UC-Davis shows vitamin E role in treating equine neurologic disease

UC-Davis shows vitamin E role in treating equine neurologic disease

Horses' condition makes it easier for vitamin E to do its work protecting cells from free-radical damage.
Dec 01, 2009

Photo 1: A horse with EMND showing postural muscle weakness with generalized muscle wasting. Note the position of the horse's hind legs.
Some inflammatory or degenerative neurologic diseases that affect horses — equine degenerative myeloencephalopathy (EDM) and equine motor neuron disease (EMND) — are linked to vitamin E deficiency. Vitamin E is a dietary antioxidant that protects cell membranes and tissues from oxidant free-radical damage, which is believed to play a role in the etiology and progression of the diseases.

Now, researchers at the University of California-Davis say horses with neurologic disease may respond differently to vitamin E treatment because of disruption of the blood-brain barrier or increased oxidant damage associated with the underlying disease.

Photo 2: A horse with EDM shows proprioceptive deficits.
The blood-brain barrier of horses with neurologic disease may be potentially compromised, allowing vitamin E to cross more easily, show higher cerebrospinal fluid (CSF) concentrations and be more effective in reducing oxidant free-radical damage in the brain.

Conversely, vitamin E may be more readily metabolized due to increased oxidant damage, and therefore show lower CSF values at the desired site of action. The antioxidant "demand" for older horses might be greater, especially those with neurologic disease.

The researchers demonstrated that daily oral administration of 10,000 IU vitamin E, as micellized d-alpha-tocopherol, crosses the blood-brain barrier in healthy horses. Leading the work were Jamie Higgins, DVM, Dipl. ACVIM, fellow in large-animal emergency medicine and critical care in the UC-Davis School of Veterinary Medicine, and colleagues, including Nicola Pusterla, DVM, Dipl. ACVIM, associate professor in equine internal medicine.

Vitamin E may benefit horses with neurologic disease, the researchers say. CSF samples they collected from the atlanto-occipital space provided accurate values of alpha-tocopherol concentrations around the brain and cervical portion of the spinal cord, which is where the most damage to the central nervous system is detected in horses.

They found that serum alpha-tocopherol concentration increases rapidly in a nonlinear manner if 10,000 IU of d-alpha-tocopherol supplement is given orally daily, compared to 1,000 IU.

Serum alpha-tocopherol concentrations in both groups increased significantly throughout the period of vitamin E administration. From baseline values at Day 0, they reached a plateau by Day 10 (mean, 2.96 µg/ml, 1,000 IU; 6.6 µg/ml, 10,000 IU).

Median and maximum CSF alpha-tocopherol concentrations were higher in horses treated with 10,000 IU d-alpha-tocopherol, compared with those receiving 1,000 IU, suggesting that high doses of supplemental vitamin E are likely of greater antioxidant benefit.

Both groups within 10 days showed a 1.3- to 3.4-fold increase in CSF alpha-tocopherol in nine out of 10 horses.

In another study, Pusterla, Higgins and colleagues showed that feeding of natural, micellized d-alpha-tocopherol showed greater bioavailability than synthetic (d,l-alpha-tocopherol), when fed on an equal basis to produce greater plasma and CSF alpha-tocopherol levels.

It was concluded that, because maintenance of sufficient cerebral alpha-tocopherol concentrations is essential for neurologic function, and of even greater importance when brain function is impaired by degenerative or inflammatory neurologic disorders, supplementation of a micellized alpha-tocopherol should be used preferentially over synthetic vitamin E when treating horses with neurologic disorders.

Horses presented to UC-Davis with neurologic disease routinely get 10,000 IU daily of alpha-tocopherol.