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The importance of nutrition in coat quality and skin health of dogs and cats

PUBLICATION DATE:  21/06/2007
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AUTHOR:  B.M. VESTER and G.C. FAHEY, JR. (Courtesy of Alltech Inc.)
Nutrition plays a key role in maintaining healthy skin and coat condition in dogs and cats. The hair coat of an animal is its first line of defense. Maintaining a coat that is healthy in appearance is important to the animal and to the owner for aesthetic reasons.

The skin, the largest organ in the body, serves as the second barrier to outside antigens.

Cracks in the skin may allow bacteria and toxins from the environment to enter the body. The health of both the skin and coat of dogs and cats is affected directly by the nutrition of the animal. Therefore, feeding a complete and balanced diet is critical in maintaining skin and coat health.

Nutritional deficiencies and excesses both can have detrimental effects; however, genetic defects in some animals also may result in a decrease in absorption of some essential nutrients needed for optimal skin and coat health. The most notable nutrients involved in skin and coat health include protein, fatty acids, and zinc, as well as select vitamins and trace minerals. Each will be discussed in brief in the following paragraphs.


Skin

Thickness of skin varies between dogs and cats. Cats have the thickest skin on the dorsal neck, lumbar, and sacral regions while the thinnest lies on the lateral sides of the lower legs and thigh area. Thicknesses of 375 to 1,900 μm were noted in cats (Strickland and Calhoun, 1963).

It was observed that, in general, the thickness of a cat’s skin decreased moving dorsal to ventral along the trunk and proximally to distally on the legs (Strickland and Calhoun, 1963). The thickest skin in dogs generally was found covering the head and neck region while the thinnest skin covered the ears and inguinal and axillary regions of the body (Webb and Calhoun, 1954).

The skin of dogs and cats consists of three primary layers, the epidermis, the dermis, and the subcutis. The epidermis includes five layers, stratum corneum (the dead layer), stratum granulosum, stratum lucidum, stratum spinosum, and stratum germinativum (the living layers) (Thomsett, 1986).

Appendages of the epidermis include hair, nails, claws, and apocrine, eccrine, and sebaceous glands (Thomsett, 1986).

The stratum corneum contains several immunologically important substances including immunoglobulins, complement proteins, and albumin, and it functions to prevent excess water loss in the animal (Thomsett, 1986; Laflamme, 2004).

The living layers of the epidermis function as the site of cell replication, differentiation, and keratinization. These cells eventually move to the stratum corneum and are eventually sloughed from the body. Cell turnover rate for the epidermis is approximately 21 to 23 days (Baker et al., 1973).

The epidermis in the hairy skin regions of the cat consists of four distinct layers, stratum germinativum, stratum spinosum, stratum granulosum, and stratum corneum (Strickland and Calhoun, 1963).

The stratum lucidum layer is noticeably absent in these areas, but is present in non-hairy skin regions of the cat (Strickland and Calhoun, 1963).

The epidermis in mongrel dogs consists of all five of the regions mentioned above.

However, it was found that the stratum lucidum was absent in the head, neck, shoulder, axillary, sternal, and abdominal regions of the dog (Webb and Calhoun, 1954).

Beneath the epidermis layer of the skin is the dermis. The dermis functions to provide structure, for water storage, and as a protective layer against trauma (Thomsett, 1986).

This thicker layer is composed of collagen fibers, fibroblasts, mast cells, and histiocytes.

It also contains hair follicles, sebaceous and sweat glands, blood and lymph vessels, nerves, and arrector pili muscles (Laflamme, 2004). The skin of dogs was noted to have a thick dermis layer in areas where thick skin was found, such as the head and neck regions, while only a thin layer of epidermis was present (Webb and Calhoun, 1954).

The subcutis layer in both dogs and cats contains connective tissue, elastic fibers, blood vessels, nerves, and fat cells (Thomsett, 1986). It provides the animal with insulation and further protection from trauma.


Hair

The coat of a dog or cat is the first line of defense against environmental antigens and bacteria. However, many owners are most concerned with the aesthetic qualities of the coat of the animal. Hair covers nearly the entire body of both cats and dogs.

Areas not covered by hair in these species include regions where there is a transition from skin to mucous membrane and in specialized regions such as foot pads and the nose (Thomsett, 1986).

The hair of dogs and cats includes three parts, the cortex, medulla, and cuticle (Thomsett, 1986).

Glycine/tyrosine-rich proteins, due to their effects on gene expression, determine the keratin protein composition of the hair (Rogers and Powell, 1993). The cortex is the region of the hair that provides the hair coat color.

In dogs, primary and secondary hairs are found in groups of up to 20 hairs within the dermis region of the skin (Webb and Calhoun, 1954). These hairs are separated into groupings of three hairs through sebaceous glands and circular connective tissue in the dermis (Webb and Calhoun, 1954).

Cats have compound follicles that allow multiple hairs to emerge from one opening (Cline, 2004). Hair is found in clusters of 2, 3, 4, or 5 groups of hairs with at least one guard (primary) hair, although 2 or 3 guard hairs may be present in one follicle, particularly on the dorsal region of the body (Strickland and Calhoun, 1963).

Three phases exist in the hair cycle of dogs and cats (Thomsett, 1986). In the anagen phase, the hair is undergoing active growth, with new hair forcing the old hair within the follicle up to the skin surface.

The next phase, the catagen phase, is marked by the cessation of active growth and the base of the follicle begins the degenerative process.

The final phase is the telogen phase, a resting phase when hair is shed from the follicle.

These phases proceed at different rates depending on the type of hair, primary or secondary, and photoperiod. This feature allows for coat density changes due to climate conditions (Thomsett, 1986).

Dog coats are divided into three categories based on breed characteristics (Thomsett, 1986). Dogs with a normal hair type have long primary hairs and fine secondary hairs (e.g., German shepherds). Dogs with short coats are those with fine or coarse short hairs (e.g., smooth-coated terriers or boxers). Dogs with long coats also can be divided into those with fine or coarse long hairs (e.g., spitz breeds and Bedlington terriers, respectively).

In cats, the tabby coat coloring is the wild type pattern and all other patterns are derived from this (Cline, 2004). Self-coated cats are one color from base to the tip of the hair. Tip-coated cats have a characteristic coloring where the hair is a pale color except for the very tip of the hair, which is a dark pigment. Multicolor-coated cats have either a tortoiseshell or piebald coloring (Cline, 2004).


Protein

Protein is the main constituent (~95%) of hair of dogs and cats and is composed of primarily cystine and methionine, sulfur-containing amino acids. Protein also is necessary for proper kertanization of the skin. Therefore, protein is vital to good skin and coat health of cats and dogs.

Protein deficiencies are rarely observed in today’s pets due to the well balanced diets available. However, deficiencies in protein may be observed in dogs after starvation, anorexia, excessive protein loss due to disease (e.g., pancreatic disease), or prolonged feeding of a nutritionally imbalanced diet (Watson, 1998). This is most often experienced in young, growing animals and lactating and pregnant females where the animal has an increased requirement for protein (Watson, 1998).

Deficiency symptoms are noted in both the skin and hair of the animal. The hair of dogs and cats deficient in protein will become dry, dull, brittle, and will shed easily and may be slow to regrow (Mosier, 1978; Watson, 1998; Cline, 2004). Edema of the feet and legs, inelasticity, and hyperpigmentation of the skin may occur in these animals and, with severe protein restriction, lesions may develop (Mosier, 1978; Watson, 1998; Cline, 2004).

Another important function of protein includes hair pigmentation of black hair in cats. In recent years, it has been found that the NRC (1986) tyrosine requirement for cats was below the minimum requirement to maximize black pigmentation of the hair coat in cats (Anderson et al., 2002; Morris et al., 2002).

Tyrosine is required to produce the two pigment constituents of melanin, eumelanins (black and brown pigmentation), and pheomalanin (yellow to reddish-brown pigment) (Morris et al., 2002).

The pathway to produce the melanin substrates requires tyrosine to produce L-3,4- dihydroxyphenylalanine (L-DOPA), which then must be converted by tyrosinase to dopaquinone, a precursor to both eumelanins and pheomelanins (Morris et al., 2002).

Tyrosinase is again required further along the pathway to produce dihydroxyindolemelanin, which is responsible for black pigments (Morris et al., 2002). Black cats fed diets containing less than 18 g of phenylalanine + tyrosine/kg diet showed decreased concentrations of pyrrole-2,3,5-tricarboxylic acid (PTCA), a product of the oxidation of eumelanin, and red hairs were present on those cats (Anderson et al., 2002).

Because phenylalanine and tyrosine, both aromatic amino acids, were the only nutrients that differed between the diets, it was concluded that the aromatic amino acids play a pivotal role in coat color development and maintenance in black cats.

Furthermore, the coat of the cats became red when fed diets containing less than 18 g phenylalanine + tyrosine/kg but would return to normal black coloring when fed a diet adequate (>18 g/ kg) in phenylalanine and tyrosine (Anderson et al., 2002; Morris et al., 2002). Therefore, it was determined that the NRC (1986) requirement to maximize growth was not adequate to maximize black coloring in cats (Anderson et al., 2002; Morris et al., 2002).


Food allergy/ sensitivity

Food allergies occur as an immune-related response to food, often due to a protein but also to specific ingredients in the diet (Hall, 1994; Watson, 1998). These proteins often are heat- and acid-stable proteins and glycoproteins (Hall, 1994). Although a very small amount of protein is absorbed intact through the brush border of the intestine (~0.002%), this small amount is sufficient to elicit an allergic response (Hall, 1994). Immunological responses to a diet can be classified as IgE-mediated and non-IgE-mediated (Hall, 1994).

A food allergy is believed to develop after a long presentation of the diet to the gut tissue where the animal is able to tolerate the antigen present (Carlotti et al., 1990; Hall, 1994). Antigens able to bypass the immune system protective functions, or an increased absorption of the offending antigen, may lead to a food allergy presenting clinical signs (Hall, 1994).

A food allergy often is difficult to distinguish from food sensitivity in a clinical setting due to owner incompliance. To diagnose a true food allergy, the animal must be removed from the offending diet and fed a hypoallergenic diet. Once symptoms clear, the original diet should again be fed to see if the diet elicits a response (Paterson, 1995; Watson, 1998).

Pruritis is the most common clinical sign noted in dogs suffering from food allergies although gastrointestinal distress also may be observed (Carlotti et al., 1990; Watson, 1998). Of the several studies assessing food allergies in dogs, no predisposition was reported for breed, sex, or age of onset of reaction (Carlotti et al., 1990; Jeffers et al., 1996; Watson, 1998).

Treatment of food allergies requires feeding a diet where no offending antigen is presented. This often is accomplished with a diet containing a novel protein source, such as lamb or venison. However, an allergy may develop to this new diet.

Another more recent option is to feed a commercial hypoallergenic diet where all proteins have been enzymatically digested. Therefore, there is no protein large enough to elicit an immune response in the animal. One concern related to these diets is that they often contain additives that some animals may respond to, although this occurs rarely.


Lipids

Fatty acids have long been known to have a direct effect on skin and coat condition of dogs and cats. An animal fed a diet deficient in an essential fatty acid (EFA) for 2-3 months will develop a dull, dry coat with fine scaling of the skin (Watson, 1998).

Symptoms will worsen with a prolonged deficiency, including alopecia, greasy skin, and secondary pyoderma (Watson, 1998). However, an EFA deficiency is rare but may be caused by feeding a diet deficient in EFAs (e.g., poorly formulated home-made diets), anorexia, and oxidation of the fat source in the diet (Watson, 1998; Cline, 2004).

These deficiency signs are due to the central role that fats play in the integument system. Essential fatty acids act as structural components in cell membranes and as precursors to eicosanoids (Watson, 1998).

Supplementation of EFAs and omega-3 fatty acids has been evaluated for use in treating inflammatory skin disorders. Polyunsaturated fatty acids have been evaluated for their effects on canine and feline atopy.

Linoleic acid, an 18-carbon fatty acid, is converted to longer chain omega-6 fatty acids through Δ6 desaturase. However, this enzyme is not present in the skin of dogs or cats, and cats have low concentrations of this enzyme overall.

Mixed results have been noted in research evaluating the efficacy of EFA supplementation in dogs and cats (Harvey, 1991; Bond et al., 1993; Marsh et al., 2000).

One study found increased serum linoleic acid concentrations in 6 of 8 cats with miliary dermatitis when supplemented with EFAs (Harvey, 1991). This was coupled with an improvement in pruritus and coat condition after 6 weeks of supplementation (Harvey, 1991).

These results differ from those of a second study where supplementation of linoleic acid only resulted in no significant improvement in skin health or coat condition of dogs (Marsh et al., 2000). Supplementation of atopic dogs with EFAs did not affect intradermal testing when compared to non-supplemented dogs (Bond et al., 1993).

Omega-3 fatty acids are found in marine sources, flax, and linseed, and are antiinflammatory due to the eicosanoids produced from the breakdown of omega-3 fatty acids resulting in less of an inflammatory response than eicosanoids produced from the breakdown of omega-6 fatty acids (Nesbitt et al., 2003).

It is difficult to assess the effectiveness of omega-3 fatty acid supplementation due to variation among studies; therefore, no clear conclusion has resulted (Scott et al., 1997; Rees et al., 2001; Nesbitt et al., 2003; Mueller et al., 2005).

It appears clear that both the amount of omega-3 fatty acid in the diet and the omega-6:omega-3 ratio are important as regards response to supplementation (Nesbitt et al., 2003). Researchers also have indicated that the differences in response to supplementation may be due to a defect in linoleic acid metabolism, possibly a deficiency in Δ6 desaturase (Scott et al., 1997).


Zinc


Zinc-responsive dermatosis in dogs is divided into two syndromes, namely syndrome I and syndrome II.

Syndrome I is a genetic disorder where dogs have a decreased ability to absorb and utilize zinc. This occurs primarily in northern breed dogs (Columbini, 1999). Syndrome II occurs in puppies in a rapid growth stage or any animal fed a diet deficient in zinc. In dogs, this syndrome is often referred to as ‘generic dog food disease’ (Columbini, 1999).

Syndrome I and II clinical manifestations both include cutaneous lesions around the eyes, ears, nose, mouth, and footpads. Secondary infections are likely to follow due to low zinc concentrations, creating suppressed immunocompetence and a breakdown of the epithelial barrier (Columbini, 1999).

Young animals may exhibit decreased growth rates, anorexia and, eventually, weight loss (Watson, 1998). Adult animals also may have decreased intake, weight loss, conjunctivitis, and inflammation of the eye.

Treatment for zinc-responsive dermatosis includes ensuring the dog is on a ‘complete and balanced’ diet and zinc supplementation to rid the animal of lesions.


Minerals and vitamins

Other minerals and several vitamins also may have an effect on skin and coat health. Deficiencies in copper will result in a decrease in tyrosine and melanin production that will create a dull, rough coat (Cline, 2004). A deficiency in iodine, responsible for a normal functioning thyroid, will create skin lesions and poor hair coat (Cline, 2004).

Although rare, vitamin deficiencies can result in several skin and coat problems. Vitamin A is important in proper keratinization of the skin. Deficiencies will result in hyperkeratinization, poor hair coat, and alopecia (Watson, 1998). Vitamin B-complex vitamins, namely biotin, will manifest similar deficiency symptoms as vitamin A.

However, most lesions of the skin characteristically occur around the face and eyes (Watson, 1998). A deficiency is rare, although it may be caused in animals fed raw eggs due to avidin, a protein that binds biotin, rendering it unavailable to the animal (Watson, 1998).



Conclusion

Due to the high quality of today’s prepared commercial diets, nutritional deficiencies are rare in companion animals.

However, these deficiencies still occur on occasion.

Owners of companion animals view the skin and coat health of their animal as a way to assess the overall health of the animal.

Therefore, nutritional strategies that enhance skin and coat health remain important when considering the overall health and well being of companion animals.


References

Anderson, P.J., Q.R. Rogers and J.G. Morris. 2002. Cats require more dietary phenylalanine or tyrosine for melanin deposition in hair than for maximal growth. J. Nutr. 132:2037-2042.

Baker, B.B., H.I. Maibach, R.D. Park, L.Z. McFarland and T.R. O’Brien. 1973. Epidermal cell renewal in the dog. Amer. J. Vet. Res. 34:93-94.

Bond, R., D.H. Lloyd and J.M. Craig. 1993. The effects of essential fatty acid supplementation on intradermal test reactivity in atopic dogs: A preliminary study. Vet. Derm. 4:191-197.

Carlotti D.N., I. Remy and C. Prost. 1990. Food allergy in dogs and cats: A review and report of 43 cases. Vet. Derm. 1:55-62.

Cline, J. 2004. The skin and coat and its role as a protective system for cats. In: Feline Protective Systems: Nestle Purina Pet Care. The Gloyd Group, Inc., Wilmington, DE, pp. 1-14.

Columbini, S. 1999. Canine zinc-responsive dermatosis. Vet. Clin. N. Amer. Sm. Anim. Prac. 29:1373-1383.

Hall, E.J. 1994. Gastrointestinal aspects of food allergy: a review. J. Sm. Anim. Pract. 34:175-179.

Harvey, R.G. 1991. Management of feline miliary dermatitis by supplementing the diet with essential fatty acids. Vet. Rec. 128:326-329.

Jeffers, J.G., E.K. Meyer and E.J. Sosis. 1996. Responses of dogs with food allergies to single-ingredient dietary provocation. J. Amer. Vet. Med. Assoc. 209:608-611.

Laflamme, D.P. 2004. Dermatology and nutrition: Review of the science. In: Focus on Veterinary Medicine. Watt Publishing Company, Mt. Morris, IL, pp. 10-20.

Marsh, K.A., F.L. Ruedisueli, S.C. Cole and T.D.G. Watson. 2000. Effects of zinc and linoleic acid supplementation on the skin and coat quality of dogs receiving a complete and balanced diet. Vet. Dermatol. 11:277

Morris, J.G., S. Yu and Q.R. Rogers. 2002. Red hair in black cats is reversed by addition of tyrosine to the diet. J. Nutr. 132:1646S-1648S.

Mosier, J.E., 1978. Relationships of nutrition and skin problems. Mod. Vet. Pract. 59:105- 109.

Mueller, R.S., M.J. Fettman, K. Richardson, R.A. Hansen, A. Miller, J. Magowitz and G.K. Ogilvie. 2005. Plasma and skin concentrations of polyunsaturated fatty acids before and after supplementation with n-3 fatty acids in dogs with atopic dermatitis. Amer. J. Vet. Res. 66:868-873.

Nesbitt, G.H., L.M. Freeman and S.S. Hannah. 2003. Effect of n-3 fatty acid ratio and dose on clinical manifestations, plasma fatty acids and inflammatory mediators in dogs with pruritus. Vet. Derm. 14:67-74.

Paterson, S. 1995. Food hypersensitivity in 20 dogs with skin and gastrointestinal signs. J. Sm. Anim. Pract. 36:529-534.

Rees, C.A., J.E. Bauer, W.J. Burkholder, R.A. Kennis, B.L. Dunbar and K.E. Bigley. 2001. Effects of dietary flax seed and sunflower seed supplementation on normal canine serum polyunsaturated fatty acids and skin and hair coat condition scores. Vet. Derm. 12:111-117.

Rogers, G.E. and B.C. Powell. 1993. Organization and expression of hair follicle genes. J. Invest. Dermatol. 101:505-555.

Scott, D.W., W.H. Miller, Jr., G.A. Reinhart, H.O. Muhammed and M.S. Bagladi. 1997. Effect of an omega-3/omega-6 fatty acid-containing commercial lamb and rice diet on pruritis in atopic dogs: Results of a single-blinded study. Can. J. Vet. Res. 61:145-153.

Strickland, J.H. and M.L. Calhoun. 1963. The integumentary system of the cat. Amer. J. Vet. Res. 24:1018-1029.

Thomsett, L.R. 1986. Structure of canine skin. Brit. Vet. J. 142:116-123.

Watson, T.D.G. 1998. Diet and skin disease in dogs and cats. J. Nutr. 128:2783S-2789S.

Webb, A.J. and M.L. Calhoun. 1954. The microscopic anatomy of the skin of mongrel dogs. Amer. J. Vet. Res. 15:274-280.


Authors: B.M. VESTER and G.C. FAHEY, JR.
Department of Animal Sciences, University of Illinois, Urbana, Illinois, USA
PUBLICATION DATE:  21/06/2007
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AUTHOR:  B.M. VESTER and G.C. FAHEY, JR. (Courtesy of Alltech Inc.)
 
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