Asian Rickets and Osteomalacia

Abstract

Crowded buildings, sunless alleyways, industrial pollution and Northern latitudes set the scene for privational rickets, first described in European cities in the 17th century and reaching its peak in Victorian times. Recognition of the antirachitic effects of sunlight and discovery of the sources and effects of vitamin D made prevention possible so that so-called 'nutritional' rickets disappeared from the indigenous population of all but the most deprived cities, and attention turned to its metabolic causes. In the USA, where vitamin D deficiency occurs only in unusual circumstances [1], this trend continues. In the UK, in contrast, lateonset rickets and osteomalacia made a dramatic reappearance with the immigration of Asians in the 1960s—particularly, but not exclusively, in our Northern cities [2-4]. Superficially, the main causes in this population were the same as those in Victorian Caucasians; in addition, Asians tended to keep well covered up, preventing their lightly pigmented skin from taking advantage of even the small amount of ultraviolet light available for the synthesis of vitamin D. Their habitual diet, often vegetarian, was deficient in vitamin D but high in fibre and high extraction flour in the form of chapattis [4]. Thus rickets and osteomalacia in the Asian population was thought to result from a lack of both endogenous (dermally synthesized) and exogenous (dietary) vitamin D. The relative importance of these sources was unknown and the term 'nutritional' was widely used to cover this ignorance. However measurement of plasma 25-hydroxyvitamin D (25-OHD), a newly found indicator of vitamin D status, gave interesting clues [5]. It was shown that the 25-OHD levels of Asian immigrants was low (and fell further after their arrival in the UK), and was often undetectable in those with rickets and osteomalacia. Even in Scotland, these low levels could be increased by outdoor exposure, so that although plasma 25-OHD levels of Asians living in Stornaway were less than those of Caucasians, they were higher than those of Asians living in Glasgow. The same investigators showed, by separate measurements of plasma 25-OHD3 (largely endogenous) and 25-OHD2 (from the diet), that the contribution of 25-OHD2 to total circulating 25-OHD in normal white adults was negligible. In support of this conclusion they demonstrated that the plasma concentration of total 25-OHD in nuclear submariners receiving a good diet fell during a two-month undersea patrol when they received no light of the wavelength required for the dermal synthesis of vitamin D. Such ingenious observations emphasized the overwhelming importance of the endogenous cutaneous synthesis of vitamin D and the normally negligible contribution of dietary vitamin D to circulating concentrations of 25-OHD.