Vitamin D is one of prohormones that are fat-soluble with the two primary types being vitamins D2 (ergocalciferol) and D3 (cholecalciferol). Other forms are: D1, D4 (22-dihydroergocalciferol) and D5. It is not a hormone per se, but is converted to an active hormone- 1, 25-Dihydroxyvitamin D. Vitamin D helps in the maintenance of organ systems. It controls blood phosphorus and calcium levels by accelerating their absorption in the intestines and calcium re-absorption in the kidneys thus facilitating proper bone mineralization thus avoiding hypocalcemic tetany.
Vitamin D is also required by osteoblasts and osteoclasts for bone growth and remodeling. It supports calcification of soft tissues when vitamin K is absent and in the presence of drugs that hamper vitamin K metabolism. It prevents secretion of parathyroid hormone by parathyroid gland. It promotes phagocytosis and immonumomodulatory activities of the immune system (Stolzt, 2006, p. 17). Deficiency can be occasioned by: insufficient intake, inadequate sunlight exposure, malfunctions that reduce its absorption, blockage of its conversion into metabolites and hereditary malfunctions.
Vitamin D deficiency leads to improper bone mineralization, children rickets, bone softening ailments, osteoporosis and adult osteomalacia. Vitamin D deficiency results in a number of disorders including: children rickets, characterized by impaired growth and disfiguration of long bones; adult osteomalacia, a bone-thinning ailment signified by weakness of proximal muscles and bone brittleness; osteoporoisis, signified by reduced bone mineral density and heightened bone brittleness.
Vitamin D malnutrition is also associated with heightened vulnerability to a number of chronic ailments, for instance, high blood pressure, cancer, TB, periodontal malady, chronic pain, multiple sclerosis, seasonal affective disorder, cognitive impairment, peripheral artery disorder and autoimmune ailments. The human body does not synthesize vitamin D2 thuds it is derived from plants and fungi. The skin makes vitamin D3 during the reaction of dehydrocholesterol with UVB ultraviolet light.
D3 is also obtained from animal sources (Dexter, Burton, 2005, p. 24). Blood calcidiol (25-hydroxy-vitamin D) analysis is the universal way of establishing vitamin D nutritional status. The optimal concentration of calcidiol is 35-55ng/ml. aged people, dark-skinned individuals and those with limited exposure to UV radiation ought to consume additional vitamin D from food supplements of vitamin D–fortified foods. These high-risk individuals ought to daily consume 25 ug (1000 IU) according to the 2005 Dietary Guidelines for Americans.
Daily dosages of 250 micrograms (10,000IU) are sufficient. Tolerable Upper Intake Level for adults and children is 50 micrograms (2,000 IU) daily as per the US Dietary Reference Intake. Tolerable UL for infants (birth to 12 months) is 25 micrograms (1,000 IU) per day (Stolzt, 2006, p. 74). Foodstuffs like yoghurt, milk, margarine, breakfast cereals, bread, oilspreads, and pastries are fortified with either vitamin D2 or D3 or both in many nations.
Natural vitamin d sources include: fatty fish, for instance, herring, salmon, mackerel, catfish and sardines; fish liver oils like cod liver oil; whole eggs; and beef liver. Synthesis of body vitamin D is tightly controlled and thus toxicity is mostly occasioned by excessive intakes. Toxicities are determined by analysis of serum calcidiol levels. Calcidiol levels in healthy persons range from 80 to 175 nmol/L (32-70 ng/Ml). In toxic instances, these levels could be as much as fifteen times.
Continuous daily intake of 2500 micrograms over a few months (100,000 IU) can lead to toxicity. Vitamin d daily intakes of 1000 micrograms (40,000 IU) results to toxicity within 1 to 4 months in infants. Levels of 500-600 micrograms per kilogram body weight per day signify toxicity in humans (Kragballe, 2000, p. 55). Most historical cases of vitamin d overdose were occasioned by industrial and manufacturing mishaps. Symptoms of vitamin d toxicity are due to hypercalcemia (increased blood calcium levels) occasioned by elevated calcium intestinal absorption.
Elevated blood pressure is also caused by vitamin d overdose. Anorexia and vomiting are GIT symptoms of toxicity. Polyuria (excessive urination), polydipsia (heightened thirst), nervousness, weakness, pruritus (itching) and kidney failure then ensue.
References
Dexter, E & Burton, J (2005). Vitamin D: New Perspectives in Drawing. New York: Phaidon Kragballe, K. (2000). Vitamin D in dermatology. London: Informa Health Care Stolzt, V (2006). Vitamin D. New York: Nova Publishers