Folic acid is the synthetic version of folate. However, to make things more confusing, "folate" can refer to either the natural version, or the generic term for both the synthetic form and natural form together.
Folate has very few roles in the horse, but the roles it does play are very important. It is involved in reactions necessary for the creation of DNA as well as methionine (an important amino acid).
Because both DNA and methionine are needed in large quantities when cell growth or turnover (old cells being replaced by new cells) are taking place, it is vital for tissues in these states.
Examples would be fetal growth and development, tissue repair after an injury or other trauma, and constant regeneration of the digestive tract lining.
As with other B vitamins, there is limited information about folate and folic acid in the horse.
Alfalfa appears to have the highest concentration of folate in the horse's diet, followed closely by timothy hay, then trailed by the cereal grains.
Horses that are on pasture have a higher serum concentration of folate than those that are eating hay, suggesting that fresh forage has a higher concentration than preserved feeds.
It also appears that folate can be synthesized by the microorganisms in the horse's digestive tract.
Folate deficiency is characterized by megaloblastic anemia (anemia resulting from inability to synthesize DNA in blood cells) and leukopenia (decreased circulation of white blood cells) in other species, but has never been reported in horses.
However, owners treating horses for EPM with sulfadiazine and pyrimethamine should be aware that these two substances can affect folate levels in the horse.
Sulfadiazine affects folate status by inhibiting the microorganisms in the tract from creating folate. Pyrimethamine affects the status by inhibiting the metabolism and absorption of folate.
A study done by Piercy et. al (2002)* reported clinical findings of folate deficiency in a horse treated with these drugs for 9 months. The clinical findings included hematological defects, hypoplastic bone marrow (decreased bone marrow), and dysphagia (difficulty swallowing) caused by oral ulcers and glossitis (swelling of the tongue).
The treatment for EPM was accompanied by folic acid supplementation, which appeared to make the problem worse by competing with the active form of folate for absorption.
Another study supported this hypothesis. That study was done on pregnant mares that were treated for EPM and supplemented with folic acid anywhere from the last 3 months of pregnancy to 2 years. The newborn foals were born with congenital defects.
Folate is considered non-toxic in the horse (and most other animals). However, if a rat is administered 1000 times the dietary requirement via injection, it can cause epileptic convulsion and renal hypertrophy.
*Piercy, R.J., K. W. Hinchcliff, and S. M. Reed. 2002. Folate deficiency during treatment with orally administered folic acid, sulphadiazine and pyrimethamine in a horse with suspected equine protozoal myeloencephalitis (EPM). Equine Vet. J. 34:311-316.