Origin and Structure of Vitamin D

As the industrial revolution began to take hold in Northern Europe in the 17th century, it was quickly associated with a new disease that caused severe growth retardation and bony deformities in young children (Figure 1). This disease was commonly known as rickets or 'English disease' and plagued the children of the industrialized cities in Europe and North America for more than 250 years. Although Sniadecki in 1822 and Palm in 1890 both recognized that it was lack of exposure to sunlight that was the likely cause of rickets in children, Huldschinsky, in 1919, was the first to prove that exposure of the skin to ultraviolet radiation could cure rickets. Within 2 years, Hess and Unger reported that exposure of several rachitic children to sunlight was adequate for curing this bone-deforming disease.

Steenbock and Black and Hess independently recognized that exposure of animals and their food to ultraviolet radiation imparted antirachitic activity. This led to the recommendation for the ultraviolet irradiation of foods as a means of fortifying them with vitamin D. This resulted in the addition of provitamin D to milk followed by ultraviolet irradiation. As soon as it was possible to commercially synthesize vitamin D in large quantities, it was added directly to milk and other foods.

The first vitamin D was isolated from the irradiation of the yeast sterol ergosterol (Figure 2). This vitamin D was thought to be identical to that produced in the skin of animals and humans. However, studies revealed that when vitamin D produced from yeast was fed to chickens, they were unable to utilize it and developed rickets. When chickens were fed natural vitamin D from fish liver oil, rickets was prevented. This led to the conclusion that vitamin D originating from yeast was different from that in fish liver oil and animal and human skin. In 1937, this mystery was solved when the structure of provitamin D from pig skin was determined. A structural analysis revealed that provitamin D derived from ergosterol differed from that derived from pig skin. The provitamin D (ergosterol; provitamin D2) that came from yeast had a double bond between carbons 22 and 23 and a methyl group on carbon 24.

Figure 1 This is a typical presentation of a child with rickets. The child is suffering from severe muscle weakness, has bony deformities including bowed legs, and knob-like projects in the middle of his ribcage called the rachitic rosary. (Reproduced with permission from Fraser D and Scriver CR (1979) Disorders associated with hereditary or acquired abnormalities of vitamin D function: hereditary disorders associated with vitamin D resistance or defective phosphate metabolism. In: De Groot LJ et al. (eds.) Endocrinology, pp. 797-808. New York: Grune and Stratton.)

Figure 1 This is a typical presentation of a child with rickets. The child is suffering from severe muscle weakness, has bony deformities including bowed legs, and knob-like projects in the middle of his ribcage called the rachitic rosary. (Reproduced with permission from Fraser D and Scriver CR (1979) Disorders associated with hereditary or acquired abnormalities of vitamin D function: hereditary disorders associated with vitamin D resistance or defective phosphate metabolism. In: De Groot LJ et al. (eds.) Endocrinology, pp. 797-808. New York: Grune and Stratton.)

The provitamin D in animal skin had a side-chain that was identical to cholesterol, i.e., it did not contain either a double bond or methyl group on carbons 22-23 and 24, respectively, and was identified as 7-dehydrocholesterol (provitamin D3) (Figure 2). The vitamin Ds generated from ergosterol and 7-dehydrocholesterol were called ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3), respectively.

Breaking Bulimia

Breaking Bulimia

We have all been there: turning to the refrigerator if feeling lonely or bored or indulging in seconds or thirds if strained. But if you suffer from bulimia, the from time to time urge to overeat is more like an obsession.

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