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VITAMIN D RCN


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Low blood calcidiol (25-hydroxy-vitamin D) can result from avoiding the sun. Deficiency results in impaired bone mineralization, and leads to bone softening diseases including:

  • Rickets, a childhood disease characterized by impeded growth, and deformity, of the long bones which can be caused by calcium or phosphorus deficiency as well as a lack of vitamin D; today it is largely found in low income countries in Africa, Asia or the Middle East and in those with genetic disorders such as pseudovitamin D deficiency rickets. Rickets was first described in 1650 by Francis Glisson who said it had first appeared about 30 years previously in the counties of Dorset and Somerset. In 1857 John Snow suggested the rickets then widespread in Britain was being caused by the adulteration of bakers bread with alum. The role of diet in the development of rickets was determined by Edward Mellanby between 1918–1920.Nutritional rickets exists in countries with intense year round sunlight such as Nigeria and can occur without vitamin D deficiency. Although rickets and osteomalacia are now rare in Britain there have been outbreaks in some immigrant communities in which osteomalacia sufferers included women with seemingly adequate daylight outdoor exposure wearing Western clothing. Having darker skin and reduced exposure to sunshine did not produce rickets unless the diet deviated from a Western omnivore pattern characterized by high intakes of meat, fish and eggs, and low intakes of high-extraction cereals. The dietary risk factors for rickets include abstaining from animal foods. Vitamin D deficiency remains the main cause of rickets among young infants in most countries, because breast milk is low in vitamin D and social customs and climatic conditions can prevent adequate UVB exposure. In sunny countries such as Nigeria, South Africa, and Bangladesh where the disease occurs among older toddlers and children it has been attributed to low dietary calcium intakes, which are characteristic of cereal-based diets with limited access to dairy products. Rickets was formerly a major public health problem among the US population; in Denver where ultraviolet rays are approximately 20% stronger than at sea level on the same latitude almost two thirds of 500 children had mild rickets in the late 1920s. An increase in the proportion of animal protein in the 20th century American diet coupled with increased consumption of milk fortified with relatively small quantities of vitamin D coincided with a dramatic decline in the number of rickets cases.
  • Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is characterized by proximal muscle weakness and bone fragility. The effects of osteomalacia are thought to contribute to chronic musculoskeletal pain,there is no persuasive evidence of lower vitamin D status in chronic pain sufferers.

Adequate vitamin D may also be associated with healthy hair follicle growth cycles.There are also associations between low 25(OH)D levels and peripheral vascular disease,certain cancers, multiple sclerosis, rheumatoid arthritis, juvenile diabetes,Parkinson's and Alzheimer's disease.However these associations were found in observational studies and vitamin D vitamin supplements have not been demonstrated to reduce the risks of these diseases.

Research shows that dark-skinned people living in temperate climates have lower vitamin D levels.

It has been suggested that dark-skinned people are less efficient at making vitamin D because

melanin

in the skin hinders vitamin D synthesis, however a recent study has found novel evidence that low vitamin D levels among Africans may be due to other reasons.

Recent evidence implicates

parathyroid hormone

in adverse cardiovascular outcomes, black women have an increase in serum PTH at a lower 25(OH)D level than white women.

A large scale association study of the genetic determinants of vitamin D insufficiency in Caucasians found no links to pigmentation.

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