The dog-show world—the American Kennel Club in particular—is often blamed for having created these genetic diseases through an obsessive preoccupation with physical appearance in breed definitions. But that criticism misses most of the point. Selecting for one thing (such as looks) doesn't mean you can't also select for other things (such as herding behavior and good health) at the same time. Breeders can narrowly select for traits that suit their fancy and still not unlock recessive diseases or lose desirable behaviors—if they start from a large founding population and make sure that they keep a broad representation of the founders' gene pool in all subsequent generations. Working foxhounds are intensely scrutinized for body conformation at competitions; they are also meticulously selected for their ability to follow a fox's trail and to work together as a pack, and their readiness to speak when they find scent. Border collies are selected for herding ability; they almost all happen to have white collars and white tips on their tails as well.
The real source of genetic trouble in many breeds is not so much that dogs are being bred for looks or to meet other narrow criteria as that the breed has relatively few founders. Many breeds suffer from the "popular sire effect" as well, and here criticism of the breeding world is more justifiable. A stud dog that wins a blue ribbon at a major show may father hundreds of litters, swamping the gene pool with his virtues—and defects—and crowding out some other ancestral lines altogether. The problem is worse in breeds that have gone through a genetic bottleneck. A number of breeds that exhibit strange recessive ailments, including Irish wolfhounds, flat-coated retrievers, Portuguese water dogs, and Shar-Peis, almost disappeared at some point during this century and were reconstituted from very small populations.
Streaks of aggressiveness in a breed like the springer spaniel could likewise be the result of recessive traits being inadvertently locked in to a closed population with a relatively small founder base. But selection may play a role too, and this is another instance in which the show ring may be to blame. Dogs that carry their heads and tails erect catch the attention of judges, and thus tend to win shows. Those are also the marks of a dominant, hence aggressive, dog. Some show-dog breeders don't actually live with their dogs (the dogs stay in kennels), and so are willing to put up with bad traits in a single-minded pursuit of the perfect coat or the half-pricked ear.
One strikingly counterintuitive conclusion of modern genetic studies is that the worst way to correct these mistakes of the past is to weed the carriers of genetic diseases out of the breeding population. The central fallacy of the racist view of eugenics was embodied in the claim that purity is genetically invigorating. In fact just the opposite is true—genetic diversity is invigorating (thus "hybrid vigor," well known to agricultural breeders), because it helps to ensure that breeding for homozygosity in desirable traits doesn't at the same time breed for homozygosity in undesirable traits at other sites on the genome. Even disease carriers have a valuable contribution to make in preserving heterozygosity: a dog that carries an epilepsy gene, for example, could also very well carry a gene that protects against cancer. That is a point that Deborah Lynch, of the AKC Canine Health Foundation (which spends about $1 million annually on academic research into canine diseases, about half of that in genetics), emphasizes.
The key is not to cull the carriers (that is, animals that possess just one defective gene and so don't exhibit the ailment) but, rather, never to breed two carriers. "The first thing a novice breeder will do is say, 'Oh, my gosh, there's a problem in my line, I'm going to get rid of everything and start over,'" Lynch says. "Well, all you're doing with that is starting over with someone else's problems." The solution is to keep parentage as diverse as possible while correcting the problem—and correcting it will become easier and easier as more genetic probes for specific canine ailments are developed.
Clearly, dog breeders are becoming far more sophisticated in their understanding of genetics and more forthright in facing up to inbred problems that just a few years ago they tended to disregard. But old habits die hard, and amid the eclat of new genetic research one can occasionally make out strains of Leon F. Whitney's old tune. A number of breeders are seeking genetic probes not to detect disease but rather to measure "genetic purity"—to test, for example, if a Vizsla really is a Vizsla, or if (horrors) tainted blood has crept in. But breeding for the purity of the breed is like hiring a storyteller not on the basis of how well he tells stories but after looking at how many generations of Irishmen he has in his background. The fact is that any genetic markers that happen to be associated with a given breed are just a matter of chance. Yes, it is possible, owing to the high degree of inbreeding in dogs, to find some (usually junk) DNA that is unique to one breed. But that is a matter of genetic chance, not genetic necessity, and a breeder who set out to foil the system could easily do so. A dog might be bred deliberately to pass the Vizsla genetic-purity test while looking like a cross between a Pekingese and a coyote. A more sensible strategy would be to breed dogs for chosen characteristics and for the maintenance of genetic diversity. From a scientific point of view, it is perfectly possible to do this while satisfying the desires of dog breeders to maintain distinctive breeds. Zoo keepers go to great lengths to ensure that subsequent generations of the rare species in their care—considered as a worldwide population—will reflect the total range of existing genetic diversity within the species. Zoos are continually swapping breeding animals or frozen semen.
Individual dog breeders do not have the same incentive to act in concert; the short-term rewards still go to those who can offer puppies that were sired by a champion dog. In the long run, however, the increased availability of genetic tests will make it obvious which breeders have sacrificed good genes in their quest for puppies with flashy pedigrees. Already there are genetic probes available to detect carriers of cystinuria in Newfoundland dogs; Von Willebrand's disease, a bleeding disorder, in poodles and Manchester terriers; and copper toxicosis in Bedlington terriers. Many breed clubs are requiring, or providing strong incentives for, the use of such tests as they become available.
The sheer diversity of dog breeds, and the fact that up until a hundred years ago—a blink of an eye in terms of evolutionary time scales—genes flowed freely throughout the global dog population, together imply that we still have ample genetic reserves that can be drawn on to undo any damage recently done. Taken as a whole, the genetic diversity of the dog remains as great as that of its wild ancestors.
We can take some reassurance, too, from the fact that mutts, owned and unowned, will always be with us. Despite the efforts of neo-eugenicists to ostracize them, mutts constitute a vibrant reservoir of canine genetic diversity. Mutts tend to be healthy dogs, because of hybrid vigor. They also tend to be good dogs. And in a very real sense mutts today embody the evolutionary heritage of the True Dog—that animal that evolved with us, that adapted to and exploited our society, and did so largely on his own terms. Defiant of human fashion and whim, selected only in accordance with the ancient evolutionary dictate that demands nothing more than an ability to get along with rather gullible human beings, mutts are really what dogs are about. If worst comes to worst, perhaps they will set us straight, just as their ancestors so ably did—at least for 99,900 of the past 100,000 years.