Agriculture Reference
In-Depth Information
More common than retinol excess is chronic carotenoid excess. Unlike retinoids,
these do not appear to carry significant risks other than hypercarotinemia and yel-
lowed skin.
v
i t a m i n
a s
t a t u s
Vitamin A status is not easy to assess reliably. Clinical signs present late. A dietary
history is, as usual, important. In relatively small population studies, conjuncti-
val impression cytology estimates the conjunctival epithelial damage, and this has
proved useful. Serum retinol is more commonly used, but this falls with infection,
with malnutrition, and with zinc deficiency, so there are likely to be many false
positives. Where available, the best estimate of individual status is the relative dose
response test (RDRT), which measures the increase in plasma retinol after a dose of
vitamin A.
vItAmIn d
Vitamin D is a hormone precursor and an unusual vitamin as it is only conditionally
essential in the diet. The condition is insufficient conversion, by the sun's ultraviolet
B (UV-B) rays, of 7-dehydrocholesterol to cholecalciferol in the skin. Unfortunately,
this often pertains. Therefore, a knowledge of sources of dietary vitamin D is neces-
sary; indeed, reference nutrient intakes (RNIs) and recommended daily allowances
(RDAs) have been laid down for those at most risk, including infants, the elderly, and
those unable to enjoy exposure to the sun (Geissler and Powers 2006). There is little
doubt that rickets was present in the first century A.D., but the first good descriptions
were published in the midseventeenth century. In the nineteenth and early twentieth
centuries, when air pollution due to industry was severe in cities like Glasgow in
northern Britain, rickets was rampant. In 1919, Mellanby showed that cod liver oil
cured rickets in dogs, and this was quickly followed by human studies with similar
results. In 1922, the dietary component “essential” for bone health was named vita-
min D (Rajakumar 2003).
Since then, much has been learned about vitamin D's numerous roles in metabolism.
Cholecalciferol itself is inactive. It is converted in the liver to 25-hydoxycholecalcif-
erol, or calcidiol and then by 1-hydroxylase in the kidney to 1,25-dihydroxycholecal-
ciferol, or calcitriol, the most active form of the vitamin. Calcitriol's primary activity
is to raise plasma calcium by increasing its intestinal absorption, its renal reabsorp-
tion, and its release from bone. It has numerous other effects, mainly in nuclei via
genes but also via cell surface receptors. These include effects on hormones such as
parathormone, calcitonin, and insulin and on cell proliferation and differentiation,
particularly in lymphocytes and monocytes, cells involved in immune processes.
Although not confirmed, it has been implicated in the metabolic syndrome, in can-
cer, and in atherosclerosis. Excessive vitamin A has been shown to inhibit some
nuclear actions of vitamin D by interfering with the dimerization of the vitamin D,
which is necessary for vitamin D's activity.
Today, in temperate and subarctic regions, there is usually insufficient exposure
to UV-B during the winter. In certain cultures, women are rarely exposed to UV-B
