A recent editorial in the American Journal of Clinical Nutrition1 raised some important questions about the neuroprotective effects of vitamin D. Until relatively recently, vitamin D was considered important only in its role to maintain adequate calcium balance. In this regard vitamin D was seen as important in the prevention of rickets in children and in the prevention of osteomalacia in adults. Within the last two decades however, interest in alternative roles for vitamin D have been investigated as improvements in molecular and cell culture techniques allowed a more detailed understanding of the cellular role of the hormonal vitamin. Research has shown a possible protective role for adequate vitamin D status on both cardiovascular disease and type 1 and type 2 diabetes, perhaps because of effects of vitamin D on the insulin signal cascade. In addition, studies have highlighted possible protective effects for vitamin D against a range of cancers. However, the neuroprotective effects of vitamin D are perhaps less well understood.
Evidence from clinical trials for the role of vitamin D in mental decline is limited but some trials have shown possible protective effects on brain function. For example, optimising the 25-hydroxyvitamin D plasma levels of patients with Parkinson disease, stabilises their condition, whereas taking placebo tablets causes continued decline. The important thing to understand is that vitamin D is not acting pharmacologically here, but is repleting plasma status to optimal concentrations in those with low sunlight exposure and low levels of vitamin D intake from the diet. Studies show that the number of individuals with low plasma levels of the vitamin D metabolite 25-hydroxyvitamin D is high in countries in high latitudes. This is particularly true during winter and spring months, and in the elderly and those not able to expose themselves to ultraviolet light during the summer months. The dietary intake required to cause optimal 25-hydroxyvitamin D status in adults may be as high as 2000 IU per day.
The vitamin D receptor is expressed in the dopamine rich areas of the brain such as the substantia nigra. In addition, vitamin D may increase the expression of tyrosine hydroxylase, the rate limiting step in the formation of all catecholamine hormones. That low vitamin D status may be linked to accelerated neurodegeneration is increasingly being raised as a reality based on the ability of vitamin D to modulate the proliferation of cells, which may detrimentally affect brain remodelling. That vitamin D may protect the brain from neurotoxins and increase resistance of cells to damage by exogenous agents has also been found to have some merits. The effects of vitamin D on brain function may therefore be subtle, but this is generally the way of nutrients, and large rapid improvements in neurological action should not be expected with repletion. As vitamin D is a steroid hormone, it is not surprising that it may be involved in neurodevelopment and that optimal levels may confer protection from development of disorders such as schizophrenia.
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