Fat Soluble Vitamins

Of the fat-soluble vitamins, vitamin A (retinol) has been the most studied in relation to the CNS. The others have been much less well examined, though vitamin E is currently of some interest, because of its function as an antioxidant. The CNS is not thought to be a major focus of action for vitamins D and K, and thus little information is available regarding their roles in brain function.

The principal role of vitamin A in the CNS is as a component of the photoreceptive pigment of the eye, rhodopsin. In the blood, vitamin A circulates bound to retinol-binding protein and transthyretin (preal-bumin). Its transport into retinal cells occurs at the blood-retinal barrier (the retinal pigmented epithelial (RPE) cells), after the retinol-protein complex binds to retinol-binding protein receptors. Once bound, retinol is released into the RPE cell. The retinol-binding protein and transthyretin molecules are released back into the circulation. Inside the RPE cell, retinol binds to a specific protein, and ultimately is esterified to a fatty acid. This molecule serves as the substrate for the conversion of retinol into the visually active form of the molecule, 11-cis-retinaldehyde, which then finds its way into the photoreceptor cell to be bound to opsin to form rhodopsin, the light-responsive pigment of the eye. When light strikes rhodopsin, phototransduction occurs and 11-cis-retinaldehyde is isomerized to all-trans-retinaldehyde, hydrolyzed from opsin, and released by the photoreceptor into the extracellular space (the opsin is retained and reused). The all-trans-retinaldehyde is shuttled into the RPE cell, where it is reconverted into 11-cis-retinaldehyde, and then recycled to the photoreceptor cells again to form rhodopsin.

From the nutritional perspective, retinal cells have an efficient system for managing and maintaining vitamin A pools. Hence, depletion of retinal vitamin A pools secondary to dietary deficiency only occurs over an extended time period. Deficiency appears functionally as 'night-blindness,' as rhodopsin levels decline. Extended vitamin A deficiency leads to a loss of photoreceptor elements, and eventually of the photoreceptor cells themselves. The cause of this cellular degeneration is not well understood.

Vitamin E is an antioxidant and free radical scavenger that protects fatty acids in cellular membranes. It is transported in blood associated with lipoproteins. The mechanism of its transfer into nervous tissue is unknown. Dietary vitamin E deficiency is extremely rare in humans. It occurs in association with certain abnormalities of vitamin E transport and fat absorption, and sometimes in individuals with protein-calorie malnutrition. The neurological manifestations are peripheral nerve degeneration, spinocerebellar ataxia, and retinopathy. Vitamin E has been proposed to play a role in a number of CNS diseases linked to oxidative damage. One example is Parkinson's disease, a movement disorder caused by the degeneration of certain groups of brain neurons. Evidence of oxidative damage is present in the brains of Parkinsonian patients, though controlled clinical trials of vitamin E supplementation have proved to be of no benefit. Such negative findings question the likelihood of a vitamin E link to the etiology of the degenerative changes. A second example is Alzheimer's dementia, which is associated with a progressive, ultimately catastrophic degeneration of the brain. Several types of oxidative damage have been found in the brains of Alzheimer's patients, though it is presently unclear if this damage is cause or effect. Vitamin E supplementation can slow the progression of Alzheimer's disease. However, such findings do not indicate if vagaries in vitamin E intake over an extended period of time are a cause of the disease.

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