Minerals for Horses: Copper and Zinc

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 Written By Dr. Kris Hiney

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.

Cu and its functionsCopper 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.

Are horses different than other animals?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.
Zn and its functions. 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.
The role of Cu and Zn in bone disorders. 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.

Cu and Zn requirements. 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.


Minerals for Horses: Magnesium and Iron

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 Written By Dr. Kris Hiney

This month we continue on our path of discussing minerals required by horses. We will actually be mixing a macro-mineral (magnesium) and trace mineral (iron) together. However, our goal has been to visit minerals in the order of their level of concern by the horse owner and their frequency of need for supplementation.

Function of MagnesiumMagnesium is an important mineral involved in many enzymatic reactions (as so many of the minerals are). The largest store of Mg in the body is in bone (60%), with a relatively small amount present in the blood. Magnesium also acts as an electrolyte as well and therefore is essential for normal nerve and muscle function. Magnesium is a key component in enzymatic reactions involving the synthesis of nucleic acids, protein, carbohydrates and lipids. Magnesium and ATP are almost always found complexed together in the body. In all, Mg is involved in over 300 enzymatic reactions.
Mg requirements Most equine feeds contain Mg in a range between 0.1 to 0.3%. If we use our average horse of 1100 lbs (500 kg), that horse would receive between 10 and 30 g of Mg per day if he was consuming 2% of his body weight per day. Remember, that is our normal goal for feeding. Currently the recommendation for Mg intake for a mature horse is 7.5 g of Mg/d for a 500 kg horse, or 15 mg/kg of body weight per day. Therefore, most horses easily meet their Mg requirements by consuming their regular diets. For young growing horses, the requirement on a percent of their body weight is higher (approximately 21 mg Mg/kg), due to their need to accumulate Mg in growing tissues. As their growth rate tapers off, the concentration of Mg in their diet can be lowered. Pregnant mares do not actually have a much higher Mg requirement than a maintenance horse, and suggested to only be 15.3 mg/kg of body weight per day. Therefore mares should easily be able to consume that amount. For example a 500 kg mare would need 7.7 grams of Mg per day. Only 200 mg more than our maintenance horse! From our above description of the normal Mg content of feeds, this would be easily obtainable by the mare simply eating 2% of her body weight. Remember if allowed, mares will consume much more feed than this! Once our mare has foaled and begins to produce milk, her requirements will increase in order to support her growing foal. During peak lactation she will need 22.2 mg of Mg/kg of body weight or 11.1 g total for that 500 kg mare. Again, this is probably easily obtainable unless she is consuming a marginally deficient diet.Now let’s shift our focus to the exercising horse, who we would expect to have a greater Mg requirement due to sweat losses. To account for changes due to sweating, assume an increase in consumption of 1 – 2 g per day, depending on sweating rate, for a light to moderately exercised horse. If the intensity of the exercise increases and thus the accompanying heat load, the requirement of Mg is suggested to double. Therefore, for those 3 day eventers or endurance horses, they should receive 30 mg/kg body weight or 15 g of Mg per day. It is possible for these horses on a normal diet to end up being deficient in Mg. In several studies in young growing exercised horses, it appeared bone Mg deposition was greater when horses were fed diets higher than previously recommended in Mg. However, in these studies, horses were also fed more Ca which may have led to greater bone formation and thus the accompanying increase in Mg retention. However, because of this interaction between both exercise and growth in the young horse, the Mg requirements of these horses should be treated more like an intensely exercised horse, or 30 mg/kg body weight.
Magnesium deficienciesTypically, acute Mg deficiencies in horses are quite rare, compared to the relatively more common occurrence in cattle. In horses, Mg tetany (or a bout of muscle contraction causing locking of the muscles) has occurred in stressed horses (typically transported) and in lactating mares. Presumably in transported horses, there would have been increased Mg losses in feces (increased intestinal motility while being nervous) or through sweating. In mares, a loss of Mg in milk while on a Mg deficient diet would contribute to an acute Mg deficiency. Rapidly growing pastures are typically low in Mg and high in K may be a risk factor in Mg deficiency, but this is much more of a concern for cattle than for horses, which absorb Mg more efficiently.Some individuals have suggested that magnesium should be supplemented to horses presumed to have insulin resistance. Magnesium does play a role in insulin release by the pancreas and its activity. This idea presumably originates from data in humans. Frequently those with type II diabetes (25-35%) have lower serum magnesium levels than those without the disease. The hyperglycemia associated with type II diabetes may result in increases loss of Mg through the kidney. It is not known if the hypomagnesia is a consequence or a potential cause of type II diabetes and insulin resistance. Studies in humans using Mg as a potential treatment of type II diabetes and insulin resistance have yielded conflicting results, with some having positive results and some with no change in insulin and glucose homeostasis. To date, no such studies have been performed in horses.
Function of IronIron (Fe) is most commonly known for its role in hemoglobin and oxygen transport. It is also a very important ion in the electron transport chain, carrying electrons in order to produce ATP. Thus it is integral in body function. Most equine feeds range between 100-250 mg of Fe/kg of feed. Grains may be lower than forages. Iron absorption in the diet is highest in newborn animals, and also in animals that are fed Fe deficient diets. The body simply becomes more efficient out of necessity and therefore absorbs proportionally more of the iron in the diet.The quickest observable sign of iron deficiency is anemia. Ironically, most animals will never be deficient in iron if they have access to soil. So horses grazing pastures should be adequate in Fe status, but horses which are continually stalled may be at a higher risk of Fe deficiency. Supplementation of Fe has been unable to show any change in hemoglobin or the oxygen carrying capacity of the blood, and therefore may be unwarranted in horses fed normal diets. Over supplementation of Fe has been reported, with clinical signs of iron toxicity disappearing after withdrawal of the supplement. Horses in this study were being fed 0.6 mg/kg Bw/d of ferrous sulphate. Thus owners should be careful about being too enthusiastic in their supplementing regimens. However, others have found no ill effects from feeding horses 500 and 1000 mg/kg feed although serum and liver Zn were reportedly lower. Supplemental iron may be toxic to young foals due to their greater efficiency of absorption. Even when fed at the rate of manufacturer’s suggestions for adult horses, death can quickly result.The requirements for iron in the mature horse are estimated at 40 mg/kg DM and 50 mg/kg for young foals, pregnant mares and lactating mares. For our 500 kg horse, then they should consume 400 mg of Fe per day. Remember when nutrients are listed on a concentration basis, it is assumed that the horse would be consuming 2% of their body weight per day. If our horse was eating 10 kg of feed ranging between 100 and 250 mg Fe/kg, he would receive 1000 to 2500 mg of Fe per day (or 1 – 2.5 g) of Fe. Again, most horses do consume adequate Fe. In a fairly recent study looking at blood mineral profiles, the Fe status of horses with pica (consumption of unusual objects including soil) was lower than in horses who did not perform this behavior. That would make sense as soil does indeed provide the normal grazing horse (they pick up soil inadvertently as they eat) with additional Fe. Therefore, if your horse is performing this behavior, it might be advisable to examine his diet more closely. 

Remember, the temptation of most horse owner’s is to over supplement their horses. However, this is often unwarranted, contributes to the expense of managing the horse, and may provide no benefits to the animal. Certainly overzealous supplementation may actually be harmful to the horse.

Key terms:Hypomagnesia – lowered blood levels of magnesiumHomeostasis –physiological ability to maintain an equilibrium through an interaction of complex relationships. For example, glucose homeostasis is an interaction between key organs (liver, kidney and pancreas) and the hormones (insulin, glucagon, cortisol etc)to keep glucose at a relatively constant levelNext month: We wrap up the left over minerals! Manganese, cobalt, chromium and iodine 


Minerals for Horses: Sulfer, Manganese, Cobalt & Chromium

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Written By Dr. Kris Hiney

This month we wrap up our discussion of minerals required by horses with a random mix of macro and micro-minerals. We will focus on sulfur, manganese, cobalt and chromium. What these minerals share in common is that they are typically in adequate supply in the average horse’s diet. However, they still warrant attention and understanding as they are vital for the health of the horse. Next month, we will start a new series on protein.

Sulfur is technically a macro-mineral, as it is required in larger amounts in the diet. Sulfur is most commonly found incorporated into two amino acids, cysteine and methionine. In the body, sulfur would be found in proteins (as cysteine and methionine) as well as some key vitamins: thiamin, biotin, and lipoic acid. Proteins containing sulfur include most structural proteins, as well as insulin, heparin and key enzymes: gluthathione peroxidase (an anti-oxidant enzyme) and as part of coenzyme A (an essential part of energy metabolism). Horses ingest sulfur in the diet mainly through consumption of protein. Horses receiving adequate protein that is of sufficiently high quality typically do not need additional sulfur in the diet. The total amount of sulfur in the diet should be about 0.15% on a dry matter basis. Therefore, unless the horse is suffering from protein malnutrition, or is deficient in these specific amino acids (most likely methionine), the horse should be adequate in sulfur. To this date, no one has been able to confirm a sulfur deficiency in horses provided that they are not deficient in protein. Some inorganic sulfur (in the form of a sulfur salt) can be incorporated into chondroitin sulfate (an important component of joint health) (Figure 1) and insulin in the body. More benefits are seen when feeding inorganic sulfur to ruminant animals, due to the ability of the rumen microbes to synthesize the sulfur-containing amino acids de novo (or from scratch). While this can indeed occur in the horse, the site of microbial synthesis is past the primary location of protein digestion and absorption and therefore does not yield the same benefits as seen in the ruminant animal. So bottom line for sulfur, if you are not deficient in cysteine and methionine, you are likely to be adequate in sulfur.



Cobalt is a trace mineral which is found in the body solely as cobalamin or vitamin B 12. Cobalamin’s function, and thus cobalt’s, is rather exclusive, limited strictly to serving as a cofactor for only two enzymes. While only two, they are vital for RNA and DNA synthesis and integral in carbohydrate and lipid metabolism. Those familiar with human nutrition know that cobalamin is found only in animal products, and thus can be deficient in vegans unless they supplement their diet. So how would a horse, who clearly is an herbivore, meet their cobalamin requirement? Bacteria in the hindgut of the horse are able to incorporate cobalt into the complex structure of cobalamin (See Figure 2). Vitamin B12 is then absorbed from the gut of the horse, thus supplying their needs. Currently no cobalt or B12 deficiencies have been reported or induced in horses. They actually seem to be more efficient at extracting cobalt from their environment or conserving cobalamin in their tissues than are ruminants. Horses have remained healthy on pastures that induced deficiency symptoms in cattle. Suggested toxicity limits for cobalt are 25 ppm in the diet with recommended dietary intakes set at 0.5 ppm.


Manganese is a trace mineral involved in both carbohydrate and lipid metabolism and is needed for the synthesis of chondroitin sulfate, whose structure is seen above in Figure 1. Manganese is also part of two key gluconeogenic enzymes as well as arginase, an enzyme in the urea cycle. It also functions as an anti-oxidant incorporated into a form of super-oxide dismutase. Remember that these enzymes function to eliminate the superoxide free radical, converting it to hydrogen peroxide in the body. Hydrogen peroxide is further reduced by other anti-oxidant enzymes in the body. Manganese has even been researched as its potential use an anti-oxidant drug for horses through infusions of inorganic manganese salts.

Most commonly manganese deficiencies are reported to impair cartilage metabolism and may result in growth abnormalities such as contracted tendons, epiphysitis etc. This is due to its role in the synthesis of chondroitin sulfate and thus in articular cartilage In Figure 3. You can see the bottle brush appearance of the proteoglycans attached to hylaronic acid. This provides the resistance, or cushioning effect of cartilage during use of the joints. When cartilage is not allowed to form properly, abnormal growth usually results.

The current recommendation for manganese is 40 ppm in the diet, with typical horse feeds ranging between 15-140 mg/kg. Forages are typically higher in manganese (40-140 ppm) than concentrates. Therefore, the average horse should be adequate in manganese. The source or form in which manganese is fed does not seem to matter. In the current literature, there does not appear to be any difference in bioavailability between organic and inorganic sources of manganese. Yearling horses fed below the recommended value did exhibit a slower growth rate compared to horses fed a diet at twice the recommended intake of manganese. However, in this example it would be difficult to determine if a faster growth rate was achieved due to managnese supplementation, or a slower growth rate resulted from manganese deficiency. Manganese toxicity is a concern in many species, and excess manganese can interfere with P absorption. The safe level of intake of manganese in the horse is suggested to be at 400 ppm. While never researched in horses, in humans Fe supplementation can inhibit manganese absorption (another reason to not over-supplement minerals!)



Finally, chromium is an important mineral for both carbohydrate and lipid metabolism. Chromium enhances or prolongs the time that insulin is bound to its receptor, thus amplifying its effects. The exact mechanism by which it does so is not yet known. Thus it has created much interest in those individuals looking to enhance insulin sensitivity both in humans and in horses. In humans with insulin resistance or type II diabetes, supplemental chromium has been reported to improve glucose dynamics, but the results have not been consistent. In general, the majority of human studies have yielded very mixed results, with more benefits in humans with altered glucose metabolism, but not in diabetics. In addition, insulin resistance increases chromium excretion, which may be leading to a chromium deficiency. As of yet, chromium supplementation in a population of insulin resistant horses has not been performed. However, there has been some equine work that suggests a positive benefit to supplementation. Exercising horses supplemented with 5 mg of chromium from a yeast source had lower glucose values during exercise, as well as lower insulin levels following a carbohydrate meal. This effect was not seen when horses were unfit and sedentary. Other groups have shown either little, or no effect from supplementation of chromium. One study even suggested deleterious effects on the exercise capabilities of horses when supplemented with chromium. At this point in time, the exact amount of chromium horses should receive is unknown. There may be a benefit to feeding chromium to a select group of horses that have demonstrated insulin resistance, but widespread supplementation may be unwarranted, or even harmful to the general population.

On a final note, remember that many minerals interact in very complex ways in the body. Indiscriminate supplementation of one mineral may upset a very delicate balance in the ability to absorb and utilize other minerals. While data in other species may indicated positive benefits of supplementation, it is best to address supplementation in horses thoughtfully, with the goal of providing a proper diet to the animal, which only enhances, and does not detract, from their health.


The list of Omega-3 medical benefits is growing.

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In two separate recent studies published in the American Journal of Clinical Nutrition, scientists found that Omega-3s protected against cognitive decline in a group of older men at risk for cardiovascular disease. At the end of the five-year study, those taking supplements had less cognitive decline than people who didn’t.

The other study was conducted at many sites throughout the United States. One study measured plasma fatty acid levels in a group of 2,251 men living in Minnesota between 1990 and 1992 and from 1996 to 1998. During that time, investigators at the University of Minnesota, in collaboration with colleagues at the University of North Carolina and the Johns Hopkins University School of Public Health in Maryland, conducted three neuropsychological tests to study attention and memory.

Again, those taking omega-3 fatty acids had less risk of “global cognitive decline,” the authors reported. What’s more, a number of cardiovascular factors were pushed in the direction of better health.

Omega-3 fatty acids help lower blood pressure and increase the flexibility of the vascular wall. High blood pressure can make the wall more rigid. Omega-3 fatty acids can also penetrate red blood cells, making them more flexible and better able to get through narrowed arteries.

There are more cardiovascular benefits, according to a study published in Lancet. Japanese researchers at Kobe University studied 18,000 people with high cholesterol and some kind of unhealthy heart history. Everyone was prescribed statins, the cholesterol-lowering agents, and half of them also received omega-3 fatty acids while the others swallowed a placebo.

They were followed for more than four years, at which time the scientists found 20 percent fewer cardiac events, including heart attacks, in those on 12 grams of fish oil a day.

Omega-3’s most potent effect is as an anti-inflammatory agent. It is now being used in a number of inflammatory disorders, including arthritis, lupus and some cancers. Studies have shown that Omega-3 regulates genes involved in inflammation. Human genes have co-evolved with the foods we have eaten for centuries,” Sears said.

So why are the Omega-3 essential fatty acids found in flaxseed so vital to good health?

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Omega-3 fatty acids have been shown to regulate gene transcription and expression, thus altering enzyme synthesis, and to modify several risk factors for coronary heart disease, including reducing serum triglycerides and blood pressure. They also protect against thrombosis and a variety of cancers, plus they enhance immune response and inhibit inflammatory reactions.

EFAs are required for maintaining the structure of cell membranes and the permeability of the skin. They are also needed as precursors for eicosanoids such as prostaglandins and thromboxanes, and in cholesterol transport and metabolism. EFAs — Hearty Protectors. Once again population studies reveal that a diet high in Omega-3 significantly reduces the risk of developing heart disease.

It is interesting to note that of all the common causes of premature death — heart attack, stroke, cancer, accidents, diabetes, and infectious diseases — the odds of dying from a heart attack are greatest. That goes whether you are male or female. Most assume that cardiovascular disease afflicts primarily men, mainly because the symptoms show up ten years earlier in men. But following menopause, women catch up rather quickly. In fact, every year more women die from heart attacks than men. Per annum, five times more women die from a heart attack than from breast cancer. As you can see, heart attacks don’t play favorites when it comes to gender. It is an equal opportunity disease.

Until recently, heart-healthy diets and nutrients good for the heart usually have only one goal; to lower cholesterol levels, which is helpful to the heart. But as research into what makes the heart tick continues, new revelations on how to achieve and maintain heart health are coming to light. True heart health is achieved through a variety of means, not just one. For instance, one might also consider lowering other blood fats besides cholesterol, lowering blood pressure, lowering homocysteine levels, increasing arterial flexibility, and decreasing blood platelet stickiness.

Flaxseed oil assists in the prevention of cardiovascular heart disease (CHD) by helping to lower LDL (bad) cholesterol, raise HDL (good) cholesterol, lower blood pressure, and lower platelet stickiness. In clinical trials, Omega-3 rich flaxseed exerts a positive effect on blood lipids. Overall clinical findings suggest that significant reductions in total cholesterol and LDL-cholesterol levels can be achieved, without a change in HDL-cholesterol levels, by adding flaxseed or flaxseed oil to the diet.

Substituting flaxseed oil for saturated fats in the diet enhances its beneficial effect. Epidemiologic studies have been excellent ways in which to study the effects of Omega-3 on heart health.


What is flax?

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Flax is one of the most ancient of useful herbs. Its Latin name, Linum usitatissimum, means “most useful.” Flaxseed excavated from ancient Greek archeological sites has been dated back to 1900 to 1700 B.C., and the use of flaxseed is inscribed on tablets at Pylos. Both the Greek historian Thucydides and the Roman Pliny mention the use of flax for food. In fact, so impressed with this gift of nature Pliny wrote, “What department is to be found in active life in which flax is not employed?” Of flax Bartholomew had this to say, “None herbe is so needfull to so many dyurrse uses to mankynde as is the flexe.” And Dioscorides extolled flaxseed’s power for “mollifying all inflammation inwardly and outwardly.” Hippocrates encouraged the use of flaxseed for the relief of abdominal pains, while Theophrastus recommended flax mucilage as a cough remedy. Hildegarde of Bingen used flax meal in hot compresses for the treatment of both external and internal ailments.

The value of flax to these early cultures is reflected in the rich folklore that surrounds the plant. Flax was believed to be a blessed plant; one that could bring good fortune and restore health. French leader Charlemagne, so impressed with the herb’s culinary, medicinal, and domestic usefulness, passed laws and regulations requiring its cultivation and consumption. Flax was much loved and widely cultivated throughout Europe after that, and its cultivation and use continued to expand to other lands and cultures. 

Omega Fields Mission

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 Our mission is simple.

We believe we produce the best stabilized ground flax supplements for your horses, dogs, chickens, goats and yourself!  We believe our customers and the animals they love can improve their health by using the products created by our proprietary flax stabilization and food safety technology.  We believe that you should have an exceptional experience with our products, our staff, and our retailers.


Our commitment in order to achieve our mission is simple: offer the finest quality, most nutritious flax based supplements for you, your horses, dogs, chickens, and goats at a fair price and provide outstanding customer service.  I hope you try our products, and tell you friends about them.  Then we’d love to hear from you!


Sean & Brenda Moriarty


Omega Fields remains committed to keeping “quality” as our number one focus, with the emphasis on natural, human-grade, non-GMO ingredients, no “filler” ingredients, shelf stability, nutritional value, and excellent Customer Service. It is because of our uncompromising insistence for quality that we choose to source our flaxseed from North America — not from less proven sources such as Eastern Europe or China.
 Although Omega Fields does not have an organic product line, we take great pride in being able to assure our customers that all Omega Fields’ products are natural, without added chemicals or preservatives, to provide good health and well-being for people and their animals. You can have confidence in the Premium, Human-Grade, Non-GMO, 99.9% Pure, Triple-Cleaned, Human-Grade, Stabilized, Ground, Fortified, Full-Fat, Whole-Food Flaxseed we use in all our formulas — as it is protected from rancidity or loss of nutritional value. It is the whole seed ground, so it contains 100% of the Omega 3 oils naturally present in the flaxseed.
Another naturally occurring phenomenon that especially protects flax seeds in the field from outside toxins is that they are formed and stored by the flax plant in a tight boll (see attached photo). This means flax seeds are much more protected than corn, oats, wheat, etc. — in which plants the seeds are 100% exposed to toxins.

How A Big German Shepherd, An Anxious Siberian Husky And A Rogue Collie Helped Me Get My First Dog

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Written By Barbara O’Brien
Now I am only going to tell you once. If you happen to be the parent to a horse crazy, dog crazy or cat crazy kid and you try to keep them from having a pet they will do everything their power to find animals on their own. Once they leave you and start their own lives, they may end up with a houseful of stray cats and dogs a barn full of horses and chickens and sheep and an always empty pocket just make up for lost time.Or at least that was the way it was with me. If you remember from my last column, my parents were not keen on the idea of letting me have a pet so it became my mission to be around animals no matter what.I remember being only about eight or nine when I began searching the neighborhood for houses that had dogs. There was a dog a block or so away that I could only catch glimpses of between the boards of their 6 foot privacy fence. From the pieces of it I did see, I could tell it was big and yellow.It would run to the fence and try to press his nose through the boards while I lay on the ground and reached under the fence to touch him. He would comply by lying on his back so I stroke his soft belly fur. I could only reach with the tips of my fingers. It was awful to be so close yet not be able to really see or play with him.When I was a little older I began to approach people out walking their dogs and beg to pet them. Pretty soon I became known as that kid who was crazy about dogs and that I would be happy to take them for walks when their owners didn’t have time. 

By the age of 12 I had a pretty tidy little business going. I would take a dog for a walk for the princely sum of 50 cents. Word spread and soon I had up to 6 clients a week. Everything from a nosy Beagle to a high strung Siberian Huskie that could pull me on my bike like the wind. One of my favorite dogs was a big male German Shepherd that acted like he owned the world but would never hurt anyone. Because of him, I have always tried to have a German Shepherd in my life.

About this same time I joined 4H. I was to participate in the horse project and the dog project. I had the horse thing figured out, I had begun to lease a horse from a local barn but the dog project required I find a suitable dog to train. I signed up for the free dog obedience classes offered by the county extension office on the hope my parents would see that I just had to have a dog of my own.Again I pleaded with my parents to let me get a dog but again I was told, NO PETS.It was clear that my parents were not going to give in. No matter how many tears and promise of extra chores it just wasn’t going to happen. Family allergies and a hectic lifestyle made that perfectly clear.So I had to settle for the next best thing, one of my dog walking customers had a beautiful sable collie and they agreed that I could take the dog to classes and show him at the county fair. His name was Cheetah and he was to become my partner for the summer.And so began my first taste of real dog training. Every Tuesday night for the next eight weeks our 4H leader would load us up with our dogs and haul us to a school grounds in a nearby town where we fell under the watchful eye of the 4H Dog Obedience Instructor. She dutifully taught us how to work with our dogs and make it fun for them while they learned to sit and stay and prepare for the big show at the county fair. 

Cheetah was a quick learner and worked hard at understanding what I wanted from him. He seemed to know when I was down and would rest his head on my lap while I petted him. He was a good dog and I loved him but it always made me sad when I gave him back to his real family he seemed to forget me the minute I let go of the leash.

We went to the fair and we did well at the show. Cheetah and I earned a blue ribbon. My parents were pleased that I seemed to filling my dog needs and I was happy to have at least one dog to love, even if he wasn’t mine.

Things probably could’ve gone on for some time like this. My parents were happy, Cheetah and his owners were happy, and I was as happy as I could be with a borrowed dog.

The fair was over and we were still meeting on Tuesday nights preparing for the state 4H Dog Show when Cheetah and the dog next to him decided to get into a fight. It was a good sized shepherd mix and I grabbed at Cheetah’s collar to separate them. Cheetah reared back still fighting and bit me in the face. I fell back, pulling Cheetah away as the dogs owner, a teenage boy got control of his dog.

Blood begin to drip from the puncture wound on my cheek as I fought back tears.How could Cheetah bite me? The Instructor came to me and handed Cheetah to my friend to hold while she gently took me inside and washed my face. The bite didn’t hurt so much as the fact that Cheetah had turned on me. I was devastated. The dog leader tried to explain to me dogs act out of instinct and Cheetah’s aggression wasn’t directed at me.We went outside and I took Cheetah back. He wagged his tail and licked my hand as if nothing had happened. I petted his head and tried to forgive him, but I was still hurt.When we dropped him off and the owners saw what had happened they told me that perhaps it was better I didn’t walk Cheetah anymore. And although they weren’t blaming me for the incident, they didn’t want to see me get hurt again.Not only had I been bitten by a dog I loved, but now he was being taken away from me. 

I held back my pain the rest of the way home, but when I opened the door and found my parents watching TV in the living room I burst into tears. They held me close as I told them what had happened and how not only did I get bit, but also that they (Cheetah’s owners) had told me I couldn’t see Cheetah anymore. It just wasn’t fair!

And then it happened. Something changed and my Dad looked at my Mom and said that enough was enough. They couldn’t have me getting bit like this. I had to have my own dog. My mother began to object but one look at my anguished face convinced her that maybe the time had come after all.

I could not believe my ears. Did my dad say I could get a dog? A real dog! Visions of collies and shepherds and goldens and mutts began to dance in my head. A dog! A dog! My own dog!I began to jump up and down wanting to shout this to the world when my mother suddenly laid out her conditions. It would have to be a Wire Haired Fox Terrier and nothing else. Her sister in Idaho had one and they didn’t shed. It had to be a male and to top it off it had to be $50.00 or less.My heart sank. She may as well have told me to find a needle in a haystack and I would have better luck. Fox Terriers were a rare bred in our area and even common breeds of purebred dogs didn’t go for less $200.Even though it was fairly late, I found the paper and quickly scanned the want ads, Beagles, Cockers, English Setters, Lab puppies and then I saw it, an ad for Fox Terriers. In all my years of scanning the ads for dogs I wished I could have, I had never seen an ad Wire Haired Fox Terriers. I joyfully showed the ad to my parents. They were surprised that I had found some so quickly and my dad said, call them up. I picked up the phone and a man answered. Breathless, I asked if he still had any puppies. I have one left, the man said. It’s a little male with a black patch on his eye. My heart leapt in my throat. What does he cost? I asked. Waiting for bad news, I said a prayer under my breath, please please, please…Well, he is the last one, the man said. You can have him for 50 bucks. Miracle of miracles! I turned to my parents and said, 50 bucks, he wants 50 bucks! My dad seeing how close he was to having a dog said, tell him you only have $40. I only have $40, I said and he said ok, you can have him. 

I was stunned. It was really happening! I handed the phone to my dad and he got the address and arranged to get the puppy the next day. I hugged my parents and jumped around and danced around the room, it was finally happening!

My mom began to cry when she saw how happy I was. Maybe she never realized how important to me having a dog was. She smiled and told me I better go clean my room if I ever to hope the find the puppy again in all that mess once I brought him home.

Thank you! Thank you! Thank you, God! I was happy as a child could be.

The next morning my dad and I drove to St. Paul and picked up the eight week old Fox Terrier puppy from the breeder. We didn’t have a crate so I held him in my arms all the way home.

He licked my face and I knew that even though he wasn’t a shepherd or a collie or a lab at least he was mine.

That was many years ago and much to my chagrin my parents have always had a dog ever since.

Don’t say you haven’t been warned.

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