Vitamin D for your horses
What it is
The discovery of vitamin D followed a similar sequence to that of many other vitamins. The curative properties of products containing it were known for a long time before the vitamin itself was identified. In the middle of the 1700s it was found that cod liver oil was an effective treatment for rickets but it was not until the beginning of the present century that the particular substance influencing rickets was separated and examined.
Two compounds have this effect on rickets: ergocalciferol (or vitamin D2) which has a vegetable origin and cholecalciferol (vitamin D3) which derives from animals. In general they are not found in these chemical forms. Plant materials contain ergosterol and animal products 7-dehydrocholesterol which are absorbed by animals and then converted into the active vitamin D form by the action of ultra-violet light on the skin. Before they can be utilised further chemical changes must take place. The first step is the formation of the 25-hydroxy product in the liver and then further hydroxylation to 1:25 dihydroxy cholecalciferol [1,25(OH)2CC]. While 25-OH CC can be effective, the 1,25(OH)2CC is the major active form.
Since 1,25(OH)2CC is created in the organs of animals there is controversy whether it is a vitamin or a hormone.
What it does
Both vitamin D2 and vitamin D3 have similar activities in horses. The main function of the vitamin is the control of the absorption, transport and deposition of calcium and, to a lesser extent, phosphorus. The first action in this sequence is the promotion of intestinal absorption of calcium. This occurs mainly in the duodenum and many experiments have shown that little calcium is absorbed in the absence of vitamin D. By far the major activity is the deposition and mobilisation of bone calcium. Calcium is transported in the blood plasma from the intestine via liver and kidneys to bones and other calcified structures and in the opposite direction from bones to the kidneys where some may be excreted. Vitamin D controls the levels of calcium and phosphorus in blood at a super-saturated level which permits deposition in bone. A less than saturated level withdraws calcium from bones. A further related activity is the control of the reabsorption of phosphorus, calcium and sodium in the renal tubules of kidneys.
If too much is given
There can also be problems from grossly excessive supplies of vitamin D. Since it controls calcium absorption, excess vitamin D leads to excessive calcium in the blood (hypercalcaemia). This extra calcium has to be dumped and may be
deposited in the heart or blood vessels, in the bone joints, in the pericardium or in the intestinal walls. This leads to heart failure, or stiffness or intestinal problems. The excess amount necessary to produce such conditions varies with age. Levels greater than ten times the allowances recommended should be avoided.
How it is measured
Vitamin D3 - cholecalciferol - is usually taken as the standard.
Recommendations are generally given in International Units which are identical to USP units (United States Pharmacopoeia).
1 International unit of vitamin D = 0.025 mg cholecalciferol
1 mg cholecalciferol = 40,000 I.U. vitamin D
Assessment of status
It is exceedingly difficult to assess the vitamin D status of a horse. Actual hypocalcaemic conditions can be identified by X-ray radiography or by histology but little is known about the amounts of cholecalciferol or its active metabolites in blood and other tissues. Very sophisticated analytical techniques are needed to extract, separate and quantify the hydroxy forms of cholecalciferol and such assays cannot be used for routine assessments of vitamin D status. This has made it difficult to identify vitamin D stores in the body which are not believed to be very extensive.
Relationships with other ingredients
The relationship with calcium and phosphorus is obvious. The balance between them is fundamentally important and a ratio of calcium to phosphorus of between 2:1 and 1:2 must always be maintained. While age variations occur, the normal ratio is 1.4:1 or 1.5:1. There also appears to be some influence from sodium, potassium and magnesium.
Other essential micro-nutrients also affect bone strength. These include zinc, manganese, niacin, choline and biotin.
Some mycotoxins appear to interfere either with vitamin D absorption, vitamin D metabolite production or vitamin D-induced calcium absorption, and rickets or osteoporosis can occur under these conditions in spite of correct Ca/P ratio and adequate dietary vitamin D.
Requirements and allowances
The minimum amounts of vitamin D required by horses are very small. Young growing horses actively depositing new bone require proportionally more than fully grown adults. The allowances for optimum growth have to be assessed very carefully because of the risk of hypervitaminosis D.
In general, the allowance, measured in I.U., should be one tenth of the amount of vitamin A. Thus, as a guide,:
I.U. / kg I.U. / day
Adult performance horses in training 600 6000
Adult performance horses in light work 800 5000
Ponies, hacks & hunters 800 2500
Mares & stallions 1000 4000
Young horses 1-2 years 800 2500
Foals & yearlings less than 1 year 1000 1000-3000
Both forms of vitamin D are affected by light and are made inactive by oxidation. The close presence of heavy metal ions such as copper greatly accelerates oxidation. Moisture, particularly in the form of saturated air, can also assist the rapid destruction of vitamin D.
Only protected forms of vitamin D3 should be used in feeds. Gelatine matrix or spray-drying protection methods are equally effective in minimising oxidative destruction. Even so, some 5% is lost during feed pelleting and a similar amount during each month of storage. Meal mixtures and vitamin concentrate mixes lose very little during mixing but may lose 2-5 % per month of storage. Vitamin/mineral premixes containing aggressive trace minerals may lose 10-20% between mixing and use within 4 weeks. It is generally recommended that an overage of 30% vitamin D should be added to pelleted feeds to allow for anticipated losses during production and storage.