Tracy Meyer, Nutritionist, Advit
This will be the beginning of a series of articles highlighting the importance of vitamins and minerals in pig nutrition. I will not be making recommendations but will rather be giving a brief overview of the function of each vitamin and mineral in the animal and why it is important to include a premix in your feed. Most vitamin and mineral premix packs make up approximately 0.4% of the total ration. This is a small percentage but without the premix, growth and production can be affected. In this article the importance of Vitamin A, D, E and K will be noted. This group of vitamins are commonly referred to as the fat-soluble vitamins.Vitamin A:
Vitamin A is essential for reproduction, growth and maintenance of epithelia, vision and mucus secretions. Combs (1999) also showed the importance of vitamin A in embryonic development, bone development, gene transcription, immunity and hematopoiesis (formation of blood cellular components). Pigs are able to store vitamin A in the liver where it is made available when there is a low intake. The requirement for vitamin A depends on what one is evaluating e.g., weight gain requirement may be different to liver storage. In a recent study by Lindemann et al. (2008) it was determined that the requirement for vitamin A in sows for maximal performance may vary with age, and this requirement may not be completely met with supplementation in the diet.
Vitamin A deficiency: blindness, posterior paralysis, reduced weight gain, incoordination, decreased plasma levels, increased cerebrospinal fluid pressure and reduced liver storage. Sows may fail to show oestrus, have poor conception rates, early embryonic death, reabsorb fetusus or produce weak, dead or deformed pigs.
Vitamin A toxicity: scaly skin, blood in urine / faeces, periodic tremors, rough hair coat, sensitive to touch, bleeding from cracks in skin above hooves and inability to stand up.
Nitrate and nitrite may affect vitamin A requirement. Aflatoxins reduce serum retinol but increase liver vitamin A Baker (1995) found that moisture in premix and feed ingredients has a negative effect on the stability of Vitamin A. The water causes the vitamin A beadlets to soften and they are then more sensitive to oxygen. In order to ensure maximum retention of Vitamin A in the premix the pH should be above 5 and as moisture-free as possible.
There are two major forms of Vitamin D – vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). These forms are converted by the kidneys and liver into a form that the body is able to utilise. The hormonal metabolites of vitamin D as well as vitamin D itself act on the mucosal cells of the small intestine and form calcium-binding proteins. These proteins are involved in the absorption of calcium, phosphorus and magnesium. Parathyroid hormone, calcitonin and the vitamin D metabolites work together to maintain calcium and phosphorus homeostasis. Vitamin D also plays a role in immunity, reproduction and endocrine and neurological function.
Vitamin D deficiency: insufficient bone calcification – rickets in young growing pigs and osteomalacia (decreased bone mineral content) in mature pigs. It may take 4-6 months for deficiency signs to show. In severe cases the pigs may show signs of calcium and magnesium deficiency (to be convered in later articles).
Vitamin D toxicity: reduced feed intake and growth rate, reduced weight of liver, radius and ulna, calcification in aorta, kidney, lung and heart. Toxicity signs vary with dose of vitamin d and age of pig. Excessive levels in breeder diets may lead to milk fever and stillborn piglets.
The primary function of vitamin E is as an antioxidant at the cell membrane level as well as having a structural roll in cell membranes. Offspring rely on colostrum and milk to meet their daily vitamin E requirements as transfer from sow to fetus is minimal. In turn the concentration of vitamin E in the colostrum and milk is dependent on the vitamin E content of the sow diet.
Vitamin E deficiency: mulberry heart disease, gastric ulcers, liver necrosis, anemia, fat tissue discolouration, sudden death, gastric parakeratosis and skeletal and cardiac muscle degeneration. In the sow there may be increased incidence of mastitis, metritis and agalactia as well as reduced litter size and increased pre-weaning mortality. Vitamin E deficient piglets have a low tolerance to iron-dextran injected intramuscularly. In order to prevent this reaction selenium / vitamin E should be injected at least 24 hours prior to the iron treatment.
Vitamin E toxicity: to date vitamin E toxicity has not been demonstrated in pigs (NRC, 2012). Excess vitamin E reduces the intestinal absorption of vitamin A.
vitamin E and vitamin C and vitamin E and selenium have synergistic relationships excess vitamin A increases vitamin E requirement
Fe, Cu, Zn, Mn and Cd in excess increase vitamin E oxidation (250ppm Cu or 1000ppm Fe increase vitamin E destruction to almost zero in 3 weeks in a starter diet). Aflatoxins reduce serum vitamin E levels. Stress, cold / damp environment, infection and physical exertion increase vitamin E requirement
Vitamin K is essential for blood clotting as it is involved in the synthesis of prothrombin, factor VII, factor IX and factor X. These factors are synthesized in the liver where they are inactive – vitamin K converts them to biologically active compounds.
Vitamin K deficiency: prolonged bleeding resulting in haemorrhages and death. The level of vitamin K stored in the liver is depleted very rapidly even during short periods of vitamin K deficient diet consumption. Mycotoxins may also have a negative effect on vitamin K level in the body (NRC, 2012).
Vitamin K toxicity: trials have shown a tolerance for high vitamin K levels with no negative effect (NRC, 2012).
The vitamin K level in the premix can be negatively affected by moisture, choline chloride, trace elements and alkaline conditions. Coating of the vitamin K has shown to improve the stability in the premix.