eMJA: Mason & Diamond, Vitamin D deficiency and multicultural Australia

Editorial

Vitamin D deficiency and multicultural Australia

Oral vitamin D supplementation may be needed in women with dark skin pigmentation or dress codes which prevent adequate sunlight exposure

MJA 2001; 175: 236-237

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Although the first written descriptions of rickets date from the mid-1600s, it was not until the 1920s that the problem was linked to a deficiency of vitamin D. With the widespread use of vitamin D supplementation, rickets became a rare syndrome. However, in the 1970s, immigrants from the Indian subcontinent living in the United Kingdom began presenting with florid symptoms of osteomalacia — bone pain, myopathy and pseudofractures.¹

Vitamin D occurs in two forms, cholecalciferol, or vitamin D₃, and the plant-derived ergocalciferol, or vitamin D₂. These two forms are biologically equivalent in human beings. For most ambulatory people, the majority of the vitamin D in the body is derived from the action of ultraviolet B light on 7-dehydrocholesterol in the skin, converting it to previtamin D₃, which, at body temperature, thermally isomerises into vitamin D₃.² A smaller proportion of vitamin D comes from dietary sources, particularly oily fish, eggs, butter and margarine.³ In contrast to the United States, few foods in Australia are fortified with vitamin D. Vitamin D made in the skin or ingested in the diet is biologically inert and must undergo conversion to 25-hydroxyvitamin D₃ in the liver and then in the kidney to 1,25-dihydroxyvitamin D₃ (calcitriol).

The amount of high energy ultraviolet B light reaching the skin depends on factors such as latitude, season, smog (which reduces penetration of ultraviolet light through the atmosphere), and the actual amount of direct sun exposure, which is further modified by clothing and the use of sun protection agents.^2,4 Vitamin D deficiency was therefore thought to be a rare disorder in populations living at latitudes where sunlight abounds for most of the year, and for this reason no recommended daily allowance for vitamin D has been established for Australia. Vitamin D deficiency, however, is now known to affect a substantial proportion of older people in this country, including those in institutions, patients with dementia and older men with hip fracture.^5-8 In older people, the factors leading to this problem are reduced mobility; limited sunlight exposure; the assiduous use of sun-protection agents; and, in particular, a reduced ability of aged skin to produce vitamin D from a given dose of ultraviolet B light.

In this issue of the Journal, two independent reports by Grover and Morley⁹ and Nozza and Rodda ¹⁰ draw attention to a new high-risk group for vitamin D deficiency in multicultural Australia. Grover and Morley report that 80% of dark-skinned or veiled women attending an antenatal clinic at the Royal Women's Hospital in Melbourne who took part in the study had biochemical evidence of vitamin D deficiency, with values of 25-hydroxyvitamin D₃, the major blood metabolite, below the reference range.⁹ Nozza and Rodda examined paediatric records to identify children with vitamin D deficiency.¹⁰ In just over four and a half years, 55 children had presented with clinical features of rickets, including delayed walking, leg bowing, seizures and failure to thrive. Of those tested for parathyroid hormone levels, over 80% had secondary hyperparathyroidism. At the time of each child's presentation, none of the mothers had volunteered symptoms of vitamin D deficiency in themselves, but over half had 25-hydroxyvitamin D₃ concentrations measured, and 81% of these had values below the reference range (< 25 nmol/L). All except one of the mothers of the children presenting with rickets were from Africa, the Indian subcontinent, the Middle East or southern Europe. The one mother of northern European descent was agoraphobic and depressed. As well as identifying a new high-risk group for vitamin D deficiency, these two reports highlight an important message for medical practitioners -- not only patients presenting for medical attention, but also other members of the family, may have vitamin D deficiency.

As most of the vitamin D in neonates is acquired from maternal transfer,¹¹vitamin D deficiency in mothers is likely to have adverse consequences for their infants. In adults, vitamin D depletion causes a reduction in intestinal calcium absorption, resulting initially in a negative calcium balance, leading to secondary hyperparathyoidism with high bone turnover, bone loss, low bone density and an increased risk of vertebral and hip fractures. This may occur with serum 25-hydroxyvitamin D₃ concentrations of less than 40 nmol/L, a value within most reference ranges.^12,13 After a prolonged period, osteomalacia may become evident, manifested by an accumulation of demineralised bone, radiological pseudofractures or progressive bone pains with myopathy and a waddling gait. These clinical findings usually occur with frankly low serum 25-hydroxyvitamin D₃ concentrations of less than 20 nmol/L.

Women who are veiled or have dark skin pigmentation are susceptible to vitamin D deficiency because most clothing effectively absorbs ultraviolet B irradiation and increased melanin pigmentation reduces the cutaneous production of vitamin D.^2,4 The absolute ultraviolet dose required to stimulate skin synthesis of vitamin D₃ is about six times higher in African-Americans than in people of European descent.¹⁴ It has been estimated that, for lightly pigmented skin, exposure of hands, face and arms to a suberythemal dose of summer sunlight for about 15 minutes about three times per week is likely to be adequate for normal vitamin D requirements, even in the north-east of the United States.⁴ The presence of darker pigmentation and/or veiling may significantly impair adequate sun-derived vitamin D production, even in sunny regions like Australia.

It remains unclear whether dietary factors, such as low calcium intakes, contribute to the problem. During the epidemic of rickets among Asian immigrants to the United Kingdom in the 1970s, it was speculated that diets low in calcium and containing certain types of cereal contributed to the development of vitamin D deficiency.¹⁵ Furthermore, there is evidence for accelerated metabolic inactivation and removal of vitamin D in primary or secondary hyperparathyroidism.^16,17

Two recent reports also noted the significant clinical morbidity associated with vitamin D deficiency in the high-risk groups identified by Grover and Morley⁹ and Nozza and Rodda.¹⁰ In the first, Muslim women presenting with bone densitometric evidence of osteoporosis, most of whom were veiled, were found to be 2.5 times more likely to have biochemical evidence of severe vitamin D deficiency than women of European descent.¹⁸ In the second, a group of Arab women with vitamin D deficiency living in Denmark experienced decreased muscle function and muscle pain and weakness, which improved after three months of vitamin D treatment.¹⁹

How much vitamin D is required to prevent vitamin D deficiency in multicultural Australia? In regions where sunlight abounds, educational programs should encourage cutaneous production of vitamin D, with due deference to the problems of overexposure. When dark skin and/or veiling prevent adequate exposure, supplementation with oral vitamin D is likely to be required. The active hormone, calcitriol, which requires careful monitoring of serum and urinary calcium levels, is not the agent of choice in these circumstances. As there is a large therapeutic window, the risk of hypercalcaemia with plain vitamin D, such as ergocalciferol, is low.²⁰ Susceptible groups, including pregnant women, should have their serum 25-hydroxyvitamin D₃ concentrations measured. As there are no high-dose oral or intramuscular vitamin D preparations available in Australia, supplementation with oral vitamin D (eg, ergocalciferol 1000 units daily) is indicated if serum 25-hydroxyvitamin D₃ concentrations are below 20-40 nmol/L.

Rebecca S Mason
Associate Professor
Department of Physiology, and Institute for Biomedical Research
University of Sydney, NSW
rebeccamATphysiol.usyd.edu.au

Terrence H Diamond
Senior Endocrinologist
St George Hospital; and Conjoint Associate Professor
Faculty of Medicine, University of New South Wales, NSW

Reprints: Associate Professor T H Diamond Department of Endocrinology, St George Hospital, Private Medical Complex, Kogarah, NSW 2217

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