Vitamin D toxicity can occur from high intakes of supplements containing vitamin D, but not from dietary intake. Prolonged sun exposure also does not result in vitamin D toxicity because the previtamin D3 is degraded as the skin heats up, and also because of the formation of various other non-functional forms of vitamin D from the thermally activated compound. Long term intakes of vitamin D above the upper limit recommended causes symptoms of toxicity. However, the intakes must be higher than about 40,000 IU/day, or the serum level of 25-hydroxy above 500-600 ng/mL, and the patient is usually also taking excessive amounts of calcium as well. Components of vitamin D toxicity Vitamin D toxicity comprises different metabolic features, namely: The last two are not invariable findings in vitamin D toxicity, though they are common. The symptoms of toxicity include: Such as calcification of blood vessels and tissues in the heart, kidney and other organs, called metastatic calcification or calcinosis.
In addition, there is nausea, constipation and dehydration. A serum calcium measurement above 14 mg/dL causes critical multisystem malfunction, requiring emergency treatment. This includes adverse effects on the heart (such as heart arrhythmias), blood vessels, central nervous system and kidneys. The fat-solubility of vitamin D means that toxic effects may linger for months after the cessation of exogenous supplementation or ingestion. Hypertension, loss of appetite and weight loss Hypercalcuric symptoms, such as polyuria and renal calculi Long-term toxicity, including increases in mortality from all causes, increased risk of pancreatic cancer, cardiovascular events and falls leading to fractures in the elderly To prevent toxicity, tolerable upper intake levels have been fixed for vitamin D as follows: Table 1: Tolerable Upper Intake Levels for Vitamin D Diagnosis of vitamin D toxicity Biochemical parameters are not the sole criterion for toxicity.
This is because hypervitaminosis D is not a critical condition provided the patient is normocalcemic. Toxicity has been reported at a serum level between 80 and 150 ng/mL. However, up to 50000 IU/month has not been associated with either high serum vitamin D levels or any laboratory findings of toxicity. Treatment of vitamin D toxicity Hypercalcemia due to vitamin D intoxication must be treated on an emergency basis once the serum calcium is determined to be above 14 mg/dL. avoidance of external sources of vitamin d low dietary intake of calcium and phosphorus intravenous hydration with non-calcium containing saline infusions loop diuretics to help excrete calcium glucocorticoids, calcitonin and bisphosphonates are also used in the management of vitamin d intoxication Further ReadingWhat is Vitamin D?Vitamin D BiochemistryVitamin D DeficiencyVitamin D Supplementation Last Updated: Mar 22, 2016 Vitamin D deficiency linked to increased risk of chronic headache
My level was 19 with a normal range of 30 – 100 ng/ml and he put me on high doses of Vitamin D3. Imagine my surprise when six months later, I didn’t need my daily asthma inhaler and I didn’t have a cold all year! Today, there are mountains of research into a myriad of issues that can be affected by Vitamin D. There is also a forward-thinking Vitamin D Council that will keep you apprised of current findings. In the Council’s December 21, 2013, newsletter, it reported about a study done in South Korea which found a link between vitamin D deficiency and autoimmune thyroid disease (AITD). The researchers found that “people who were deficient in vitamin D were much more likely to have TPO-Ab positive tests.” TPO-Ab is a marker for autoimmune thyroid disease and measures the level of antibodies specific to fighting thyroid-related cells. The Council newsletter went on to say, “The researchers calculated that those who were severely deficient in vitamin D had nearly twice as high the risk of a positive TPO-Ab test compared to those who were sufficient.”
So, does that mean vitamin D deficiency leads to autoimmune disease or that those with autoimmune disease are more likely to be deficient in Vitamin D?? Unfortunately, the researchers haven’t figured that one out yet and/or only offer opinion. The one thing researchers do know is “thyroid treatment isn’t optimal — and may not work — if you do not have adequate vitamin D for the crucial final metabolic step, which takes place at the site where thyroid hormone actually works. This happens inside the nucleus of the cell. Vitamin D needs to be present at sufficient levels in the cell in order for the thyroid hormone to actually affect that cell. That is why vitamin D is so crucial.” 1) The 25-hydroxy (25OHD) vitamin D blood test. The 25-hydroxy represents your body’s primary circulating form of vitamin D and the precursor to the below. 2) 1,25-dihydroxy vitamin D blood test, which is the active form. This is the test which recommendations of where you want to fall are based on.