Calcium for Rickets

Probably yes, as part of treatment alongside vitamin D, for children with rickets whose diet is very low in calcium. In Nigerian children eating a median 203 mg of calcium a day, 61% given calcium alone and 58% given calcium plus vitamin D reached the healing target at 24 weeks, versus 19% given vitamin D alone (Thacher 1999). A Cochrane review of four small trials found low-certainty evidence that calcium, with or without vitamin D, heals rickets better than vitamin D alone (Chibuzor 2020), and the 2016 global consensus recommends at least 500 mg of calcium a day, from food or a supplement, for every child treated for nutritional rickets (Munns 2016).

It does not work the same way everywhere. In Indian children who were also short of vitamin D, the combination healed 50% against 11.7% for calcium alone (Aggarwal 2013), and a small Turkish trial favoured vitamin D (Kutluk 2002). Calcium has not been shown to prevent rickets: the Nigerian prevention trial had too few cases to tell (Thacher 2012). Rickets is diagnosed with blood tests and X-rays and treated under a clinician, so this page describes what the trials tested, not a home treatment.

In rickets, growth cartilage does not mineralise normally, which can leave lasting changes in bone structure (NIH ODS). Nutritional rickets is usually blamed on vitamin D, but in sunny countries with cereal-based diets and little dairy, low calcium intake is the likelier culprit (Pettifor 2004). The consensus guideline reports that in children over 12 months a calcium intake under 300 mg a day raises rickets risk regardless of vitamin D status, and that no nutritional rickets was seen at 500 mg a day (Munns 2016).

Children with rickets in Nigeria showed the blood pattern of calcium deficiency: low blood calcium, very low calcium excretion, and raised 1,25-dihydroxyvitamin D and parathyroid hormone (Thacher 2000). In India, children with rickets ate 204 mg of calcium a day against 453 mg in healthy controls, drew less of it from dairy (41.7% against 88.6%), and ate more phytate, a plant compound that binds calcium (Aggarwal 2012). NIH notes that absorption from dairy and fortified foods is about 30%, while some plant foods give much less (NIH ODS).

Calcium deficiency is not the whole story. In the same Nigerian case-control study, healthy controls ate just as little calcium (214 against 217 mg a day), so the authors concluded that low intake alone does not account for rickets and probably interacts with genetic, hormonal and other nutritional factors (Thacher 2000). Children with rickets absorbed calcium about as well as controls (61% against 63%; only 10 children per group could be measured), and absorption was higher (81%) when re-measured after the disease had resolved, which the authors link to resolution of active disease rather than to the extra calcium itself (Graff 2004).

Calcium and vitamin D also feed into each other. Studies in Asian children and African American toddlers suggested that low calcium intake increases breakdown of vitamin D and can lead to vitamin D deficiency (Pettifor 2004). A systematic review describes nutritional rickets as a spectrum from isolated vitamin D deficiency to isolated calcium deficiency (Creo 2017), and the Indian case-control study found rickets arose when low calcium coexisted with low or borderline vitamin D (Aggarwal 2012). That is why the consensus pairs the two nutrients in treatment.

The 2016 consensus recommends at least 500 mg a day of oral calcium, as food or a supplement, routinely alongside vitamin D for treatment, regardless of age or weight. Its vitamin D treatment dose is at least 2,000 IU a day for a minimum of 3 months (Munns 2016). Trials used a range of calcium doses: 1,000 mg a day (Thacher 1999), about 938 mg twice daily (Thacher 2014), about 920 to 952 mg a day (Thacher 2015), 75 mg/kg a day (Aggarwal 2013), 3 g a day of calcium lactate, with the elemental amount not reported (Kutluk 2002), and 500, 1,000 or 2,000 mg a day in a dose-finding trial (Thacher 2016).

In that dose-finding trial of 65 Nigerian children, 1,000 mg and 2,000 mg healed rickets faster than 500 mg, but 2,000 mg was no faster than 1,000 mg. By 24 weeks 87% on 1,000 mg, 67% on 2,000 mg and 67% on 500 mg had reached the healing score (P=0.21). Forearm bone density rose faster on 2,000 mg (Thacher 2016). The trial abstracts do not give the calcium salt used in every case, so ask the clinician which product and how much elemental calcium is meant.

The central trial randomised 123 Nigerian children (median age 46 months) with rickets to vitamin D (600,000 units by injection), calcium 1,000 mg a day, or both, for 24 weeks. Dietary calcium was low in children with rickets and in controls alike (median 203 and 196 mg a day). The healing target, alkaline phosphatase at or below 350 U/L plus near-complete healing on X-ray, was reached by 61% on calcium, 58% on the combination and 19% on vitamin D alone (P<0.001) (Thacher 1999).

A follow-up trial gave 72 children limestone calcium (about 938 mg twice daily) and randomised them to vitamin D2 50,000 IU monthly or placebo. Among the 68 children who finished, 67% with vitamin D and 44% without reached the healing target, a difference that did not reach significance (P=0.06) (Thacher 2014). A third trial of 96 children compared powdered limestone (920 mg) with ground fish (952 mg) daily for 24 weeks: 55% and 66% reached the target (P=.39), and both groups improved markedly (Thacher 2015). The dose-finding trial in 65 children is described under Dosing (Thacher 2016).

In 67 Indian children aged 6 months to 5 years, dietary calcium was just as low (204 mg a day) but 82.1% also had vitamin D below 20 ng/mL. After 12 weeks, normal alkaline phosphatase plus complete healing on X-ray was reached by 50% on vitamin D plus calcium, 15.7% on vitamin D alone and 11.7% on calcium alone (Aggarwal 2013). The authors concluded the combination worked best.

A small placebo-controlled trial in 42 infants in Istanbul, a sunny city, found the biggest rise in blood calcium with vitamin D plus calcium, and concluded vitamin D deficiency was the main problem there; vitamin D, alone or with calcium, did better than calcium alone (Kutluk 2002). Its abstract gives no outcome numbers, and follow-up was short. Results differ by country: calcium alone beat vitamin D alone in Nigeria but not in India, and the Turkish trial favoured vitamin D. In the one trial that checked, baseline vitamin D status did not change the effect of adding vitamin D to calcium (Thacher 2014), and the consensus notes that blood tests may not separate vitamin D from calcium deficiency as the main cause, which is why it pairs the two (Munns 2016).

A Cochrane review found four randomised trials with 286 children, two in India and two in Nigeria, with follow-up of 12 to 24 weeks. None had a low risk of bias in all domains and three had a high risk of bias in at least one (Chibuzor 2020). At 24 weeks, calcium alone healed rickets more than vitamin D alone (RR 3.26, 95% CI 1.59 to 6.69; one study, 71 children; low certainty), and vitamin D plus calcium beat vitamin D alone (RR 3.06, 95% CI 1.49 to 6.29; one study, 75 children; low certainty).

Whether vitamin D plus calcium beats calcium alone is unclear (RR 1.17, 95% CI 0.72 to 1.90; two studies, 140 children; very low certainty). The review could not draw conclusions about fractures or adverse events (Chibuzor 2020). The Turkish trial was not among the four included studies.

Prevention is less well supported. In 647 Nigerian children aged 12 to 18 months, calcium carbonate (400 mg a day) or ground fish (529 mg) was compared with none for 18 months. Rickets developed in 1, 1 and 2 children in the three groups, and the authors said a larger sample would be needed to judge the effect on rickets. Forearm bone density rose more with calcium (P<0.04) (Thacher 2012).

In 158 Bangladeshi children given a milk-powder supplement with 50 to 500 mg of calcium, none of those who had no leg signs at the start and finished 13 months developed rachitic leg signs. There was no unsupplemented group, so the judgement of benefit rests on earlier rates in the same cohort (Combs 2008). A Tibetan trial of calcium, vitamin D or both found no difference in rickets between groups after 3 years (Rooze 2016). A Cochrane prevention review, whose trials included vitamin D in Turkey and a combined vitamin D, calcium and counselling programme in China, advised offering vitamin D or calcium to high-risk groups while data are scarce (Lerch 2007).

The calcium trials are small, and the four Nigerian treatment trials share authors (Thacher, Fischer and Pettifor), so independent replication is thin. We found no trial of calcium alone in children who are vitamin D deficient but eat adequate calcium. The trial abstracts do not report adverse events.

In Kabul, vitamin D alone did not lower rickets (5.3% against 5.5% on placebo) in infants eating an average 372 mg of calcium a day, though height gain was slightly better in those eating more than 300 mg (Crowe 2021). That is a vitamin D trial, not a calcium test, and the calcium-intake pattern was a borderline subgroup result for height rather than rickets, so treat it as a hypothesis. The consensus defines nutritional rickets as excluding heritable disorders of vitamin D metabolism and congenital or acquired hypophosphataemic rickets, which these trials do not cover (Munns 2016).

The trial abstracts do not report adverse events from calcium, and the Cochrane review found adverse-event data in only one small study per comparison. The point estimates were higher on the combination (for example RR 4.76, 95% CI 0.24 to 93.19, in 39 children) but far too imprecise to interpret (Chibuzor 2020). That is an absence of data, not proof of safety.

NIH sets upper intake levels for calcium of 1,000 mg a day for ages 0 to 6 months, 1,500 mg for 7 to 12 months, 2,500 mg for ages 1 to 8 and 3,000 mg for ages 9 to 18, from all sources. NIH says higher intakes of supplemental calcium might increase the risk of kidney stones, and that hypercalcaemia (high blood calcium) and hypercalciuria (high urine calcium) usually result from other conditions such as primary hyperparathyroidism (NIH ODS). Hypercalcaemia can cause constipation, nausea, weight loss, fatigue, poor muscle tone, kidney problems and heart rhythm disturbances (NIH ODS). The dose-finding trial's highest arm gave 2,000 mg a day, below the upper level for children aged 1 or over (Thacher 2016).

NIH also notes that calcium supplements can cause gas, bloating and constipation, and that calcium carbonate does so more than calcium citrate. Smaller, more frequent doses or taking the supplement with meals can ease this (NIH ODS). High vitamin D doses, which treatment regimens pair with calcium, can cause hypercalcaemia, high urine calcium and, if prolonged, kidney calcification (Munns 2016). Severe nutritional rickets itself can cause hypocalcaemic seizures and tetanic spasms (Munns 2016).

Calcium supplements bind or interfere with several medicines. The advice below comes from NIH and the drug labels it cites, and applies to children and adults taking these medicines (NIH ODS).