1. Introduction
Vitamin D deficiency is a major world pandemic [1,2]. The first
clear indication that such a deficiency can cause disease emerged
when rickets was found to result from a decline in calcium (Ca2þ)
uptake across the intestine caused by low levels in Vitamin D.
Subsequently, such Vitamin D deficiencies have been linked to
many other human diseases such as Alzheimer's disease (AD),
cancer, cardiovascular disease, hypertension, type II diabetes,
multiple sclerosis (MS), Parkinson's disease (PD) and various inflammatory
disorders such as tuberculosis [3]. The role of vitamin D
in preventing rickets depends on its ability to increasing the
expression of Ca2þ pumps and buffers to facilitate the uptake of
Ca2þ across the intestine as part of vitamin D's role in regulating
whole body Ca2þ homoeostasis. In the case of all the other diseases
mentioned above, there is no general consensus as to how Vitamin
D might function despite the overwhelming evidence of its
important health benefits.
In this review, I will develop the concept that Vitamin D may act
by maintaining the stability of intracellular signalling pathways.
This Vitamin D phenotypic stability hypothesis will be illustrated
through its role in regulating the cellular mechanisms responsible
for maintaining the Ca2þ and redox signalling pathways