In the last issue we began our discussion on the necessity of vitamins in ruminant diets. We looked at Vitamin A extensively and we saw the importance of this compound in the animal's diet. As a nutritionist I have always found it interesting how the nutrients required in the smallest amounts can have such a profound effect on performance and health in the animal.
The following takes a similar look at a number of the other vitamins required by the ruminant. Vitamins D and E, like vitamin A, fall into the fat-soluble classification of vitamins. In this day and age we seldom see signs of a deficiency of these vitamins in cattle. More critical, however, are the small imbalances that take place from time to time. Some of this falls into the “if a little is good a lot has to be better,” ideal. We know from research that higher feeding levels of some vitamins have shown positive results in characteristics such as increased meat tenderness (vitamin D), extending the shelf life of meat (vitamin E), etc. At the same time, feeding excessive levels of vitamins such as D can have a negative impact on intake levels, potential calcification of kidney tissue and so on. Because of this it is very important that we are careful in formulation and feeding of diets where feeding levels of nutrients such as the vitamins is above the norm.
Ok, the following is just a little complicated so bear with me as we trudge through this. Vitamin D is formed by the action of sunlight or other sources of ultraviolet light rays upon certain sterols. A sterol in the skin of animals,
7-dehydrocholesterol, is converted to vitamin D3 by ultraviolet rays of sunlight. Glass filters ultraviolet rays from sunlight, so animals kept indoors do not form vitamin D.
Ergosterol, a sterol in green plants, is converted to D2 when the plant is harvested and cured in sunlight. Many commercial products of vitamin D are sold in concentrated form. Irradiated yeast has a high potency of vitamin D2. Both vitamin D2 and D3 are biologically active for cattle and other four-footed animals. Vitamin D3 is about 100 times as active as D2 for poultry.
Young, growing animals have a greater requirement for vitamin D than mature animals. Under normal conditions, cattle receive adequate vitamin D from exposure to direct sunlight or from consumption of three to four pounds of sun-cured forages daily. Experiments with calves indicate a requirement of approximately 300 I.U. of vitamin D per 100 pounds of body weight.
As suggested above, some work has shown that feeding of increased levels of vitamin D, for the last 3 to 4 weeks of the finishing period in slaughter cattle has resulted in improved meat tenderness.
Vitamin D is important in a number of critical physiological areas. These include:
1) An increase in the absorption from the digestive tract and metabolic use of calcium and phosphorus.
2) Regulation of blood calcium levels
3) Conversion of inorganic to organic phosphorus.
4) Aids in the formation of sound bones and teeth.
5) It's specific role in the prevention of rickets in young animals or osteomalacia in mature animals is associated with its involvement in the metabolism of calcium and phosphorus.
Rickets is characterized by soft, porous, poorly developed bones. Early signs of vitamin D deficiency in calves are poor appetite, decreased growth, stiff gait, weakness and labored breathing. Later signs include swollen joints, slight arching of back, bowed legs and bent knees. Bones that are easily broken are a sign in all ages of animals. A deficiency in pregnant animals may result in dead, weak or deformed calves.
Most rations fed to beef cattle are inadequate in vitamin E. Adding two to five I.U. of vitamin E per pound to high-grain rations devoid of leafy roughages has increased feedlot cattle performance in a few Corn Belt trials, but not in others. Injecting new feeder cattle with Vitamin E may reduce the incidence and severity of sickness in the starting phase as it has shown a positive effect on immune response
The specific physiological function of vitamin E is not clear. Its principal role may be as a chemical antioxidant to reduce the destruction of other vitamins and essential fatty acids both in the digestive tract and after their absorption. A vitamin E deficiency impairs reproduction in rats and other laboratory animals, but this effect has not been confirmed in farm animals. Stiff-lamb disease and white-muscle disease in calves (both degenerative muscle diseases) have been prevented and cured by use of vitamin E. Selenium, a trace mineral, spares or replaces vitamin E in the prevention or curing of these two diseases. A close relationship exists between selenium and vitamin E, but each is thought to be irreplaceable on a total basis for normal body metabolism.
Vitamin E activity is present in several tocopherols that occur in nature as high molecular weight alcohols, but alpha-tocopherol is the principal one with any significant biological value. One I.U. of vitamin E is defined as the activity of 1.0 mg. of dl-alpha-tocopherol acetate. Other tocopherols vary from one-third to one-hundredth the biological potency of the alpha form. Common assay methods do not distinguish between these forms, resulting in the vitamin E potency of feeds being overestimated in many cases (see Table 1). Alfalfa meal contains a high percent of alpha-tocopherol. Green leafy forages and whole grains are sources of vitamin E. Much of the vitamin E is in the oil of the seed.
Table 1. Tocopherol content of feedstuffs.1
C.R. Adams, Hoffman La Roche Co., 19th Montana Nutrition
The need for vitamin E in beef cattle rations has not been clearly demonstrated. Until we know more about this vitamin, however, the following conditions might be suspected as causing a deficiency:
1) High-grain rations with limited or no roughage, especially high-moisture harvested grains
2) Feeding grains or roughages that are low in selenium
3) High fat levels in ration
4) Lengthy storage of feeds
5) High drying temperatures for feeds
6) Feeds that have a small portion of their vitamin E assay value from alpha-tocopherol
Use about 50 I.U. per animal daily if vitamin E supplementation of feedlot rations is deemed advisable.
Rumen bacteria make vitamin K in quantities to meet the needs of cattle under most conditions. One exception is death loss from internal hemorrhage or surgery that may occur when cattle are fed moldy sweet clover hay or silage. Other moldy legumes can possibly cause a similar problem. Vitamin K is essential in the liver for the production of prothrombin. Low levels of prothrombin in the blood lengthen blood clotting time and cause internal bleeding. Dicumarol (active substance found in some rat poisons) is the substance in moldy sweet clover hay that interferes with the function of vitamin K in the production of prothrombin by the liver. Vitamin K administration and removal of the moldy feed are the most effective ways to overcome this condition.
Included in the B-vitamin complex are thiamin, biotin, riboflavin, niacin, pantothenic acid, pyridoxine, folic acid, vitamin B12 and choline. Once the rumen becomes functional, bacterial synthesis is considered to supply the normal requirement of cattle for B-vitamins. Milk is a source of B-vitamins for the calf.
The lack of a trace mineral, cobalt, can result in a vitamin B12 deficiency in cattle. This is because cobalt is a part of the vitamin B12 compound and is essential for rumen bacteria to manufacture this vitamin.
Choline supplementation of rations for fattening cattle has appeared to increase performance in Washington State trials, but has not been effective in most other areas of the United States.
You can tell from this discussion that we know a lot about vitamin nutrition in cattle. This discussion also tells you that we have much left to learn. Remember that in feeding vitamins a little can go a long way. Always make sure you have highly accurate information when determining what levels you need to be feeding.
Dr. Steve Blezinger is a nutritional and management consultant with an office in Sulphur Springs, Texas. He can be reached at P. O. Box 653 Sulphur Springs, TX 75483, by phone at (903) 885-7992 or by e-mail at firstname.lastname@example.org.