ARE SOMALI IMMIGRANTS LIVING IN COUNTRIES WITH MODERATE CLIMATE
at RISK of VITAMIN D DEFICIENCY
PRESENTED BY
DR AHMED DALMAR
Vitamin D is a steroid hormone producing more than one effect on calcium and phosphorus metabolism and the immune system. This precursor is converted in the liver to 25–hydroxyvitamin D [25(OH) D], the primary storage form of the vitamin D and the best clinical indicator of vitamin D intake and body stores. This form of vitamin D is inactive and must be converted in the kidneys by 25-hydroxyvitamin D-1ά-hydroxylase (1-OHase) to the biologically active form 1, 25(OH) 2 D.
The clinical manifestations of a severe vitamin D deficiency are rickets in children and osteomalacia in adults, resulting in soft bone, pain and muscle weakness. However, even milder states of deficiency have recently been implicated in the pathogenesis of diabetes mellitus, cancer, hypertension and other chronic diseases involving low-grade chronic inflammation. In Minneapolis (USA) and Sweden, vitamin D deficiency has been implicated in the rising number of cases of Autism among Somali children.
Vitamin D is naturally present in very few foods: Fatty fish, fish liver oil, and milk, margarine and butter where vitamin D has been added (vitamin D2), but the main source of Vitamin D is sun exposure (vitamin D3). In fact, a 0.5-h exposure to the summer sun in a bathing suit ( 3 times the minimal erythemal dose) will initiate the release of 50 000 IU (1.25 mg) vitamin D into the circulation within 24 h of exposure in white persons. Dark skin people require up to 5 times this solar exposure to achieve the same response.
Much debate has taken place over the definition of vitamin D deficiency. Data taken from the Mayo Medical Laboratories in Rochester, MN, list the normal range to be 15–80 ng/mL. In sun-rich environments, circulating 25(OH) D ranges from 54 to 90 ng/mL. Several factors alter ‘normal’ levels of vitamin D, including race, lifestyle habits, sunscreen usage, age and latitude.
Vitamin D deficiency in immigrants has been known in UK for 30-40 years. Other countries (Denmark, Norway, and Sweden) have become aware of the problem only recently. Studies in Germany, Denmark, Dutch, Sweden and UK on vitamin D in Asians, Turkish, Arab-Muslims and Somalis have shown an increasing number of these people with vitamin D deficiency. Like their brothers in Northern Europe, most Somali immigrants in USA live in Midwest with moderate climate and face the same risk factors for vitamin D deficiency. The reason why vitamin D deficiency is common in immigrants to moderate climate countries is explained by the following:
I. The cutaneous release of vitamin D is completely blunted because of the following factors preventing UVB 
penetration into the skin: A) Lack of sun light during late fall and winter (November-April).B) Clothing covering the whole body. C) Dark skin. D) Old age. E) Staying home or in the shade.
penetration into the skin: A) Lack of sun light during late fall and winter (November-April).B) Clothing covering the whole body. C) Dark skin. D) Old age. E) Staying home or in the shade. II. Diet poor in vitamin D containing foods III. Lack of supplementation
IV. Prolonged exclusive breastfeeding for children from vitamin D deficient mothers.
Although to date, representative data on vitamin D among Somalis is lacking, we suspect that there is an epidemic of vitamin D deficiency in Somalis living in countries with moderate climate. Future studies will determine and there are plans to conduct Vitamin D screenings.
At the mean time what are the interventions needed to eliminate this epidemic? Since most Somalis in the diaspora are health illiterate, the most cost-effective intervention in this epidemiologic transition is health education and health promotion. This will allow to raise awareness in the community to help prevent deficiency by encouraging those at risk to take vitamin D supplements, sun exposure during spring, summer and early fall, eat food containing vitamin D and ask providers check their vitamin D level.
But the question is: What vitamin D intake is required to sustain an adequate nutritional status of vitamin D in sun-repleted adults like Somali immigrants living in moderate climate countries? Two recently reported studies provide an answer to this question: The first study to address this topic was published by Vieth et al in 2001 (1, 3). In this study, the investigators supplemented healthy adults daily with either 25 µg (1000 IU) or 100 µg (4000 IU) vitamin D for 5 months. Circulating 25(OH) D concentrations increased from 16.3 ± 6.2 to 27.5 ± 6.8 ng/mL and from 18.7 ± 6.0 to 38.6 ± 5.8 ng/mL in the 1000- and 4000-IU groups, respectively. Not a single adverse event or episode of hypercalciuria was observed in the 60 subjects enrolled in the study. In an even more detailed report, Heaney et al (2) studied 67 men divided into 4 groups that received 200 IU (5 µg), 1000 IU (25 µg), 5000 IU (125 µg), or 10 000 IU (250 µg) vitamin D/d for 5 months. The 200-IU/d group failed to maintain circulating 25(OH) D concentrations during the study period. The remaining 3 groups responded in a dose-response fashion with respect to elevations in circulating 25(OH) D concentrations. From these data, with the use of regression analysis, it has become possible to calculate a response of circulating 25(OH) D from a given oral intake of vitamin D. The data show that for every 1 µg (40 IU) of vitamin D intake, circulating 25(OH) D increases by 0.28 ng/mL over 5 months on a given supplemental regimen. Note that a steady state appears to be achieved after 90 days of each dose (2, 3). Thus, doses of 400 IU (10 µg), 1000 IU (25 µg), 4000 IU (100 µg), and 10 000 IU (250 µg) vitamin D/d for 5 months will result in theoretical increases in circulating concentrations of 2.8, 7.0, 28, and 70 ng 25(OH) D/mL respectively, all of which values are in the normal range of circulating concentrations according to reference data. In the study by Heaney et al (2), not one case of hypercalcemia or hypercalciuria was observed.
The other issue is the treatment of those who have already become deficient. This is particularly important for women who are thinking of having children, as any baby born to a woman who is deficient, is highly likely to be deficient. Studies show preeclampsia, and C-section are more prevalent in pregnant women with vitamin D deficiency. Other non confirmed data suggest that breastfed children from vitamin D deficiency mothers are at risk of vitamin D deficiency with possible mental retardation and Autism. For more readings see following references:
1.Vieth R, Chan PCR, MacFarlane GD. Efficiency and safety of vitamin D3 intake exceeding the lowest observed adverse effect level (LOAEL). Am J Clin Nutr 2001; 73:288–94.
Vieth R, Chan PCR, MacFarlane GD. Efficiency and safety of vitamin D3 intake exceeding the lowest observed adverse effect level (LOAEL). Am J Clin Nutr 2001; 73:288–94. 2.Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr 2003;77:204–10
Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr 2003;77:204–10 3.Vieth R. Vitamin D supplementation, 25-hydroxy-vitamin D concentrations, and safety. Am J Clin Nutr 1999;69:842–56.
Vieth R. Vitamin D supplementation, 25-hydroxy-vitamin D concentrations, and safety. Am J Clin Nutr 1999;69:842–56. 4 Favus M. Laboratory values of importance for calcium metabolic bone disease. In: Favus M, ed. Primer on the metabolic bone diseases and disorders of mineral metabolism. 4th ed. New York: Lippincott, Williams &
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