A DIFFERENT APPROACH TO OXALATES
Warm-season C4 grasses store energy as starch rather than fructan and are therefore thought of as being less of a problem for horses susceptible to laminitis. The downside is that many of the C4 grasses such as kikuyu, setaria, buffel, signal and panic are high in oxalates which bind to minerals, making them unavailable for digestion and use by the horse. Oxalates have a strong affinity for calcium, but also bind other minerals such as magnesium.
The result is that the horse is mineral deficient which causes minerals to be taken from bone reserves to supply essential metabolic processes. Whilst the whole skeleton is at risk, the most noticeable feature is the loss of bone from the face that causes a swollen appearance as facial bone is replaced by hard fibrous tissue. This is known as Bighead Disease or Nutritional Secondary Hyperparathyroidism. The traditional treatment for bighead disease (and prevention) is to feed the horse large volumes of calcium and di-cal-phos (DCP). This treatment has proved effective for some horses, but many horses do not respond positively.
(Click on any image to see a larger version)
It has been found that some horses do improve very quickly with a completely different approach. On one Queensland property with predominantly setaria pasture, several horses with signs of severe bighead disease of several years' duration were given large amounts of calcium and DCP on veterinary recommendation over a long period. There was no change to their condition.
One young horse was given calcium and DCP in the hope of preventing bighead disease, but developed the characteristic facial swelling anyway.
The same high magnesium and low calcium dietary protocol that has been used for the other horses featured on this website was commenced late July 2012. The results were remarkable as can be seen from these photos tracking changes in one of the horses in less than four months.
Photos courtesy of H. Statham
20 June 2012
20 October 2012
18 September 2012
6 November 2012
20 June 2012
20 June 2012
There was also some evidence of improvements to jaw alignment. As shown here the lower jaw is protruding less than before diet change.
6 February 2013
Prior to diet change, this pony was standing in a braced posture leaning over his front feet. This can be one of the signs of magnesium deficiency.
After diet change, this pony has a normal body posture with a lengthened topline.
6 February 2013
Despite these dramatic improvements after years of failure with conventional treatment, there is no room for complacency. Removing the horse from oxalate pasture is still the preferable option, as any other dietary approach must be maintained continuously.
Subsequent to the November 2012 photo above, the pony’s large intake of magnesium was reduced to half from December 2012, with one week of no magnesium at the end of January 2013. The pony quickly regressed with increased facial swelling as can be seen in this photo of 6 February 2013.
Rory, the aged chestnut TB whose documented lifestory can be read on the RORY main page, grazed the worst of the oxalate grasses, setaria, for over 8 years. He was given very little additional calcium and did not consume any high-calcium feeds such as lucerne during that period. Add to that his history of laminitis and Cushings, and he could be expected to have significant bone loss in his vulnerable coffin bones. To the contrary, he continues to have excellent strong bone.
How could a low calcium diet reverse Bighead Disease?
It does seem extraordinary that a disease manifesting as lack of skeletal calcium can be improved by a low-calcium diet. A clue to understanding those results can be found in neurosurgeon Russell Blaylock’s explanation of calcium and magnesium metabolism in his book ‘Excitotoxins, The Taste That Kills’. Dr Blaylock states that all nerve cells take precedence for the body's use of calcium and that calcium will flood into nerve cells any time the cell channels or 'gates' are open. This ‘calcium flood’ will occur regardless of whether the calcium is needed in the nerve cells or not, and regardless of how damaging that may be. Very simplistically, one of magnesium’s multiple metabolic roles is to act as a cellular 'gatekeeper', controlling the influx of calcium into nerve and other cells. During normal metabolism, when sufficient magnesium is available, only small amounts of calcium are permitted to enter cells for a specific, temporary purpose.
When the horse eats grass containing oxalates, a proportion of the calcium in the grass and also the magnesium and other minerals is passed out of the body without being digested. This is likely to leave the horse with low blood levels of both calcium and magnesium. As the body prioritizes the use of whatever minerals are available, there may be insufficient magnesium allocated to operate the nerve cell 'gates' which then allows calcium to flood into the open nerve cells. If there is not enough calcium in the blood to feed the open 'gates' because the calcium was excreted along with the oxalates, calcium is then taken from bone to supply the open nerve cell 'floodgates'.
In this situation of low magnesium, extra calcium fed to the horse may provide enough in the blood to supply the nerve cell 'floodgates' so calcium does not have to be taken from bone. If extra magnesium is given to the horse instead, the nerve cell channel 'gates' may be able to operate appropriately to exclude calcium until it is needed. Calcium is then not wasted in feeding the 'floodgates' and does not need to be taken from bone. With sufficient magnesium available, the small amount of calcium absorbed can be used for vital functions and replenishment of previously depleted bone.
There is no proof, because the research has not been done, that this is the mechanism by which the aged TB, Rory, did not get Bighead Disease and the pony has improved. Controlled research is needed to evaluate what would appear to be an effective dietary approach for some horses where conventional treatment has failed.