SUNSHINE AN IMPORTANT SOURCE OF VITAMIN D

AS the evolution of vertebrates began 400 million years ago, a stable internal phosphate pool became necessary for mineralisation. Calcium was available to primitive unicellular organisms from their immediate environment. When multicellular organisms evolved and started moving away from the seas, a strong and mobile internal skeleton was necessary. Parathormone (PTH) and vitamin D became the principal hormones of vertebrate evolution that regulated extra-cellular calcium and phosphorous homeostasis.

Vitamin D is a fat-soluble vitamin made by our body after exposure to ultraviolet (UV-B) rays from the sun, but is also found in food. Exposure to sunlight is an important source of vitamin D. UV-B rays from sunlight trigger vitamin D synthesis in the skin. Season, latitude, time of day, cloud cover, smog and sunscreens affect UV-ray exposure.

It is important for individuals with limited exposure to the sun to include good sources of vitamin D in their diet. Vitamin D exists in several forms, each with a different activity. Vitamin D promotes bone mineralisation in concert with a number of other vitamins, minerals, and hormones.

Dietary sources

Dietary sources of vitamin D are cod liver oil, cooked salmon, eel and mackerel, sardines, liver, beef, whole egg (vitamin D is present in the yolk), milk and its products and drumstick leaves.

Fortified foods are the major dietary sources of vitamin D. Milk in the United States is fortified with 10 micrograms (400 IU) of vitamin D per quart. One cup of vitamin D fortified milk supplies about one-fourth of the estimated daily need for adults.

Although milk is fortified with vitamin D, dairy products made from milk such as cheese, yogurt, and ice cream are generally not fortified with vitamin D.

Vitamin D, calcium and phosphorus are critical for building of bone. Insufficient intake of vitamin D is associated with an increased risk of fractures. Vitamin D deficiency causes rickets in children and osteomalacia in adults.

Osteoporosis, a disease characterised by fragile bones, results in increased risk of fractures. Post-menopausal women and the elderly are at risk of developing osteoporosis. Normal storage levels of vitamin D in the body may help prevent osteoporosis.

Normal bone is constantly being remodelled. During menopause, the balance between these two systems is upset, resulting in more bone being broken down (resorbed) than rebuilt.

Vitamin D deficiency occurs more often in post-menopausal women and elderly. Adequate supplements of vitamin D may reduce the risk of osteoporotic fractures in elderly subjects with low blood levels of vitamin D.

Health impact

Laboratory studies have shown that low vitamin D intake results in increased risks of prostate, breast, colon, and other cancers. Vitamin D keeps cancer cells from growing and dividing.

Well-designed clinical trials need to be conducted to determine whether vitamin D is protective against some cancers. Vitamin D has been implicated in hypertension and skin diseases like psoriasis. Corticosteroid may also impair vitamin D metabolism, further contributing to the loss of bone and development of osteoporosis associated with steroid medications. Individuals on chronic steroid therapy should seek medical advice about the need to increase vitamin D intake through diet and/or dietary supplements.


Serum 25(OH)D levels are the most reliable indicator of the vitamin D status of an individual. Since vitamin D levels are subject to variations in diet, dress code, latitude and altitude of residence, skin colour, climate etc., the normative data varies between laboratories. These genuine geographic variations in calcium homeostasis restrict the locally estimated reference range used across the countries. Thus, locally developed "population-based reference values" (derived variously from blood donors etc.) cannot be applied globally as these values are limited by other factors.

A "functional health-based reference value" which physiologically defines hypovitaminosis D (vitamin D insufficiency) as the concentration of 25(OH)D at which PTH begins to increase is largely replacing the hitherto used "population-based reference values". This classification encompasses the "vitamin D-calcium-PTH axis" and its impact on the bone. It is more apt, and based on scientific reasoning.

Vitamin D deficiency (25(OH)D levels {lt}10 ng/ml) denote a biochemical, radiological or histological abnormality as a consequence of low vitamin D status. Hypovitaminosis D (10-20 ng/ml) is defined as a low concentration of serum 25(OH)D that indicates risk of developing vitamin D deficiency. While osseous signs often diagnose severe vitamin D deficiency, biochemical abnormalities reflect the cause and effect of vitamin D deficiency.

Low vitamin D status has far-reaching implications in diseases like fluorosis where the morbidity produced due to bone deformities is severe. It can have an impact in including vitamin D as an integral part of therapy in those vitamin D deficient postmenopausal women with osteoporosis.

Scientific organisations and apex policy forming bodies should undertake multicentric studies to develop nationally relevant guidelines. It is necessary to assess and address the issue of vitamin D status in various parts of the country where the sunshine, season, dietary habits, dress code etc, vary widely.