With grateful acknowledgment to Jocelynn Jacobs-Knoll, DVM, Linda A. Frank, MS, DVM, Diplomate ACVD, and Manon Paradis, DVM, MVSc, Diplomate ACVD for their assistance in preparing this article

Coat funk is the common name for a disorder that causes adult malamutes to experience hair breakage and loss.  Accurate diagnosis of coat funk is complicated by the fact that symptoms vary widely and because other conditions may have similar clinical signs.  The condition appears in other Spitz-type breeds such as Pomeranians, Samoyeds, Chow chows, Keeshonds, and Siberian huskies.  A similar disorder is also seen in miniature poodles and occasionally cocker spaniels.  Affected animals rarely have any other physical abnormalities and usually have normal blood values.  The disorder is so little understood that most experts simply call it "alopecia X." 

Clinical Presentation

In malamutes, owners typically first notice guard hairs breaking off around the collar area.  Many owners report a pattern of abnormal shedding.  Some dogs never blow coat normally, while others shed normally for a few years and then stop shedding altogether.  This may pass unnoticed at first, but if the dog is not shedding his old coat, then he is also not growing fresh healthy coat.  As the coat ages, hairs eventually become stripped of their protein protection, causing color to fade and breakage to occur.  Guard coat tips may turn from gray or black to a burnt orange or reddish color, and the coat may begin to feel dry and brittle.  Because tail hairs in malamutes do not normally shed as often as the rest of the body, the tail takes on a sparse or hairless appearance sooner than the rest of the body.  Guard coat along the hips may begin to show wear, followed by the trunk.  Eventually, much of the guard coat is gone, leaving the dog dressed in a dry, wooly undercoat.  Except for his head and legs, he may look like he has a light-colored "puppy coat" or like a sheep with a malamute head. 

At any point in the condition's progression, the dog may begin to have bare patches which may not be all that noticeable at first.  These tend to spread as the disorder progresses, although typically the process is slow in malamutes.  Some dogs may become quite naked as they age, but most maintain the wooly appearance for many years.  Exposed skin may turn black in color and may eventually become thick and leathery in response to the lack of protective fur. 

Just as every individual human experiences disease differently, so do dogs.  The above symptoms can happen in most any order, and a given dog may have all or just a few of them.  The symptoms can progress fairly quickly, or they may take as much as eight years to develop.  Owners of CF dogs have reported other symptoms, from scaly skin and sores, to a funny odor, to a greasy feel to the coat.  Some dogs seem to spontaneously improve, then get worse again.  Symptoms can become apparent as early as two years old, but more commonly the dog is between three and five years old when the first symptoms show up.  Anecdotally, males seem more likely to get it than females, and of the females who get it, most seem to be spayed.  However, we desperately need more data to help us to understand the disease better, which dogs are affected and why, how to diagnose it, and how best to treat it.

Diagnosis

Diagnosing alopecia X, or coat funk, can be challenging.  There is no single test that definitively indicates coat funk.  Rather, endocrine disorders such as hypothyroidism and Cushing's disease must be ruled out, as well as post-shaving alopecia and Sertoli cell (gonadal) tumors.  Post-shaving (also called "post-clipping") alopecia occurs when the dog's fur is shaved close to the skin and fails to grow back, sometimes even after a couple of years.  In some veterinary literature, follicular dysplasia is another differential diagnosis, but it is unclear whether follicular dysplasia would be the primary diagnosis or whether it is usually secondary to some other underlying disease state.  In fact, the term follicular dysplasia may describe several different disorders, such as alopecia X, color dilution alopecia, and recurrent flank alopecia.  For each of these conditions, the dysplastic change is different and more or less characteristic for the disease.  Experts also recommend doing skin biopsies to aid in diagnosis.  Typically, they are consistent with endocrine disorders.  (Mueller, 2003; Paradis, 2002; White, 2001; Schmeitzel, 1999)  "Flame follicles," or telogen phase follicles with "excessive tricholemmal keratinization" in medical jargon, are strongly suggestive of alopecia X, but can also be associated with other disorders.  (Paradis, 2004)  Diagnosis is therefore achieved through careful case histories and differential diagnosis.

Research to date

Research on Alopecia X stutters along, much of it supported by Pomeranian fanciers.  So far the results have been disappointing.  Several disease processes have been postulated, but none of them have been proven.  Most veterinarians believe that the disorder is caused by an endocrine abnormality, because it so often responds to hormonal therapies.  Others believe that the problem may reside in the hair follicles themselves, which are influenced by hormone levels.  Follicles have receptors for various hormones, including sex hormones and growth hormones. 

Adrenal hyperplasia-like syndrome has been the most popular description, suggesting that the disease is caused by too much sex hormone-producing activity in the adrenal gland, which can affect hair growth.  Researchers have tended to focus on the adrenal gland, but research is complicated by the fact that these sex hormones can be produced both there and elsewhere in the body.  Growth hormone imbalances have also been suggested as the culprit because there have been reports of the disease responding to growth hormone injections.  Others postulate that the condition is caused by an abnormality within the pituitary gland because of the pituitary's effect on the secretion of many types of hormones.  (Jacobs-Knoll, 2004)

Dr. Lynn Schmeitzel first focused on the possibility that sex hormone imbalances caused by a complicated interaction of adrenal hormones played a role in disrupting hair growth (adrenal hyperplasia-like syndrome).  Along with more technical reasons having to do with adrenal function and molecular binding, Dr. Schmeitzel cited the fact that affected dogs sometimes respond well to neutering or to treatment with sex hormone altering drugs.  More recently, Dr. Schmeitzel suggested that many of the disease's characteristics might be explained by a combination of a primary hair follicle disorder that is triggered by a sex-hormone related signal.  (Schmeitzel, 1999; Paradis, 2002)  Dr. Linda Frank, of the University of Tennessee, is leaning in that direction as well.  (Frank, 2004)

Dr. Frank's group developed a study to try to answer Schmeitzel's questions about whether the disease was caused by an adrenal steroid hormone imbalance by examining data about cortisol, growth hormone, and sex hormone levels.  They did a retrospective analysis of data gathered over a period of seven and a half years on various breeds, including eight malamutes.  Comparisons of blood levels before and after adrenal stimulation with ACTH showed no striking patterns.  None of the correlations were strong enough to support any of the various adrenal theories about how the disease works.  Dr. Frank's group concluded that, "based on our results, there does not appear to be a single hormone abnormality associated with the hair loss and not all dogs or breeds have hormone alterations." (Frank, et al., 2003, 95.)  Malamutes were among the breeds that did not have much of an alteration in hormone levels, but the results are not conclusive because of the small sample size.  The study suffered from a lack of comparative norms for the various breeds, as well as the raw numbers that would be needed to achieve statistical significance.  As is often the case, its primary achievement was in ruling out any easy answers and showing where more research might be fruitful.  Dr. Frank is currently exploring the notion that estrogen receptors in hair follicles play a role.  (Frank, 2004)

Dr. Schmeitzel (1990) and Dr. Julie Yager (Paradis, 2002) have speculated that breeding for hirsutism (abnormally big fluffy coats) may have been inadvertently selecting for an unspecified adrenal disorder.  Dr. Schmeitzel suggested that when piggy-backed onto another disorder similar to male pattern baldness, the result might be runaway alopecia.  She based this hypothesis on an analogous condition in human women, which can cause either hirsutism or pattern baldness, depending on other genetic factors.  (Schmeitzel, 1999)  Yager wondered whether breeding for dogs who will carry fluffy puppy coats into adulthood (neoteny) may be causing the problem.  To date, these hypotheses are merely speculative and need additional research.   

Dr. Jocelynn Jacobs Knoll worked with Dr. Paul Bloom at Michigan State University to see whether coat funk malamutes might have any laboratory results markedly different from normal malamutes.  Not only might this shed light on the mechanism of the disorder, but a simple blood test to determine whether a dog has coat funk would make it much easier to diagnose early.  Early diagnosis is critical in order to make responsible breeding decisions and, perhaps, for treatment purposes.  Because of the small sample size (five affected dogs and five unaffected dogs for comparison), the results were indeterminate.  However, slight abnormalities in sex hormones were noted in the coat funk dogs and merit further study.  (Knoll, 2001)

Treatment

There is no proven safe and effective treatment for coat funk.  Some owners have reported coat improvement with nutritional supplements such as Missing Link (at doses from 2 to 4 times those recommended by the manufacturer) or ground flax seed or oil.  One interesting theory is that malamutes evolved on a diet rich in Omega 3 fatty acids, and that current diets do not provide them in the ratios needed.  There have been no studies on this theory, and it seems likely that if a dietary supplement was all that it took to make the problem go away, there would be many fewer dogs with active coat funk.  However, every clue is useful when you are trying to figure out such a mysterious condition.  One wonders whether a diet of seal meat would be feasible... .

Nearly all veterinarians who study alopecia X recommend neutering as the initial therapy for intact dogs.  Many dogs will regrow a normal coat either permanently or, more likely, for several months to several years.  (White, 2001; Paradis, 2004)   Pharmaceutical interventions are considerably less benign than the aforementioned dietary changes and not that much more effective.  They are therefore rarely recommended for a condition that most clinicians consider essentially cosmetic.  One drug that has been used with some success is mitotane (Lysodren), a chemotherapy agent that erodes the adrenal gland, thereby slowing production of hormones.  The drug is properly used to treat Cushing's disease (hyperadrenocorticism), whose symptoms mimic those of coat funk, but which is very rare in malamutes.  The dog has to be monitored closely to guard against throwing him into Addison's disease (hypoadrenocorticism), which can be life-threatening and difficult to treat.  Given the risks and its patchy efficacy, most veterinarians do not recommend mitotane for coat funk dogs.

Another potential treatment is the male hormone methyltestosterone, but it is both very expensive and very difficult to obtain.  More importantly, it carries a high risk of liver damage and frequently causes aggressive behavior.  The disorder has also been treated with porcine or bovine growth hormone, but most veterinarians consider it undesirable because of the high risk of iatrogenic diabetes, which may be temporary or permanent.  Like methyltestosterone, growth hormone is hard to get and expensive.  Moreover, none of these treatments have been proven to be effective more than temporarily.  Coat loss nearly always recurs.  Dr. Rosario Cerundolo has been getting promising results in Europe with trilostane, a drug that interferes with the production of adrenal steroids.  However, it has not been thoroughly tested and is not yet available in North America.  (Cerundolo, 2001; Paradis, 2002)

Dr. Manon Paradis popularized the use of melatonin in treating alopecia in dogs.  It is readily available over the counter in the United States (but not in Canada) and has minimal side effects.  (Paradis, 2004)  Some dogs may appear lethargic (melatonin has also been used to ease anxiety or as a sleep aid), but the effect goes away when doses are reduced.  Best results occur when a 3 to 6 milligram dose is administered three times daily to maintain blood levels. (White, 2001)  Melatonin is a hormone secreted by the pineal gland that affects, among other things, hair growth cycles.  (Schmeitzel, 1999)  Improvement, if it is going to happen, is usually seen within 8 to 12 weeks, at which time the dose can be lowered until it is not needed any more.  (White, 2001)  If the alopecia recurs, melatonin therapy can begin anew.  Melatonin is not advised in diabetic dogs because it may cause insulin resistance.  (Paradis, 2002)   Dr. Jacobs-Knoll has anecdotal reports that malamutes do not seem to respond to melatonin.  (Jacobs-Knoll, 2004)  Indeed, the success rate with melatonin was only about 33 percent among all dogs treated by a roundtable group studying the disorder.  Dr. Frank has reported better results from a controlled study that is currently under way at the University of Tennessee.  (Frank, 2004)   Melatonin's safety and low cost make it a reasonable therapeutic alternative.  (Paradis, 2002)  Breeding animals may experience temporary reproductive side effects, but in any case it is prudent to avoid breeding affected animals until we know more about how coat funk is inherited.  (Schmeitzel, 1999)

Mode of Inheritance

Current studies of alopecia X have so far not identified a clear mode of inheritance, either by pedigree analysis or by DNA marker.  In Japan, Dr. K. Takada and his group worked on a candidate gene (21-OH) that was identified with congenital adrenal hyperplasia (CAH) in humans.  They cloned the analogous gene in dogs and sequenced it, but there were no mutations identified.  Dr. Takada's group concluded that the 21-OH encoding gene was not responsible for the alopecia condition in Pomeranians.  (Takada, 2002)

Because coat funk appears to be more common in males, it has been speculated that it may be an X-linked disorder, i.e., the gene(s) might be found on the X chromosome.  Dr. Jacobs-Knoll collaborated with Dr. Gary Johnson of the University of Missouri on a small study to determine whether a few very specific sites on the X-chromosome might have a marker for the disorder.  (Knoll, 2000)  Luck did not smile on their efforts, but every little piece of information, in this case that the gene is not on either end of the X chromosome, moves us closer to finding a marker.  Dr. Johnson is currently working on finding a marker for the Pomeranian alopecia under CHF grant number 2290, which is nearing completion.  If he continues this work, we hope that he will add malamutes to his data collection.

In malamutes, we see clear evidence of family ties among dogs who develop the condition.  However, even closely related dogs may have very different clinical presentations, and its appearance in any given pedigree is so far frustratingly random.  Experts believe that coat funk is likely to be a polygenic disorder.  (Jacobs-Knoll, 2004; Paradis, 2002)  Because of the wide variety in the clinical signs and progression of the disease, its expression may depend upon the level of penetrance of the gene(s).  (Paradis, 2002)  In other words, one dog may be mildly affected and never get any worse, while another may develop signs early and deteriorate rapidly, all because of how "strongly" or "weakly" the genetic potential is activated.

Conclusion

As of this writing, we do not know how to predict when coat funk will strike, nor do we know how to treat it successfully.  The physiological mechanisms are likewise poorly understood.  Much more research will be necessary to help us defeat this frustrating condition.   We are working with a veterinary epidemiologist to develop a survey that will give us more information about coat funk. Please visit frequently to check on our progress. With all of us working together, we can get rid of coat funk and restore our proud breed to its natural beauty. 

References:

1. Cerundolo, Rosario, D. H. Lloyd, A. Persechino, H. Evans and A. Cauvin, "The use of trilostane for the treatment of 'alopecia X' in Pomeranians and miniature poodles," in Veterinary Dermatology  2001, 12, 225-41. 
2. Frank, Linda A., personal communication, July 2004.
3. Frank, Linda A., Keith A. Hnilica, Barton W. Rohrbach, and Jack W. Oliver, "Retrospective evaluation of sex hormones and steroid hormone intermediates in dogs with alopecia," in Veterinary Dermatology 2003, 14, 91-97.
4. Jacobs-Knoll, Jocelynn, "Coat Funk Update," presented at the AMCA National Specialty in Minnetonka, MN, October 2001.
5. Jacobs-Knoll, Jocelynn, "Canine Alopecia (Coat Funk or CF)," in Alaskan Malamute Research Foundation web site, AMRF Coat Funk Page, April 2000.
6. Jacobs-Knoll, Jocelynn, personal communication, July 11, 2004.
7. Mueller, Ralph S., "Noninflammatory alopecia in dogs," in Veterinary Medicine (June 2003): 518-34.
8. Paradis, Manon, "Roundtable Summary," in Dermatology Dialogue, summer 2002.
9. Paradis, Manon, personal communication, July 2004.
10. Schmeitzel, Lynn P., "Alopecia X of Nordic Breeds," Fifteenth Proceedings of the American Association of Veterinary Dermatologists Annual Meeting, April 1999.
11. Takada, K., H. Kitamura, M. Takiguchi, M. Saito, A. Hashimoto, "Cloning of canine 21-Hydroxylase gene and its polymorphic analysis as a candidate gene for congenital adrenal hyperplasia-like syndrome in Pomeranians," in Research in Veterinary Science, 2002, 73, 159-63.
12. White, Pat, "Identifying 'look-alike' endocrine diseases," DVM: the newsmagazine of veterinary medicine, June 1, 2001.  Pat White's article