effects from the bobtail gene, that litter sizes were not reduced, homozygous puppies and their problems never lived long enough to be born, etc. None of his assumptions were true and the bobtail gene is decidedly less wonderful the more we find out about it.

We already know that Tollers don’t live long, they have high rates of auto immune disease due to an MHC allele that is pervasive in the breed and few other alleles to turn to, as well as growing evidence of numerous other problems. We also know that the gene pool is severely limited due to a very very small founding population in the KC dogs.  Is that not reason enough?  How small of a founding population can we justify?  Only two dogs perhaps?  Is that where we’re going to draw the line.

Cattanach was wrong about the dangers of Bobtail and if he thinks there’s no justification to outcross Tollers, he’s wrong again.  Here’s a small list of conditions known to run in Tollers: Hemolytic Anemia, Addison’s Disease, Hypothyroidism, Pemphigus, Immune-Mediated Polyarthritis, Systemic Lupus Erythematosus, Congenital Deafness, Epilepsy, Pulmonary Stenosis, Steroid responsive Meningitis-arteritis, Cleft Lip and Cleft Palate, Mega-esophagus, Collie Eye Anomaly, Skeletal Dysplasia & Chondrodysplasia, and Herniated discs. More Tollers will suffer one or more of these conditions than will toll ducks even once in their lives, more will die young than will win Conformation Championships, and many more Tollers will be bred to dogs that are as close as siblings than will ever hoped to be out-crossed.

What more does Cattanach need to see?

Finally, there was a question on unneeded puppies in my breed cross. This was no problem when one presented the objective. Potential owners were told what the cross was all about. There was annual get-together where everybody met together with their dogs of different generations to observe progress It was a tea-and-cakes gathering in the garden and all were made to feel part of a research study that all could, and did, boast of participation. I still have contacts with many of the owners although the early dogs are long since dead.

Bruce Cattanach
www.steynmere.com
25 August 2011 22:56

Is Cattanach suggesting here that because the breeder of this Toller x Aussie litter isn’t a research scientist who can cloak his project in a veil of academia that these puppies aren’t going to find good homes? The sales value of “pedigree” and “purity” are as low now as it has ever been and the public’s awareness of hybrid vigor and appetite for designer dogs and other mixes is as high as ever. Given the choice between a show bred Aussie or a pedigreed Toller, I think any rational human would look at these hybrid puppies and agree that it’s a better product.

I see a resistance in Cattanach to come to terms with the health concerns in the bobtail gene in the same way Claire Wade doesn’t want to consider an outcross for MHC or any other reason. They both downplay the health concerns and I’d say both have a biased reason to do so: they are both highly invested in their dogs as they are. Wade doesn’t want to give up “purity” and Cattanach doesn’t want to reconsider the bobtail gene. Both are highly educated biologists who should know better.

Neither one thinks that you should buy what the Toller x Aussie breeder is selling, but do you buy what Wade and Cattanach are selling? I don’t.  Like a bobtail without an anus, I think they’re both full of it.

Biologist Claire Wade and her Toller "Burn" during an NSDTRC-USA Field Test.

The 2011 study A Genealogical Survey of Australian Registered Dog Breeds is a shoddy piece of work and a disgrace to the scientific method.

The world-wide population of Cavalier King Charles Spaniels descends from only 6 dogs.  This bogus study manufactured 836 observed CKCS “founders.”

GIMME AN F!

The authors Mohammad Shariflou, John Hames, Frank Nicholas, and Claire Wade did themselves and the canine community no service in writing it and I contend that Claire Wade allowed her own bias for and attachment to Nova Scotia Duck Tolling Retrievers to taint her judgment. Combined with her failure to disclose her extant conflicts of interest as a Toller owner, breeder (stud service), trainer, and breed club member, this bias and its resultant corruption of the methods and characterization of the results by the authors are de facto academic fraud.

The authors begin by suggesting that their analysis is circumspect and all encompassing when it’s anything but:

To better understand the actual nature of pedigree dog population structure on a whole-population basis, we examined data records for a representative sample of recognised pedigree breed populations in Australia.

This is a lie.  This paper did NOT look at a whole-population basis at all, in fact the researchers went out of their way to limit the information they were looking at and purposely excluded data that is both informative and readily available.

The world-wide population of Pekingese Lion Dogs descends from only 5 dogs.  This bogus study manufactured 1053 observed Peke “founders.”

GIMME AN R!

They looked at only a fraction of the data available in one registry in Australia, going out of their way to remove all known dogs before import which were certainly contained on their import pedigrees but not included in the analysis.  This means that they failed to look at the whole-population of any dog breeds  despite claiming otherwise.  They didn’t even come close.

Only one breed, the Australian Terrier, passed the 10 generations of data mark. The other native Oz breed, the Australian Cattle Dog, fell short at only 9.7 generations but this low mark still greatly surpassed the imported breeds.

Generation Equivalents (EqG): 3.0, 2.1, 3.5, 5.4, 4.4, 3.1, 3.4, 3.3, 4.8, 4.1, 4.1, 1.7, 7.6, 2.6, 10.1, 9.4, 7.7, 8.3, 8.1, 7.6, 9.7, 7.6, 6, 7.5, 7.3, 8.7, 6.6, 4.8, 6.7, 6.6, 4.9, 8
mean: 3.9

These scientists threw away so much prior-to-import data and the documented history within Australia is so limited for almost all these breeds that their results are based upon an average of only 3.9 generations! This is less information than would appear on one single import pedigree and we know that most of these breeds have many more generations of documented history.

The world-wide population of Nova Scotia Duck Tolling Retrievers descends from only 9 dogs.  This bogus study manufactured 84 observed NSDTR “founders.”

GIMME AN A!

As I’ve shown before, Nova Scotia Duck Tolling Retrievers should have between 11 and 22+ generations of documented pedigrees.  I’ve traced my own Border Collies back (including significant history in Australia) between 20 and 70 generations.

It’s really laughable then that they claim their results are “comparable with other species of domesticated animals.”  How can you compare genetic analysis of an entire species to a circumcised look at a niche registry in a remote island country?

Why would you make such a comparison when your data doesn’t support it and your methodology precludes making such comparisons in the first place? These sorts of throw away comments suggest an author with an agenda to create sound-bites for breed apologists instead of a scientist with ethics and objectivity.

Claire Wade's Toller "Burn" a.k.a. Am, NSDTRC-US CH Edlyn Seastar Dodge N Burn WC CGC CCD JD, is a conformation show champion.

Using complete national pedigree data supplied by the Australian National Kennel Council (ANKC), this study examined the levels of inbreeding and popular sire use in 32 Australian dog breeding populations with different registry sizes.

This statement is misleading.  It says “using complete national pedigree data” but as you’ll soon find out the researchers discarded much of that data, so the use of “complete” is highly inappropriate.  If you want to use the word ‘complete,’ you should include all known pedigree data, worldwide, period.

The world-wide population of Samoyeds descends from fewer than 20 dogs.  This bogus study manufactured 149 observed Sammy “founders.”

GIMME A U!

For Nova Scotia Duck Tolling Retrievers, this analysis was already completed and published before the Wade paper in 2009 by Katariina Mäkii: Population Structure and Genetic Diversity of Worldwide Nova Scotia Duck Tolling Retriever and Lancashire Heeler Dog Populations. For the Australian subpopulation, the study found an inbreeding level of 28% and looked at 13.2 complete generation equivalents worth of pedigree data.

It’s not that this data contradicts the ANKC data, it’s that the Mäki data was not artificially manipulated to exclude known relationships and create bogus founders out of thin air.

The Wade study looks at but the tip of the iceberg and pretends that everything below water doesn’t exist.

Claire Wade's Toller "Burn" is an import to Australia and a stud dog for hire. He's sired at least two litters to date.

The evaluation of data over the entire registration histories of breeds shows inbreeding trends over time.

The world-wide population of Leonbergers descends from only 5 dogs.  This bogus study manufactured 149 observed Leonberger “founders.”

GIMME A D!

This statement is misleading and if it was intended to suggest to the reader that these researchers were looking at “the entire registration histories” then it is a bold lie.

Even for the few breeds which were developed in Australia, I’d like to see some evidence that they were founded within the ANKC and that their breed is represented well within just that registry.  I have my doubts as the study claims to only have data from 1954 from the Australian Cattle Dog and 1955 for the Australian Terrier.  It’s likely that the ANKC is not the parent/founding registry for these breeds and thus their formation is not contained in their registry database (or that data has been excluded in this study).

In the genealogical analysis, animals with known parents born from 2000 to 2009 inclusive were used as the reference population. The completeness of pedigree information was determined by complete equivalent generations (EqG) in the reference population. Founders (f) were defined as animals with unknown parents (typically imported dogs with known parentage but outside of the Australian registry) contributing to the gene pool in the reference population.

This little gimmick is what completely invalidates this entire study.  They are creating “founders” out of thin air, throwing away the information which documents inbreeding and then declaring that there is no inbreeding!

This is Australia we’re talking about so almost every single breed was developed elsewhere and there’s a good chance that the two Australian breeds were not developed within the AKNC, so this one step not only obliterates evidence of the true founder effects on the breeds, it also white washes the very real import bottleneck that Australia has.

Import bottlenecks are no small matter.  Think of the rising inbreeding documented in culturally or geographically isolated human communities: Muslims in Europe & Australia; Polygamist Mormons; Ashkenazi Jews; Bedouins; Martha’s Vinyard, Pitcairn Island, Faroe Islands, Easter Island, Iceland; Hirado, Japan.

As far as dogs are concerned, Australia is no different.  Not only are they geographically isolated from the countries of origin and the largest dog markets in the world, there are also historical import barriers that prevented the easy flow of dogs into the country.  Many of these barriers still exist: it’s very expensive and laborious to sort through all the red tape, bureaucracy, and quarantine to import a dog into Australia.  This greatly limits the gene pool versus the global population of a breed.

If you read this study as presented, you’d be given the mistaken impression that Australian dog breeds are miraculously well off genetically.  This is true only if you blind yourself to reality. But that’s exactly what Wade has done:

Observed values for breed mean inbreeding coefficients are considerably lower than those reported by Maki (2010), who analysed international pedigrees of rare breeds, but are in line with those reported by others based on national data (Calboli et al., 2008; Leroy et al., 2006). For example, it is likely that the observed disagreement with the Maki analysis for the Nova Scotia duck tolling retriever breed (Australian F = 0.03 vs. International F = 0.26) is related to the treatment of imported individuals in our data and, as part of this, the lack of pedigree information from ancestors of the imported dogs. The correspondence of our breed mean results with other national data collections suggests that the majority of the inbreeding identified by Maki (2010) for this breed is probably derived from distant rather than recent co-ancestry. Recent inbreeding is expected to be more deleterious to population health (Hinrichs et al., 2007) and so inbreeding coefficients calculated over more recent population history (such as are presented in this analysis) may have more relevance to breed health than total inbreeding.

The first bit of intentional distortion here is that Mäki didn’t just look at all International data, she also published subdata which included Australia.  Wade clearly doesn’t want to point out that the Australian subpopulation of Tollers is actually more inbred than the International average at 28% inbred versus the 26% Wade quoted.

Wade is trying to claim that the post-import Australian breeders are doing such a bang-up job of avoiding inbreeding that they’ve dropped their COI numbers, this isn’t the case, obviously, as the Australian dogs are more inbred on average, not less.

The second distortion is that Toller inbreeding is “distant” versus “recent.”  Tollers are not an old enough breed to distinguish between distant and recent inbreeding.  As you saw from my recent COI post, Toller inbreeding skyrockets after only 4 generations: 9.57% at 7 generations, 19.35% at 8 generations, and 25.9% at 9 generations.  This is NOT distant inbreeding.

Wade quotes the 2007 paper by Hinrichs et al to suggest that Toller inbreeding is somehow so distant that they are protected from the effects of inbreeding.  The Hinrichs paper defined “new” inbreeding as at least 25 generations of pedigree information! Tollers don’t even have that many generations in their entire history, so the notion that the Hinrichs paper is applicable to Tollers is a joke.  The fact that Wade would try and apply the Hinrichs paper but redefine “new” inbreeding as under 4 generations and “old” inbreeding as anything over that is a horrible distortion of the truth and of another researcher’s work.

When you look at less and say it’s more, you are a liar.

When you look at more and say it’s less, you are a liar.

Claire Wade and the other authors of this paper looked at less information and claimed that it was more.  Knowing that COI levels were more, they manipulated their data to tell you it was less.  

This is fraud. 

At the end of many research papers you’ll find a signed statement that reads something like this:

The Conflict of Interest statement signed by Claire Wade

This represents a commitment to the integrity of the scientific process, the credibility of the presented findings, and a reaffirmation of public trust that is central to peer review and publication.  Conflicts of Interests arise when an author or researcher has any relationship or interest which can influence their judgement and the potential for bias can exist and should be disclosed even if the author believes that such a relationship will not affect their scientific judgment.

While financial conflicts are the most obvious (Researcher X is currently employed by Pharmaceutical Company Z whose drug Amazicure is being investigated in this study), conflicts can arise from personal relationships or rivalries, academic competition, and even a passion for the subject being studied.

Claire Wade is a Toller owner, breeder, trainer, and conformation show exhibitor.  She imported her Toller “Burn” into Australia and it’s possible that his offspring are included as data in this study.  She has a vested interest in the promotion and breeding of Tollers and that is a conflict of interest that should have been disclosed in this study and it was not.

What does that spell?  F-R-A-U-D!   F-R-A-U-D!   F-R-A-U-D! 

This is a chart of what I found as I looked at Burn’s COI from 1 Generation all the way up to 12 generations.

Claire Wade's NSDTR "Burn" has a COI of nearly 30%. If you're a fool you might pretend it's lower than that by looking at only a few generations.

COI is a measure of inbreeding in an individual and it’s almost always denoted with the number of generations that are being looked at in the calculation.  For example, a COI5 or COI(5) is looking at 5 ancestor generations and only calculating the inbreeding that is seen within those dogs.  It ignores consanguinity of any dogs further back in the pedigree for the sake of calculation simplicity.  A COI of rank N is intentionally blinded to all dogs in generations N+1 and beyond.  Some pedigree software packages treat generation 1 differently, so it’s wise to confirm just how many dogs are being looked at if you’d like to compare COIs calculated by different software packages (some count the individual as generation 1, others count the parents as generation 1).

Why would someone want to intentionally blind themselves to more information?  First, the COI calculation is not trivial and doing it by hand is time consuming and arduous for most people.  Second, the calculation requires extensive pedigree information that is not always available for many generations.  Third, looking at lower N COIs will measure recent inbreeding versus deeper inbreeding.

Am, NSDTRC-US CH Edlyn Seastar Dodge N Burn WC CGC CCD JD "Burn" A Nova Scotia Duck Trolling Retriever owned by biologist Claire Wade.

But let’s not fool ourselves that lower N COIs are better or more accurate or that higher N COIs are trivial.  COI calculations are meant to predict the level of homozygosity (doubled up alleles) in an individual due to the same ancestors showing up multiple places in the pedigree.  No matter how many generations you look at, the dog’s pedigree and ancestry doesn’t change.  Consanguinity has created a certain level of doubling up on alleles in the dog and that will not change if you blind yourself to more distant generations.  The more generations you look at, the closer your calculation will approximate the real level of inbreeding present in your dog.  That’s why a COI calculation of N+1 is in general always superior to COI(N).  More information is always equal to or better than less information.

In practice though, we run across both pedigree collapse and a limit to how far back our knowledge extends.  Once we start hitting founder dogs, going back any further generations on those dogs won’t actually give us more information because that information is lost or unknown.  If the oldest known ancestor is at most 10 generations back from our current dog, taking a COI(15) won’t really tell us anything that a COI(11) will.  But how do we know when our COIs are giving us diminishing returns?  Well, we can keep taking higher N COIs until they stop changing much.  They might stop changing because we’ve taken into account all known inbreeding or they might stop changing because we’ve run out of useful information, or both.

To illustrate this, I’ve graphed Claire Wade’s pet Toller Burn’s COI over N generations from N=1 to N=12.  You can see this chart at the top of the post.  Notice how as we look at more generations the COI quickly rises and it doesn’t start to stall until the 10th generation and we don’t see significant change only two generations after that.  If you asked me what this dog’s COI was, I’d say at least 28%.  There’s really no reason to look at fewer generations as none of those numbers would tell you anything of value.

A pedigree chart of Claire Wade's Toller "Burn" showing pedigree collapse

Now if we look at Burn’s graphic pedigree again, we can see why the COI peters out at 12ish generations: there’s really no more information after that point which can move the COI significantly.  Every dog on Burn’s complete pedigree can be traced back to Burn in 11 generations or less.  In the following chart, the “Min Gen” column shows the first generation a given ancestor shows up in and the Max Gen shows the last generation they show up in.  Count records how many times they show up in the pedigree total.  As you can see, all the ancestors show up in 11 generations or less as 11 is the largest number in the Min Gen column.

While there’s certainly information after the 12th generation, we aren’t adding any new names to the pedigree after that point, just connections between them. Each generation after we’d need to see twice the level of inbreeding just to begin to make a difference on the COI given that there are theoretically twice as many possible breedings each level. Seeing as most paths going back are already dead ends, there’s no way we can keep that up. The few lines that go to 20 generations or more are likely to have already contributed to for/against the COI in a significant way already.

In her published paper, Claire Wade would have you believe that looking at 4.1 generations of Toller data is enough. What do you think now that you’ve seen the whole truth?

“The greatest shortcoming of the human race is our inability to understand the exponential function.”

- Professor Albert Bartlett, CU Boulder

This is called exponential growth, and very few natural systems which exhibit this growth model can sustain it for very long given just how explosive the resource requirements are to maintain it.  Overpopulation alarmists use this model to project human populations looking forward in time, and it is often referred to as “The Malthusian Law” after Reverend Thomas Malthus who wrote an early and very influential doom tract on human population growth.

In pedigree analysis we use this model to look backward in time to analyze past generations instead of future ones.  As each older ancestor generation is double the size of their children’s generation, there is one more ancestor in that next oldest generation than all the previous younger generations combined.  When our knowledge of the pedigree runs out we call that last generation the foundation, and much like a real pyramid, it’s theoretically a large base upon which all further generations are built.

The 10 generation pedigree chart for my Border Collie Mercury

Although this tree grows backwards in time, we live life going forward so we can not manufacture twice the ancestors every new generation to accommodate our theoretical tree.  We quickly discover that as we go back in time the number of theoretical ancestors keeps growing as the number of actual new ancestors falls.  At 32 generations we’ve accounted for 8.5 Trillion ancestors, and this is more ancestors than total people alive today.  While it might be hard for you to think of your 32nd Great Grandfather, this actually isn’t such a great genealogical distance for dogs.

The distance between my Mercury and Old Hemp who was born in 1893 varies between 15 and 71 generations.  The dogs that show up between 25 and 35 generations ago are almost all clustered in the mid 1950s.  So one human lifetime is enough to witness a great many generations of dogs.  An equivalent number of human generations might take you back to the mid 14th century when the Black Death wiped out huge swaths of Europe’s population.

There weren’t even 4.3 trillion people on the planet in the 1350s, the number was much closer to 430 million, only one tenth the number of people we’d need to fill spaces in our 32nd generation of our pedigree.  So even if the entire population of the world at that time was one “generation” and an equal ancestor, they’d each have to appear 10 times.  This is a pedigree collapse of 90%.

80 generation pedigree chart of my Border Collie Mercury showing the diamond shaped pedigree collapse

If we choose to not repeat ancestors and give each unique ancestor only one space in our tree, but still draw branches connecting them to all their offspring and their parents, we could visualize how our actual ancestor tree differs from the theoretical.  You’ll notice in the above pedigree of my Border Collie Mercury that after expanding out in the predicted pyramid shape the pedigree eventually starts to shrink.  The resulting diamond shape is a visual representation of pedigree collapse.

Pedigree collapse is caused by inbreeding; both recent close breeding and more distant founder effects.  When a breeder inbreeds they are cutting the pedigree pyramid of their stock down dramatically.  When two cousins mate, creating a COI of only 6.25%, they have actually permanently cut out 25% of the possible ancestors for their offspring.

A normal person has 8 great grand parents, the product of a first cousin mating has only 6, a 25% pedigree collapse.

Normal Norma is not inbred and she has the expected 4 grand parents and 8 great grandparents.  Inbred Ted’s parents are first cousins, meaning that one of their parents are siblings.  This means that Ted has only 6 great-grandparents because two of them are doing double duty in his pedigree.  This represents a pedigree collapse of 25% and that continues back forever into his history.

Pedigree collapse and the resulting loss of genetic diversity doesn’t require recent inbreeding to have a devastating effect.  When breeds are formed from a small founding generation and/or go through population bottlenecks, there simply aren’t enough ancestors to go around and there aren’t enough mating combinations to sustain genetic diversity.  This causes inbreeding to rise even though breeders avoid close pairings.

A complete pedigree chart of Claire Wade's Toller "Burn" showing pedigree collapse. Burn is on the far left and the founding Tollers on the far right, sires on top, dams on the bottom.

For example, let’s look at Claire Wade’s Nova Scotia Duck Tolling Retriever: Am, NSDTRC-US CH Edlyn Seastar Dodge N Burn WC CGC CCD JD  3/8/2007 a.k.a. ”Burn.”  I’ve rotated his pedigree pyramid so that it fits nicely on a computer screen and matches the standard presentation on written pedigrees: sires over dams, older generations to the right.

Burn's 5 generation pedigree showing few repeated ancestors.

Burn’s breeding is not very close in recent generations;  his first repeated ancestors are three great grandparents.  Two of them show up again once in the next generation and one shows up twice.  But you can see from his complete pedigree chart above that Burn’s pedigree quickly collapses into only a handful of dogs.  You can even see the popular sires and dams as they have a fan of connections coming into them; each one of those lines represents ancestor loss as that connection could have been made with a unique dog, but the Toller’s foundation is so small that swift pedigree collapse was guaranteed from the founding of the studbooks combined with early and often popular sires and an aversion to outcross to new blood.

Burn's 7 generation pedigree showing many repeated ancestors.

When we look at only two more generations of Burn’s pedigree you can see that the vast majority of ancestors in those later generations is highlighted in a variety of colors indicating repeat ancestors that show up elsewhere on the pedigree.  This is inevitable in all Tollers as there are only so many ancestors they have to work with and many of those ancestors were not widely bred.

Remember that in my earlier post I showed how a founder would have to have over 10 children that each survived to pass along their genes for the gene pool as a whole to retain over 99.9% of that founder’s genome.  As you can see in the fish shaped pedigree chart above, several of those “founder” dogs on the far right had only one recorded child in the Toller studbook. At most 50% of their genes would be conserved in that child and we can see that often their children had very few children as well.  This indicates that Tollers had a very small founding population and that a big chunk of the extant genetic diversity in that small founder pool was lost almost immediately.

In my next Toller post, I’ll examine how looking at a limited number of generations for a Toller COI can attempt to hide the real situation that breed is in.

NUNC LENTO SONITU DICUNT, MORIERIS.

Now, this Bell tolling softly for another, says to me, Thou must die.

PERCHANCE he for whom this bell tolls may be so ill, as that he knows not it tolls for him; and perchance I may think myself so much better than I am, as that they who are about me, and see my state, may have caused it to toll for me, and I know not that.

- John Donne, Devotions Upon Emergent Occasions

Nova Scotia Duck Tolling Retrievers don’t know they’re genetic wrecks, they are blissfully unaware that in the transition from regional purpose-bred sporting dog into a studbook governed purebred show dog, their gene pool was severely bottlenecked and harmful diseases came to the surface.

They know not that the bell is tolling for them.  But those who are about them, breeders and scientists alike, have no excuse to deny the precarious and unsustainable genetic position the breed is in today.

This Toller probably isn't the product of a father x daughter mating, but the gene pool is so small, it has the same level of inbreeding.

Two recent genetic studies have brought this issue to light but with very different conclusions.  One study was done by Katariina Mäki (PhD Animal Science) a Finn who does not own, show, or breed Tollers and the other study was done by Claire Wade (BSc PhD) who is a breeder and exhibitor of Tollers in Australia.

One of the studies is comprehensive and looks at a near exhaustive global studbook for the breed and the other study looks at only those pedigrees that are in one country only (and not even a very important country for the breed at that) and intentionally throws away the pedigree information from the country of origin and all other countries too.

One of the studies found nearly 13 generations of Toller ancestors for their COI calculations (about 16,000 ancestors) while the other one found just over 4 generations of ancestors (about 30 ancestors).  That’s more than 500 times the information.

One study traced every dog it could back to the true founding population, the other study pretended that the second a dog landed in Australia, its pedigree was erased and it was a amazingly unrelated to all the other import dogs and was thus a “founder” of the breed.

One study looked at 28,668 Tollers and found 9.8 effective founders while the other study looked at only 589 Tollers but declared there to be 84 founders with 26 founder equivalents.

One study found that the average inbreeding coefficient in Tollers was 26%, while the other study declared it to be less than 3%.

One study found that the effective population size was only 18 individuals while the other found that the value was 47.

Which study would you trust more?  The one with 50 times as many dogs, a comprehensive pedigree analysis, done by an unbiased researcher OR the one done by a show breeder who has a vested interest in making her breed look good who intentionally limited the scope of her analysis to the dogs that were imported into her own country?

Guess which researcher claims that the Tollers are a robust and healthy breed and that any thoughts of out-crossing are scandalous and should be ignored?

Professor Claire Wade, of course, who is a biased hack that should clearly know better.  In a future post, I’ll walk you through her paper and explain her deliberate attempt to whitewash the state of her breed and how her own bias and unchecked conflict of interest drove her to commit academic fraud.

Terrierman doesn't know much about rats.

Patrick “I didn’t actually read the study I linked to…again” Burns recently posted a vapid comparison of dog population genetics to that of island rats.  His summary of the study is a complete fabrication that doesn’t reflect in any way what was looked at or concluded in the actual study.

Since he’s prone to editing his posts after the fact, here is the relevant section:

Imagine a pregnant rat jumps ship on to a large island that is 200 square miles in size.  The population of rats multiplies very rapidly but without any apparent long term problems due to inbreeding.  How is that possible?  Answer:  With rats, massive population numbers within a short period of time are possible, and a mid-sized island of 200 square miles (over 259,000 acres) can easily hold a million rats.  In this situation, genetic drift and mutation will eventually result in a population with little or no obvious genetic dysfunction.  On an island with 1,000,000 rats, in which each rat lives for a year or so, a 100-year old population of theoretically “inbred” rats will have very low coefficients of inbreeding, no inbreeding depression, and no discernible early mortality due to genetic weakness.  To be clear, this is not a theory; rats have colonized almost every island in the world exactly this way.

He tells us that the study describes his scenario EXACTLY.  But the study does no such thing.

First, the Rat study looks at a very small island:

We sampled and genotyped most individuals of a Norway rat (Rattus norvegicus) reinvasion on Moturemu island (5 ha) in New Zealand.

5 hectares is about 2 one-hundredths (0.019) of a square mile, not 200 square miles.  Patrick botched the math by a factor of 10,000.

Second, the study looked at a total population of only 30 rats on the entire island:

Population size was most likely between 30 and 33 rats.

30 rats is nowhere near the 1,000,000 rats Patrick is hallucinating.  He botched this one by a factor of over 33,000.  Even if we consider his suggested density of 5,000 rats per square mile, that equates to 19.3 rats per hectare.  This study found a population of 6 rats per hectare.

Overall, our estimatesof reproductive success suggested the population was stable or declining, possibly as a result of density dependence after reaching carrying capacity. Density dependence plays an important role regulatinginvasive rat populations at the breeding level (Efford et al. 2006), however, survival rates of offspring and adults are likely to be high given the absence of predators on the island and abundant food resources following the previous rat eradication.

Given that the population was stable or declining and the conditions for survival were good, the rat population here as likely at a stable equilibrium point.

Despite the apparently increasing inbreeding the population of invading rats had still reached a high density and probably the carrying capacity of the island.

Third, the study does not support a very rapid expansion of population in the manner Patrick is suggesting.  Rats certainly have the potential, but we don’t see that being exploited here.

In high-density populations Norway rats can breed rapidly and, although not always, in all seasons, with a gestation period of 21–24 days and average litter sizes of 6–8 (Innes 2005). They have a life expectancy of 1–2 years in the wild

The population increased from perhaps as small as one pregnant female to 30 individuals over 2 years and appears to have petered out at that level.

After the Norway rats and mice were initially eradicated off of the island in 1992, several further eradications took place:

In order to prevent reinvasion poison bait stations were established and the island was monitored annually. The island remained rat free until February 1999, when rat sign was detected. A contingency response using traps and poison to confirm presence apparently resulted in eradication, although no bodies were recovered. No further sign was detected until April 2002, when a new population was confirmed on the island 10 years after the first eradication.  Therefore, it is likely that a new population became established in 2002, and 2 years later the eradication effort provided an opportunity to study invasion dynamics.

A new eradication was conducted in May 2004, providing us with a single opportunity to sample most individuals from an approximately 2 year old invasion of a small island.

Fourth, this observation also completely invalidates Patrick’s claim that the study was looking at “long term problems due to inbreeding.”  The title of the study is “Early colonisation population structure of a Norway rat island invasion;” note the use of the words “Early” colonization, and “population structure.”  The study looked at animals after only 2 years of assumed isolation and it analysed population structure, not inbred disease specifically.  This is neither long term, nor inbred disease analysis.

Breeding was most likely seasonal but breeding cessation may also have been linked to density dependence or increased inbreeding.  However, genetic effects on population demography usually only have long-term consequences on population persistence, and inbreeding is not likely once established beyond a certain size (Jamieson et al. 2007).

Fifth, it’s worth noting what the study did not look at.  It did not measure the individual health of the rats, it did not study the mortality rate or the fertility rate, and it didn’t even manage to compare the homozygosity levels of the island rats with a likely source population on the landmass near the island.

In order to obtain samples from the putative source population, trapping programmes were also conducted at three different sites on the surrounding mainland for a total of 400 trap nights. This resulted in the capture of 4 ship rats and 14 mice but no Norway rats were obtained, consistent with their rarity outside offshore islands.

So, long story short, there’s nothing in this study that contradicts anything I’ve written about inbreeding and population genetics as Patrick implies, and everything in the study contradicts or fails to support Patrick’s fantasy scenario.  I know he didn’t read the study, but I doubt he even read the abstract.  That, or the old-timers is kicking in.  He is clearly unburdened by facts and unhampered with reason.