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The first commentary in this series described the physiological handling of vitamin D, calcium and phosphorus as well as the many aetiologies of rickets. It also listed those factors that would suggest a case of rickets was not a simple vitamin D deficiency from sun and/or diet. While there are many possible causes of rickets, in the majority of cases, the cause is a deficiency of vitamin D due to insufficient sun exposure and/or deficiencies in the diet. This second commentary in the series describes these two environmental factors, sun and diet, and their influences in more detail.
Sun
Latitude and season
The further from the equator one goes, the less effective is the process of conversion and the greater is the effect of season.
At latitudes greater than 400 N or S there is little conversion occurring from October to March, which is sometimes referred to as the 'vitamin D winter'. The latitudes of typical large cites are Birmingham UK (53 N), Paris France (49 N), Calgary Canada (51 N), Helsinki Finland (60 N), Ushuaia Argentina (55 S). There is marked seasonal variation in measurements of vitamin D status in pregnant women and children in these areas of the world and exposure to summer sunshine is essential for replenishing stores enough to get through the vitamin D winter with adequate amounts.
Exposure to sun
In Cincinnati (38 N), twenty minutes exposure a day on the hands and face were sufficient to maintain satisfactory vitamin D levels in older infants; but in Beijing, only a little further north (40 N), two hours were necessary during September and October. Exposure times for toddlers and at other latitudes have not been documented.
Clouds reduce the energy of the radiation by fifty percent and shade by sixty percent. Similarly, industrial pollution is associated with rickets. Staying indoors for any reason -- watching television, playing with a computer, reduced mobility due to handicaps and adverse weather -- reduces vitamin D formation. Window glass blocks the UV radiation.
The perception of modesty is dictated by local custom and interpretation of religious rules. The arms, legs, and sometimes the face of many Moslem girls and women are covered in public.
Prevention of sunburn, dehydration and skin cancer may all lead to less exposure, and the use of sunscreens. It has been shown that the use of sunscreens in Australia reduced vitamin D concentrations. It should be possible to choose a prudent path between exposure to the sun in amounts adequate for the formation of vitamin D and the prevention of sun damage.
Skin colour
Darker skin pigmentation limits conversion. For example, albino 'black' children in a South African school for the visually impaired had higher vitamin D levels than normally pigmented children, yet it is likely the albino children limited their exposure to sun to prevent burning. A single dose of ultraviolet radiation (UVR) increased serum vitamin D concentration up to sixty fold in white adults, but six doses were necessary to produce the same increase in black people. Asian immigrants to Britain required more UVR to produce a minimal erythemal dose and so may need longer exposure to produce vitamin D.
Diet
Vitamin D
Diet becomes an important source of vitamin D only when there is inadequate exposure to sunshine (see above). Most children have very low intakes of vitamin D from food, most of which is from such fortified foods as infant and follow-on formulas, many margarines and breakfast cereals, and, in some countries, from fortified milk. Most children would need supplements to achieve the reference nutrient intake and therefore rely extensively on skin synthesis for an adequate supply.
Breast milk contains little vitamin D. Infant and follow-on formulas and some weaning cereals are fortified (up to 2 ug/100 kcal -- in other words, 1.3ug (52 IU) per 100 ml of infant formula). After infancy, fortified foods such as breakfast cereals and yellow fat spreads become significant sources (about 1ug (40 IU) /100 kcal). Unfortified foods provide little vitamin D. Fatty fish such as salmon, pilchards, sardines, and tuna contain 3-8 ug (120-320 IU)/100 kcal) but they are uncommon items in the diet of many children.
Calcium
Milks consumed during infancy contain relatively limited amounts of calcium (Breast milk contains 50 mg/100 kcal, 35 mg/100 ml and infant formula contains 70 mg/100 kcal, 43 mg/100 ml), but the proportion absorbed and retained (about a third) meets requirements except in preterm babies.
After infancy, cow's milk (calcium 180 mg/100 kcal, 120 mg/100 ml) and milk products are major sources of calcium. Children who do not like milk or are on a milk-restricted, therapeutic diet may have much lower intakes. Consequently, in societies without a tradition of milk drinking, calcium intake is often below 300 mg per day. This is regarded as a major factor in the rickets seen in Nigerian and South Africa; but adaptation to low calcium intakes by increasing the proportion retained is well established. Some foods have a much higher calcium energy ratio than milk. Examples are fish, such as canned sardines and pilchards (including their bones), broccoli tops, spring onions, parsley, and watercress. Unfortunately, children tend to eat only small quantities of these foods.
Other food substances, such as phytate, which is present in most cereals, limit the net absorption of calcium and other minerals. High extraction flour (for whole meal bread, for example) contains more calcium and phosphorus but also more phytate, so absorption is less. Therefore, the amount of calcium absorbed from a diet containing little milk and a lot of phytate is likely to be low. In some developing countries, the addition of phytase to weaning foods is being explored as a way to improve mineral absorption using animal husbandry technology. This will also improve the dietary zinc phytate ratio, which is low in many developing countries.
See Also: Rickets, Part 1.
This commentary is partly based on the following review:
Wharton BA, Bishop NJ. Seminar: Rickets. Lancet. 2003; 362:1389-1400.
See also the following individual references concerning rickets and hypocalcaemia:
Allgrove J. Is nutritional rickets returning? Arch. Dis. Child. 2004;89 699-701.
Ladhani S, Srinivasan L, Buchanan C, and Allgrove J. Presentation of vitamin D deficiency. Arch. Dis. Child. 2004;89 781-784.
Gartner LM, Greer FR. Section on Breastfeeding and Committee on Nutrition. American Academy of Pediatrics. Prevention of rickets and vitamin D deficiency: new guidelines for vitamin D intake. Pediatrics. 2003 ;111:908-10.
Mohapatra A, Sankaranarayanan K, Kadam SS, Binoy S, Kanbur WA, Mondkar JA. Congenital rickets. J Trop Pediatr. 2003 ;49:126-7.
Singh J, Moghal N, Pearce SH, Cheetham T. The investigation of hypocalcaemia and rickets. Arch Dis Child. 2003 ;88:403-7. Review.
This material has been prepared by B A Wharton on behalf of the IFM's Advisory Committee on Child Health and Nutrition, October 2004.
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