The current government recommended vitamin D daily amounts are based largely on the ability to prevent osteomalacia in adults and rickets in children, without the need for sun exposure. However, the recommended amounts do not take into account the growing body of epidemiological and clinical data that suggest that vitamin D in higher amounts than is currently recommended may reduce the risk of developing a number of diseases such as multiple sclerosis, diabetes, cardiovascular disease and cancer. Recommendations for both adults and children are based on outdated information and understanding. For example, in England the RDA of 100 iu per day vitamin D was based on a case of 7 women with osteomalacia that responded to this amount. In addition, confusion over the toxicity of vitamin D has caused healthcare practitioners to recommend too low amounts for disease prevention.
The problems concerning the recommendations for vitamin D intakes that stem from improper use of scientific data are suitably illustrated by Vieth (1999). This author states that ‘Before 1997, the recommended dietary allowance of vitamin D for infants and children was 10 mg (400 IU). In essence, the scientific basis for this dose was that it approximated what was in a teaspoon (5 mL) of cod-liver oil and had long been considered safe and effective in preventing rickets. The basis for adult vitamin D recommendations has been even more arbitrary. Thirty-six years ago, an expert committee on vitamin D could provide only anecdotal support for what it referred to as “the hypothesis of a small requirement” for vitamin D in adults and it recommended one-half the infant dose, just to ensure that adults obtain some from the diet.’
Generally, blood levels below around 25 nmol/L (10 ng/mL) of 25(OH)vitamin D will cause severe deficiency which will result in the classic deficiency diseases of osteomalacia in adults and rickets in children. Insufficiency is a new term that refers to sub-optimal blood levels of 25(OH)vitamin D that can result in a number of difficult to diagnose chronic health conditions, but not the classic deficiency symptoms. Displaying 25(OH)vitamin D concentrations to between 25 and 40 nmol/L (10 to 16 ng/mL) will result in vitamin insufficiency (marginal deficiency) which increases parathyroid hormone concentrations and reduces levels of 1,25(OH)vitamin D (a metabolite of 25(OH)vitamin D). To increase blood 25(OH)vitamin D levels above 100 nmol/L generally requires supplementation with 100 mg (4000 iu) per day, and there is no evidence that levels below 140 nmol/L cause and toxicity in healthy individuals. .
Levels of vitamin D from sunshine exposure have been recorded as high as 250 nmol/L (100 ng/mL) in a farm worker in Costa Rica and 274 nmol/L (109.6 ng/mL) and been recorded from an individual exposed to artificial UV light. Increases in 25(OH)vitamin D are generally related to the baseline level, such that lower initial levels result in larger rises on sun exposure. Full body exposure to UV light has been reported to be equivalent to oral intakes of around 10,000 iu of vitamin D3. Sun exposure does not cause toxicity of vitamin D because as peak levels of 25(OH)vitamin D are reached, the production of further 25(OH)vitamin D are counterbalanced by its degradation. Data from submarine crews have shown that even with dietary intake from milk and fortified cereals, 24(OH)vitamin D levels declined by 30 nmol/L (12 ng/mL) in 2 months without sun exposure.
Vitamin D toxicity occur only when blood concentrations exceed ≈200 nmol/L (80 ng/mL). Toxicity is initially detected by hypercalcaemia, and can subsequently lead to symptoms such as nausea, vomiting and nervousness. Eventually renal failure occurs followed by death. Alarmist opinions on the toxicity of vitamin D have resulted in overreaction in the setting of accurate upper safety levels. For example, Vieth (1999) in his extensive vitamin D review paper states that ‘Throughout my preparation of this review, I was amazed at the lack of evidence supporting statements about the toxicity of moderate doses of vitamin D. Consistently, literature citations to support them have been either inappropriate or without substance.’ For example, the US nutrition guidelines that 5 times the RDA may be harmful is taken from a 1938 report on the bone growth in infants which is not relevant to adults.
RdB
