Blood levels necessary to cause adverse effects in adults are thought to be greater than about 150 ng/mL, leading the Endocrine Society to suggest an upper limit for safety of 100 ng/mL.
Based on risk assessment, a safe upper intake level of 250 μg (10,000 IU) per day in healthy adults has been suggested by non-government authors.
[5][6] Blood levels of 25-hydroxyvitamin D necessary to cause adverse effects in adults are thought to be greater than about 150 ng/mL, leading the Endocrine Society to suggest an upper limit for safety of 100 ng/mL.
[9] It has been questioned whether to ascribe a state of sub-optimal vitamin D status when the annual variation in ultraviolet will naturally produce a period of falling levels, and such a seasonal decline has been a part of Europeans' adaptive environment for 1000 generations.
[13] Evidence suggests that dietary vitamin D may be carried by lipoprotein particles into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages.
[25] Among descent groups with heavy sun exposure during their evolution, taking supplemental vitamin D to attain the 25(OH)D level associated with optimal health in studies done with mainly European populations may have deleterious outcomes.
Measuring melanin content to assess skin pigmentation showed an inverse relationship with serum 25(OH)D.[36] The uniform occurrence of very low serum 25(OH)D in Indians living in India and Chinese in China does not support the hypothesis that the low levels seen in the more pigmented are due to lack of synthesis from the sun at higher latitudes.
Vitamin D compounds, specifically cholecalciferol (D3) and ergocalciferol (D2), are used in rodenticides due to their ability to induce hypercalcemia, a condition characterized by elevated calcium levels in the blood.
Concentrations used in these rodenticides are several orders of magnitude higher than the maximum recommended human intake, with acute baits containing 3,000,000 IU/g for D3 and 4,000,000 IU/g for D2.