Vitamin D is actually not a vitamin at all, but a steroid hormone. Vitamin D can be ingested in the diet or can be synthesised endogenously in the skin of humans via the action of ultraviolet light on cholesterol. In the body vitamin D3 (cholecalciferol) is converted in the liver to its active form, 25-hydroxyvitamin D3 [25-(OH)D3]. If dietary vitamin D is derived from plant rather than animal sources the vitamin is in the D2 form, and the subsequent synthesis of 25-hydroxyvitamin D2 proceeds in the liver. Adequate sunlight is essential to optimal production of vitamin D and 25-hydroxyvitamin D because dietary sources are limited. Therefore those living in high latitude regions experience shortages of vitamin D synthesis in the winter which causes a drop in 25-hydroxyvitamin D when the angle of incidence of the sun increases. Recently the vitamin D requirement has been revised upwards from 25 nmol/L (10 ng/mL) to 40 nmol/L (16 ng/mL), based on evidence from scientific studies investigating vitamin D and disease.
Those individuals with 25 hydroxyvitamin D levels below 25 nmol/L (10 ng/mL) are still considered to have outright vitamin D deficiencies and are at risk of osteomalacia and rickets. However, those with plasma levels of 25-hydroxyvitamin D below 40 nmol/L (16 ng/mL) but above 25 nmol/L (10 ng/mL) are now classified as insufficient, equivalent to a subclinical chronic deficiency. Such individuals are also at increased risk of disease. Large scale epidemiological studies have assessed the associations between plasma level of vitamin D and all cause mortality, with particular reference to dose-response relationships. For example, in a German study1 of subjects between 50 and 74 years, 10,000 subjects had their plasma 25-hydroxyvitamin D levels measured at baseline and a further 5000 had their levels remeasured at 5 year follow up, with deaths being recorded from baseline to a 9.5 year follow up. During this time, 1083 people died, which included 350 cardiovascular deaths, 433 cancer deaths and 55 respiratory deaths.
Compared to subject with adequate 25-hydroxyvitamin D status (>50 nmol/L or 20 ng/mL), those with plasma 25-hydroxyvitamin D levels of <30 nmol/L (12 mg/mL) and of between 30 and 50 nmol/L (12 and 20 ng/mL) had an increased risk of mortality indicated by a hazard ratio (HR) of 1.71 and 1.17, respectively. Vitamin D deficiency was associated with an increased risk of cardiovascular death (HR: 1.39), and increased risk of cancer mortality (HR: 1.42) and an increased risk of respiratory death (HR: 2.50). The association between vitamin D and all cause mortality was an inverse nonlinear trend with increased risk starting at plasma levels of <75 nmol/L (<30 ng/mL) 25-hydroxyvitamin D. These results therefore support previous findings that show protective effects of vitamin D. Further, they highlight the increase risk of disease at plasma levels of 25-hydroxyvitamin D that are commonly found in the general population of those living in high latitude regions. This supports a role for vitamin D supplementation in human health.
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