Principles of Biochemistry Volume 3 - A. Lehninger 1985

Selected Aspects of Human Biochemistry
Human Nutrition
Vitamin D deficiency leads to rickets and osteomalacia

At one time, vitamin D deficiency was widespread in many northern countries (Section 10.15), but today it is extremely rare in the United States. In children, vitamin D deficiency leads to Rickets (the adult counterpart of which is Osteomalacia), a condition characterized by softening and deformation of the bones due to insufficient calcium. This is caused not by a lack of dietary calcium, but by a shortage of the hormone 1,25-dihydroxycholecalciferol (see Fig. 10-22), which is typically derived from the precursor vitamin D₃, or cholecalciferol. Under favorable conditions, dietary vitamin D may not even be necessary, because sufficient exposure of the Skin to sunlight converts 7-dehydrocholesterol into cholecalciferol, i.e., vitamin D₃ (Fig. 26-20), via a photochemical reaction. However, when sun exposure is inadequate, vitamin D must be obtained from food (Section 10.15). If a child's face is exposed to direct sunlight for at least half an hour daily, this is sufficient to meet the minimum daily requirement for vitamin D. Although Eskimos are virtually deprived of sunlight during the arctic winter, they manage to obtain adequate amounts of vitamin D from fish rich in this vitamin (Fig. 26-21).

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Fig. 26-20. Vitamin D.

Infants suffering from rickets generally appear well-nourished, but they exhibit reduced Muscle tone and delayed motor development. Rickets causes deformities in the BONES OF THE Skull, chest, and spine; a particularly classic sign is bowing of the legs and knock-knees. In the Cytology/cytology/16.html">Early stages of the disease, vitamin D Treatment can correct mild deformities, but at later stages the bone changes become irreversible.

In adults, vitamin D deficiency manifests as osteomalacia. Pregnant women with restricted diets are especially vulnerable to vitamin D deficiency, as the developing fetus draws Ca²⁺ ions from the maternal Skeleton.

Fig. 26-21. Vitamin D deficiency typically develops when There is a lack of ultraviolet sunlight, which is necessary to convert 7-dehydrocholesterol into vitamin D₃. It is hypothesized that human ancestors lived in the tropics and had dark skin. As populations migrated northward, dark skin pigmentation—which protects against UV radiation—became a disadvantage because it hindered vitamin D synthesis. The lighter skin color that evolved through genetic Selection facilitated better absorption of ultraviolet rays among northern populations. Eskimos did not undergo this selection pressure because they receive ample amounts of vitamin D from fish.

To combat vitamin D deficiency, irradiated ergosterol is added to foods. This Yeast sterol is readily converted into ergocalciferol (Section 10.15), which has biological effects similar to vitamin D. The virtual eradication of rickets in the United States is a direct result of fortifying cow's milk with irradiated ergosterol. The recommended daily dose of vitamin D for adults who receive no sunlight exposure is 10 µg. Doses exceeding 1.5 mg per day are highly toxic.