A few stories have appeared over the past day or so about a new study looking at vitamin D and calcium supplementation in older women that reported a significant number of cases of hypercalcemia. For example, News Medical reported that ‘Calcium, vitamin D supplements may send blood levels too high for some women‘.
This randomized, placebo-controlled trial included 163 older (ages 57 to 90) white women whose vitamin D levels were too low. The women took calcium citrate tablets to meet their recommended intake of 1,200 mg/day, and they took various doses of vitamin D, ranging from 400 to 4,800 IU/day. (The trial was limited by ethnicity because different ethnic groups metabolize calcium and vitamin D differently.) About 9% of the women developed excess levels of calcium in their blood (hypercalcemia), and 31% developed excess levels in their urine (hypercalciuria), even though they were taking normal doses of the supplements and did not have hyperparathyroidism, a condition in which the body makes too much calcium-regulating hormone. These excess blood and urine calcium levels may lead to kidney stones or other problems.
What the article doesn’t really make clear is that the vitamin D intake seems largely incidental. In the original study they concluded :
No relationship between hypercalcemia or hypercalciuria and vitamin D dose was found, and hypercalciuria was equally common in the placebo group.
So the real problem appears to be be related to the calcium intake. The study attempted to normalise the calcium intake for all of the women to 1200 mg per day, which is the recommended daily amount for women of 51 years or older.
I can see three possible causes for this. Firstly, the 1200 mg per day wasn’t adjusted for the women’s size and diet; smaller women with smaller diets may need less calcium than larger women. Therefore, the ratio between calcium intake and lean body mass may simply have been too high.
Alternatively, 1200 mg might be set just too high. However, this seems unlikely given the usually very conservative RDAs. The estimates for RDAs always feature a healthy (unhealthy?) buffer below toxic levels and are usually only just enough to stop deficiency. They rarely approach optimal levels.
Thirdly, the calcium was given in isolation which, other than for studies such as this, is never advisable. For a start calcium is antagonistic to magnesium, and one should never be supplemented without the other, except to rectify a specific deficiency, as was the case here. However, we have no idea whether the women were also magnesium deficient. At the same time, the women didn’t receive any other supplementation that should be taken alongside vitamin D including vitamins A and K2, as well as zinc and copper.
It would have been extremely interesting to have another group of women who also received a fully balanced set of minerals, vitamins and fatty acids to compare how a well fuelled body copes with 1200 mg of calcium. Unfortunately, these studies never look at people in terms of peak health.
The study adequately demonstrates the potential problem with isolated supplementation (of any kind).