By Dr. Kris Hiney, PhD, Equine Nutritionist -
Equine Nutrition Advisor to Omega Fields® - (www.omegafields.com)
Greetings fellow horse owners!
This month we will discuss two important trace minerals, copper (Cu) and zinc (Zn). We will discuss them together, as they are most commonly discussed in relation to developmental orthopedic diseases in young horses. First of all, copper and zinc are classified as trace minerals because they are required in far less quantities compared to Ca, P, Na, Cl etc. While the minerals we previously discussed were described in terms of percentages of the diet, or in grams, trace minerals are only required in mg per day. Typically their requirements are listed in ppm (or mg/kg) of the total diet. It is then assumed that a horse would be consuming a standard 2% of their body weight per day. Thus if a requirement is listed as 15 ppm, then a 500kg horse should consume 150 mg per day. Now let’s discuss what these particular trace minerals do for your horse.
Copper is a mineral that is heavily involved with collagen and elastin and their tissue integrity. Collagen is a structural protein found in skin, tendon, arteries, bone and cartilage, while elastin is found primarily in ligaments. Copper is necessary for a key enzyme (lysyl oxidase) which catalyzes the cross-linking of collagen, and thus is vital for the strength of cartilage, tendon etc. Essentially that is the connection between separate collagen fibers. That is why Cu is typically implicated in developmental issues in growing horses. Copper also plays a role in energy production as it is part of cytochrome c oxidase, an enzyme which transports electrons and helps to generate ATP (remember, that is the energy currency for cells) within the mitochondria. It is also necessary for iron (Fe) metabolism and serves in an anti-oxidant capacity. Copper easily accepts electrons and thus aids in scavenging free radicals. In fact, free Cu can actually cause free radical damage due to its ability to “grab” electrons. Thus in order to protect body tissues, Cu is found in blood bound to the protein ceruloplasmin. Both Cu and Zn are associated with the enzyme superoxide dismutase, a main player in preventing oxidative damage. The superoxide radical (oxygen with an extra electron) is one of the main reactive oxygen species (it steals electrons away from other molecules and makes them unstable) and can cause tremendous damage to the body unless it is eliminated. Superoxide dismutase catalyzes the reaction of two superoxide radicals to create hydrogen peroxide and oxygen. Finally Cu is involved in the enzyme tyrosinase, which catalyzes the production of melanin. Without melanin, hair loses pigmentation and can create funny colored animals!
Figure 1. Collagen is made up of several types of proteins. These proteins are wrapped around each other in a helical structure. The crosslinks between separate collagen molecules help to provide the stability in equine tissues such as cartilage, tendons etc.
Copper metabolism in horses differs from other species, so direct extrapolation from studies in other species may offer incorrect assumptions. For example, ruminants can suffer Cu deficiencies if fed a diet high in molybedenum. However, this does not happen in horses. In other species, alterations in hair coat due to Cu deficiency also appear more rapidly. In horses, only anecdotal evidence (never reported in trials where Cu deficiencies are achieved deliberately) supports the idea that the horse’s hair coat will differ (most often reported in black horses). And remember, sun can bleach hair coats and create a dull, reddish tinge too! Horses don’t show as extreme sensitivity to Cu overloads as well (sheep are especially susceptible) and can tolerate concentrations in the total diet as high as 250 ppm. Therefore, information concerning Cu and its metabolism, and requirements, needs to originate from equine trials.
Zinc is a ubiquitous mineral involved in over 100 enzymatic actions in the body. Key functions include digestive enzymes, bone function, and immune function, as well as the previously mentioned role as an anti-oxidant. Ironically, Zn may actually prevent free radical formation caused by other metals (primarily Cu and Fe which are highly reactive). When Zn is incorporated into proteins vs other metals, it may decrease the overall generation of free radicals. In humans, marginal zinc deficiency results in impaired taste and smell, as well as memory loss and decreased male fertility. In its anti-oxidant capacity, Zn helps to maintain cell membrane integrity, which may contribute to its immune function as well. Zinc deficiencies in animals and humans results in decreased resistance to pathogens (viral, fungal and bacterial) and even parasites and decreased antibody formation. The immunologic function of Zn is why it is commonly available in cold lozenges for people (it was clinically proven to decrease duration of the common cold). Currently no such studies have been conducted in the equine.
Deficiencies in Cu especially have been implicated in developmental orthopedic diseases in young horses. This term can encompass such disorders such as physitis (inflammation of the growth plate), flexural limb deformities, wobblers (compression of the spinal cord in the vertebrae) and most commonly osteochondrosis or OCDs. It is also commonly referred to osteochondrosis dissecans once a flap of cartilage is free floating in the joint. Osteochondrosis is typically seen as a lesion in the cartilage due to improper ossification of the subchondral bone (bone underlying the cartilage in a joint). Management of young horses including diet and exercise, rapid growth rate, as well as genetics have been implicated as causes of these disorders. Experimentally, cartilage lesions and gait abnormalities were induced in foals fed a diet deficient in Cu, but these foals were also deficient in Ca and P. Thus the absolute cause is difficult to tease out. Unfortunately subsequent studies in foal development and Cu intake have had contradictory results. Overall the most benefits in Cu supplementation in preventing OCDs may be realized by supplementing the dam in late gestation. A Cu deficiency may not result in formation of OCDs (genetics, growth rate, other nutritional factors may actually cause the lesion development) but Cu may help in the repair mechanism. Visually, it may be difficult to determine if foals are deficient in Cu as their growth rate and outward appearance is normal. On a practical note, while Cu concentrations have been increasing in commercial equine feeds, especially in feeds formulated for young horses, a decrease in OCD have not been seen generally in the equine population. Now certainly, there are many confounding factors in the pathogenesis of OCD, genetics included. In the equine industry, we are guilty of breeding horses despite them having soundness issues. Thus, we may be inadvertently perpetuating developmental diseases in our horses.
Figure 2. Alterations in the normal process of ossification can result in cartilage defects.
Ideally mature horses should receive a total diet of 10 mg/kg or 0.2 mg/kg BW/d. Therefore a 1100 lb horse which consumes 2% of its body weight in feed per day would consume 100 mg of Cu per day. Most natural horse feeds contain 3-20 ppm of Cu. Increases in Cu requirements due to exercise are slight, and most will be accomplished simply by increasing intake to meet energy demands. Current recommendations for Zn are to be fed at a rate of 40 mg/kg DM. Thus depending on the feed source of the horse, supplementation becomes more necessary. Typically mares fed a normal diet should supply adequate Cu in the milk for foal growth as no additional increases in milk Cu concentration were seen with Cu supplementation to mares. However, as a precautionary measure an increase in Cu in the diet of broodmares may be warranted. Feeds designed to be fed for foals often contain 50 ppm of Cu or greater and between 150 to 220 ppm Zn. These values are well above the current NRC recommendations as more of a safety precaution. However, overzealous supplementation of trace minerals is not a wise idea. Excess Zn can impair Cu metabolism as they share a common transport mechanism. Typically this wouldn’t be an issue unless Zn concentrations are over 200 ppm in the total diet. This might occur with a misformulation of a diet, or if the horses are pastured need a metal refinery. It is recommended for Zn to not reach a concentration over 500 ppm. Extreme levels of Zn can cause joint abnormalities but only in excessive quantities (such as 2% of the diet).
Figure 3. The cartilage defect in the hock joint is circled in red.
Next month we will discuss Mg and Fe.
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