ORIGIN OF VITAMIN D: NUTRITION AND PHOTOSYNTHESIS

Vitamin D can be obtained from dietary sources of vegetal (vitamin D 2 or ergocalciferol) or

animal origin (vitamin D 3 or cholecalciferol). About 50% of dietary vitamin D is absorbed by
the enterocytes and is transported to the blood circulation via chylomicrons. Part of this
vitamin D is taken up by a variety of tissues (fat and muscle) before the chylomicron
remnants and its vitamin D finally reach the hepatocytes. The best food sources are fatty
fish, but it is also found in small amounts in butter, cream, and egg yolk. Both human’s and
cow’s milk are poor sources of vitamin D, providing only 15 to 40 IU/L, and they include
equally minimal concentrations of 25OHD or 1,25(OH) 2 D. 15 Only an intake of
pharmacologic amounts of vitamin D (6000 IU/day) can increase the vitamin D
concentration of milk to a level equivalent to the daily requirements of an infant. 16 Vitamin
D intake is a poor predictor of serum 25OHD concentrations in subjects with an intake
between 2 and 20 μg/day. 17 It is difficult to obtain adequate vitamin D from a natural diet.

However, in North America, 98% of fluid and dried milk (>400 IU/L), as well as some
margarine, butter, and certain cereals, is fortified with vitamin D 2 (irradiated ergosterol) or

D 3 , but the real vitamin D content is frequently differ-

ent from the labeling standard. Vitamin D is remarkably

stable and does not deteriorate when food is heated or

stored for long periods. The Second National Health and

Nutrition Survey (NHANES II) reported a median intake

of about 3 μg/day in adults, 18 but much higher values

were found in NHANES 2002 to 2006 (6 to 9 μg/day). 19

The mean intake of vitamin D in Germany, however, is

still about 3 μg/day, probably related to different policies

in the vitamin D supplementation of food. 20 In view of

the low vitamin D content of a vegetarian diet (natural

vitamin D intake is indeed related to the intake of animal

fat), vitamin D deficiency and rickets are risk factors for

strictly vegetarian children with insufficient sun exposure

or inadequate vitamin D supplementation. 21

Nature probably intended that most vitamin D would be

generated by photosynthesis in the skin, with minor contri-

butions from food sources. However, exposure to sunlight

also increases the risk of dermal photodamage and several

skin cancers, including melanoma. This was no real problem

during human evolution, but with increasing life expectancy,

the benefits of UV light for the photosynthesis of vitamin D

should be compared with the lifetime risk of skin damage,

especially because vitamin D supplementation can safely

replace the skin synthesis. The recommended dietary allow-

ances by the U.S. Food and Nutrition Board of the National

Research Council and the 2010 updated recommendations

are presented in Table 59-1, and older recommendations

are gradually updated in Europe. 22-24 There is, however, no

unanimity regarding these recommendation (vide infra).

Hypervitaminosis can occur when pharmaceutical vita-

min D is taken in excess, and this includes a wide variety of

symptoms and signs related to hypercalciuria, hypercalce-

mia, and metastatic calcifications (Table 59-2). The toxic

dosage has not been established but toxicity should always

be monitored when daily doses markedly exceeding the

present upper limit of more than 100 μg are administered

for a longer period. Overproduction of renal 1,25(OH) 2 D

by abnormal hormonal stimuli (as seen in fibroblast growth

factor-23 [FGF-23] or Klotho-null mice) or absence of

CYP24A1 (see text that follows), the main catabolizing

enzyme, causes the same calcemic side effects, with severe