Milk-and-Dairy-Products-in-Human-Nutrition-FAO

Chapter 4 – Milk and dairy products as part of the diet 131
4.4.7 Calcium-deficiency rickets
Rickets is a progressive disease that begins with hypocalcemia and progresses to low
mineralization of the growth plate of growing bones. The classic clinical symptom is
deformity (bowing) of the arms and legs. Severe rickets is associated with deformities
of the chest. Nutritional rickets may be caused by deficiency of either vitamin
D or calcium, or more often by a combination of both (Pettifor, 2008). Vitamin-
D-deficiency rickets is most prevalent within the first 18 months of life (Thacher
et al., 2006a), and is more common in countries lying at high latitudes both north
and south of the equator (Pettifor, 2008). It can also occur when vitamin D is in
the normal range but dietary calcium is very low (less than 300 mg/day). Calcium
deficiency depletes vitamin D status (measured by the amount of the inactive form)
as conversion of vitamin D to its active form calcitriol is accelerated (Thacher et
al., 2006b). Calcium- and/or vitamin-D-deficiency rickets have been reported in
young children in 59 countries (Thacher et al., 2006a). In Africa and some parts of
tropical Asia, calcium deficiency is the major cause of rickets, typically occurring
after weaning and after the second year of life (Thacher et al., 2006a). High-fibre,
low-calcium diets, common in these countries, can also increase clearance rates of
vitamin D (Batchelor and Compston, 1983). Calcium supplementation (between
350 and 1 000 mg/day) without vitamin D has been reported to heal rickets in
Nigeria (Craviari et al., 2008).
Although rickets had been almost eradicated in the twentieth century in many
developed countries, a recent resurgence of the disease has been recorded in a number
of developed countries. An increased risk of rickets has been recorded among
the older children and adolescents in communities of recent immigrants in these
countries, indicating that the combined effect of low dietary calcium intake and
vitamin D deficiency may be involved, as their diets are typically low in calcium and
high in phytates (Pettifor, 2008). The re-emergence of rickets has also been reported
in Kenya (Bwibo and Neumann, 2003). The identified risk factors included: a low
intake of milk (hence of calcium and phosphorus), no intake of ocean fish (hence
a low vitamin D intake) and perhaps reduced exposure to sunshine and ultraviolet
light. The lack of milk in the diet was highlighted as a major factor by the authors,
and provision of milk supplements and vitamin D 3 for one month led to a noticeable
regression of rickets in affected children (Bwibo and Neumann, 2003).
Minimal dairy intake is often a common characteristic associated with rickets.
Rickets is not a result of impaired calcium absorption efficiency (Graff et al., 2004),
nor was calcium absorption efficiency improved with vitamin D supplementation
in Nigerian children (Thacher et al., 2009). Fischer, Thacher and Pettifor (2008) call
for more research before widespread vitamin D supplementation is advocated to
address rickets because the complex etiology is still being clarified. The final common
pathway in the pathogenesis of rickets that has been suggested is an inability
to meet the calcium needs of the growing skeleton, whether from vitamin D deficiency
in the face of good calcium intake or from dietary calcium deficiency in the
face of vitamin D sufficiency (Pettifor, 2008). Ideally, nutritional rickets would be
prevented by ensuring all children receive adequate amounts of both vitamin D and
calcium (Thacher et al., 2006a, 2006b).