Rickets

Rickets is a bone disease of growing children in which bone tissue fails to mineralise properly, leaving soft bones and skeletal deformities (NIH Office of Dietary Supplements). Calcium and phosphate levels in the blood are abnormal, and the picture varies with age and cause: bowing of the legs, short stature and widened joints are typical (Carpenter 2017, Nature Reviews Disease Primers). Severe cases can cause failure to thrive, developmental delay, seizures from low blood calcium, muscle spasms, heart muscle disease and dental problems. Most rickets worldwide is nutritional, caused by too little vitamin D, too little calcium, or both. A systematic review of regional studies found that calcium deficiency remains a major cause in Africa and Asia, while vitamin D deficiency rickets may be increasing in the Americas, Europe and parts of the Middle East, and described a spectrum from isolated vitamin D deficiency to isolated calcium deficiency (Creo 2017). Nutritional rickets is preventable; inherited rickets is not. Heritable forms involve genes for vitamin D metabolism or action, the hormone FGF23, renal phosphate handling or bone mineralisation, and are treated differently by type: vitamin D metabolites, phosphate, or phosphate plus active vitamin D, and in X-linked hypophosphataemia the antibody burosumab, all under specialist care (Carpenter 2017). What the trials show for nutritional rickets is more nuanced than 'give vitamin D'. A Cochrane review of four small randomised trials (286 children, low-certainty evidence) found calcium alone, or vitamin D plus calcium, healed rickets better than vitamin D alone, and could not say whether vitamin D plus calcium beats calcium alone. In Nigerian children eating about 200 mg of calcium a day, 61% on calcium and 58% on calcium plus vitamin D reached the healing endpoint versus 19% on vitamin D alone. In Indian children, most of whom also had low vitamin D, the combination did best: 50% healed versus 15.7% on vitamin D alone and 11.7% on calcium alone at 12 weeks. For prevention, 400 IU of vitamin D a day is the standard infant recommendation. A separate Cochrane review of term breastfed infants (Tan 2020) found that 400 IU a day may raise blood vitamin D and may lower vitamin D insufficiency (low-certainty evidence), and that evidence on rickets itself was insufficient. Doses matter for safety. NIH sets tolerable upper intake levels for vitamin D of 1,000 IU a day for infants 0 to 6 months, 1,500 IU for 7 to 12 months, 2,500 IU for ages 1 to 3, 3,000 IU for ages 4 to 8 and 4,000 IU from age 9, including pregnancy and lactation. Too much vitamin D causes high blood calcium, and taking calcium and vitamin D supplements together may add to the risk of adverse effects. NIH's upper limits for calcium are 1,000 mg a day for 0 to 6 months, 1,500 mg for 7 to 12 months and 2,500 mg for ages 1 to 8. The trial doses described here were given to children with confirmed rickets under supervision and are not general supplement advice. Treatment is a medical matter. Children are diagnosed with blood tests and X-rays, doses are set by the clinician, and healing takes months. This page covers the evidence on calcium and vitamin D so you can understand what the trials tested; it is not a home-treatment guide.

• •Bowing of the legs
• •Widening of the wrists, knees or ankles
• •Short stature or slow growth
• •Bone pain or tenderness
• •Delayed development or failure to thrive
• •Seizures or muscle spasms from low blood calcium (severe cases)
• •Dental abnormalities

• •Vitamin D deficiency from limited sunlight
• •Prolonged exclusive breastfeeding without vitamin D supplementation
• •Low dietary calcium intake (about 200 mg a day in children studied in Nigeria and India)
• •Low maternal vitamin D status in pregnancy and lactation
• •Premature birth, or breastfed infants with darker skin
• •Inherited defects in vitamin D metabolism or phosphate handling (such as X-linked hypophosphataemia)
• •Avoiding dairy without replacing its calcium (milk allergy, lactose intolerance, vegan diets)
• •Fat malabsorption, or kidneys that cannot activate vitamin D

Nutritional rickets results from vitamin D deficiency (limited sunlight, or prolonged exclusive breastfeeding without vitamin D supplementation), from low dietary calcium, or from both together. Maternal vitamin D status may also matter: in a Bangladeshi secondary analysis, only maternal vitamin D (28,000 IU a week) given both in pregnancy and for 6 months after birth reduced biochemical (blood-test) rickets in infants, while prenatal-only dosing did not. Premature birth and breastfeeding in infants with darker skin raise risk. Inherited rickets arises from mutations affecting vitamin D metabolism or action, FGF23 production or degradation, renal phosphate handling, or bone mineralisation.