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Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111-1524
2 To whom correspondence should be addressed. E-mail: susan.harris{at}tufts.edu.
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ABSTRACT |
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 TOP ABSTRACT LITERATURE CITED |
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KEY WORDS: • vitamin D • African-Americans • 25-hydroxyvitamin D • race
There are several reasons to examine the vitamin D status and requirements of African Americans as a distinct group. First, they have lower levels of circulating 25-hydroxyvitamin D [25(OH)D]3 and a higher prevalence of vitamin D insufficiency compared with other American groups. Second, their risk for some major medical conditions associated with vitamin D status, including osteoporosis and diabetes, differs from that of others. Third, there is limited evidence that blacks may have adaptive responses to vitamin D insufficiency that reduce its deleterious effects on the skeleton.
Vitamin D acquisition. Parent vitamin D is obtained from sun exposure and diet and is converted in the liver to 25(OH)D, the primary storage form of the vitamin and the best clinical indicator of vitamin D status. Optimal blood levels of 25(OH)D with respect to skeletal health are a matter of current debate, but are likely to be in the range of at least 75–80 nmol/L (1,2). However, regardless of how vitamin D insufficiency is defined, it is far more prevalent among blacks than whites (3–5). For example, data from NHANES III show that, in the southern states, 53%–76% of non-Hispanic blacks (depending on sex and age) compared with 8%–33% of non-Hispanic whites had 25(OH)D concentrations below 50 nmol/L in the winter (4). The lower 25(OH)D of blacks and other groups with dark skin results primarily from the fact that pigmentation reduces vitamin D production in the skin. Individuals with dark skin can produce high 25(OH)D levels given sufficient UV exposure (6) but, under normal conditions at most latitudes in North America, even young, healthy blacks do not achieve optimal 25(OH)D concentrations at any time of year. This is illustrated by a study in young black and white Boston women measured four times over the period of 1 y (Fig. 1). The black women had much lower 25(OH)D levels all year long and smaller increases in 25(OH)D between winter and summer (5).
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37.5 nmol/L, so a much higher percentage clearly had levels below the desirable 75–80 nmol/L range (4).
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One potential adaptive response involves 1,25-dihydroxyvitamin D [1,25(OH)2D], the kidney metabolite of 25(OH)D and the most biologically active form of the vitamin. The relation between 25(OH)D and 1,25(OH)2D is complex because the latter is affected by calcium and phosphorus status, parathyroid hormone (PTH) levels, and kidney function, as well as the circulating level of 25(OH)D. Extremely low 25(OH)D may be associated with low 1,25(OH)2D due to lack of substrate (15), but moderately low 25(OH)D (e.g., 20–40 nmol/L) is often associated with increased 1,25(OH)2D, presumably due to increased PTH-stimulated kidney synthesis (16,17). We have only recently become aware of the influence of vitamin D status on PTH levels in general. In young and old adults of all races, low 25(OH)D is accompanied by secondary hyperparathyroidism (18), which may stimulate renal synthesis of the active form of vitamin D. As a group, blacks are observed to have higher circulating levels of PTH and, as in other groups with low 25(OH)D, they tend to have relatively high 1,25(OH)2D (3,5,18–21). However, there is some evidence that blacks may have an intestinal resistance to the actions of 1,25(OH)2D (22,23). Such an adaptation could benefit the skeleton because 1,25(OH)2D may have favorable effects on bone formation that are independent of the promotion of intestinal calcium absorption (24). More limited calcium absorption with normal renal function would theoretically protect against hypercalcemia, prevent down-regulation of 1,25(OH)2D by increased serum calcium, and thereby facilitate the higher 1,25(OH)2D levels that may be necessary for direct beneficial effects on bone.
Another potentially adaptive response among blacks may be a skeletal resistance to PTH-stimulated bone resorption (25,26). Young (5,21) and old (3,19) blacks tend to have higher PTH concentrations than whites, a difference that is only partially explained by their lower calcium intake and poorer vitamin D status (3). A skeletal resistance to PTH would improve the balance between the favorable kidney-mediated actions of PTH [increased production of 1,25(OH)2D and increased calcium reabsorption] and the unfavorable bone-resorptive effects.
Further work is needed to characterize the skeletal benefit of these apparently adaptive mechanisms. However, the beneficial effects may not fully mitigate the harmful skeletal effects of low 25(OH)D and elevated PTH in older blacks. In NHANES III, there was a positive association of 25(OH)D with hip BMD in adults aged 50 and older (Fig. 2). This association, although perhaps modestly weaker in blacks than whites or Mexican Americans, was observed in all groups and plateaued at the high 25(OH)D level of 90–100 nmol/L (27). In a smaller study, low 25(OH)D and secondary hyperparathyroidism were associated with both reduced BMD and increased bone turnover in elderly blacks (28). In contrast, a recent 3-y randomized, double-blind, placebo-controlled study found that daily vitamin D supplementation at the level of 20 µg (800 IU) for the first 2 y and 50 µg (2000 IU) for the third and final year had no effect on bone loss, bone turnover, or serum PTH levels in postmenopausal (50- to 75-y-old) black women (29). Mean baseline 25(OH)D concentrations in placebo- and vitamin D-supplemented women were 43 and 48 nmol/L, respectively, but the lack of a vitamin D effect was observed even in the subset of women with lower baseline 25(OH)D. Women in both vitamin D and placebo groups were given calcium supplements to achieve total daily calcium intakes of 1200 to 1500 mg/d, and it is plausible that consumption of calcium may have inhibited formation of the active metabolite of vitamin D and suppressed bone turnover independent of vitamin D status. Actual calcium intakes of black women are only about 500–800 mg/d, and it is unknown whether vitamin D supplementation would be effective at these lower calcium intakes (29).
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Heart disease, cancer, and cerebrovascular disease are the leading causes of death in older adults, including both blacks and whites. Diabetes is the next most important cause of death in older blacks (59) and, in persons aged 65 and older, the death rate from diabetes is nearly twice as high in blacks as in whites (59). Mortality rates from prostate cancer are significantly higher among black men compared with white men and are inversely related to the availability of ultraviolet radiation, in other words, the availability of vitamin D from sun exposure (55). Thus, although blacks have a relatively low prevalence of osteoporosis, potentially beneficial effects of vitamin D on other, more prevalent, conditions suggest that the overall benefit of improving vitamin D status may be essential for chronic disease prevention in blacks.
Conclusions and policy implications. A high percentage of American blacks have suboptimal blood levels of 25(OH)D and levels that are well below those of American whites. Poor vitamin D status may increase the risk of blacks as well as others for osteoporosis, cardiovascular disease, cancer, diabetes, and other serious chronic conditions. African Americans should be included in well-designed intervention studies that test the benefit of improved vitamin D status on both skeletal and nonskeletal outcomes. However, even before such research is conducted, clinicians and educators should be encouraged to promote improved vitamin D status among adult blacks (and others), as they have for black infants and children (60), because of the low risk and low cost of vitamin D supplementation and its potential health benefits.
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FOOTNOTES |
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3 Abbreviations used: 25(OH)D, 25-hydroxyvitamin D; 1,25(OH)2D, 1,25-dihydroxyvitamin D; BMD, bone mineral density; DRI, dietary reference intakes; PTH, parathyroid hormone.
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LITERATURE CITED |
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TOPABSTRACTLITERATURE CITED |
|---|
1. Dawson-Hughes B, Heaney RP, Holick MF, Lips P, Meunier PJ, Vieth R. Estimates of optimal vitamin D status. Osteoporos Int. 2005;16:713–6.
2. Hollis BW. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D. J Nutr. 2005;135:317–22.
3. Harris SS, Soteriades E, Coolidge JA, Mudgal S, Dawson-Hughes B. Vitamin D insufficiency and hyperparathyroidism in a low income, multiracial, elderly population. J Clin Endocrinol Metab. 2000;85:4125–30.
4. Looker AC, Dawson-Hughes B, Calvo MS, Gunter EW, Sahyoun NR. Serum 25-hydroxyvitamin D status of adolescents and adults in two seasonal subpopulations from NHANES III. Bone. 2002;30:771–7.[Medline]
5. Harris SS, Dawson-Hughes B. Seasonal changes in plasma 25-hydroxyvitamin D concentrations of young American black and white women. Am J Clin Nutr. 1998;67:1232–6.[Abstract]
6. Brazerol WF, McPhee AJ, Mimouni F, Specker BL, Tsang RC. Serial ultraviolet B exposure and serum 25 hydroxyvitamin D response in young adult American blacks and whites: no racial differences. J Am Coll Nutr. 1988;7:111–8.[Abstract]
7. Institute of Medicine. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D and fluoride. Washington, DC: National Academy Press; 1997.
8. Calvo MS, Whiting SJ, Barton CN. Vitamin D fortification in the United States and Canada: current status and data needs. Am J Clin Nutr. 2004;80:1710S–6S.
9. Moore CE, Murphy MM, Holick MF. Vitamin D intakes by children and adults in the United States differ among ethnic groups. J Nutr. 2005;135:2478–85.
10. Barrett JA, Baron JA, Karagas MR, Beach ML. Fracture risk in the U.S. medicare population. J Clin Epidemiol. 1999;52:243–9.[Medline]
11. Bohannon AD, Hanlon JT, Landerman R, Gold DT. Association of race and other potential risk factors with nonvertebral fractures in community-dwelling elderly women. Am J Epidemiol. 1999;149:1002–9.
12. Looker AC, Wahner HW, Dunn WL, Calvo MS, Harris TB, Heyse SP, Johnston CC, Jr, Lindsay R. Updated data on proximal femur bone mineral levels of US adults. Osteoporos Int. 1998;8:468–89.[Medline]
13. Li JY, Specker BL, Ho ML, Tsang RC. Bone mineral content in black and white children 1 to 6 years of age. Early appearance of race and sex differences. Am J Dis Child. 1989;143:1346–9.
14. Bell NH, Shary J, Stevens J, Garza M, Gordon L, Edwards J. Demonstration that bone mass is greater in black than in white children. J Bone Miner Res. 1991;6:719–23.[Medline]
15. Theobald TM, Cauley JA, Gluer CC, Bunker CH, Ukoli FA, Genant HK. Black-white differences in hip geometry. Study of osteoporotic fractures research group. Osteoporos Int. 1998;8:61–7.[Medline]
16. Breslau NA. Normal and abnormal regulation of 1,25-(OH)2D synthesis. Am J Med Sci. 1988;296:417–25.[Medline]
17. Need AG, Horowitz M, Morris HA, Nordin BC. Vitamin D status: effects on parathyroid hormone and 1, 25-dihydroxyvitamin D in postmenopausal women. Am J Clin Nutr. 2000;71:1577–81.
18. Pepe J, Romagnoli E, Nofroni I, Pacitti MT, De Geronimo S, Letizia C, Tonnarini G, Scarpiello A, D'Erasmo E, Minisola S. Vitamin D status as the major factor determining the circulating levels of parathyroid hormone: a study in normal subjects. Osteoporos Int. 2005;16:805–12.[Medline]
19. Kleerekoper M, Nelson DA, Peterson EL, Flynn MJ, Pawluszka AS, Jacobsen G, Wilson P. Reference data for bone mass, calciotropic hormones, and biochemical markers of bone remodeling in older (55–75) postmenopausal white and black women. J Bone Miner Res. 1994;9:1267–76.[Medline]
20. Fleet JC, Harris SS, Wood RJ, Dawson-Hughes B. The BsmI vitamin D receptor restriction fragment length polymorphism (BB) predicts low bone density in premenopausal black and white women. J Bone Miner Res. 1995;10:985–90.[Medline]
21. Bikle DD, Ettinger B, Sidney S, Tekawa IS, Tolan K. Differences in calcium metabolism between black and white men and women. Mineral & Electrolyte Metabolism 1999;25:178–84.
22. Dawson-Hughes B, Harris S, Kramich C, Dallal G, Rasmussen HM. Calcium retention and hormone levels in black and white women on high- and low-calcium diets. J Bone Miner Res. 1993;8:779–87.[Medline]
23. Dawson-Hughes B, Harris SS, Finneran S, Rasmussen HM. Calcium absorption responses to calcitriol in black and white premenopausal women. J Clin Endocrinol Metab. 1995;80:3068–72.
24. Reichel H, Koeffler HP, Norman AW. The role of the vitamin D endocrine system in health and disease. N Engl J Med. 1989;320:980–91.[Medline]
25. Cosman F, Morgan DC, Nieves JW, Shen V, Luckey MM, Dempster DW, Lindsay R, Parisien M. Resistance to bone resorbing effects of PTH in black women. J Bone Miner Res. 1997;12:958–66.[Medline]
26. Fuleihan GE, Gundberg CM, Gleason R, Brown EM, Stromski ME, Grant FD, Conlin PR. Racial differences in parathyroid hormone dynamics. J Clin Endocrinol Metab. 1994;79:1642–7.[Abstract]
27. Bischoff-Ferrari HA, Dietrich T, Orav EJ, Dawson-Hughes B. Positive association between 25-hydroxy vitamin D levels and bone mineral density: a population-based study of younger and older adults. Am J Med. 2004;116:634–9.[Medline]
28. Harris SS, Soteriades E, Dawson-Hughes B. Secondary hyperparathyroidism and bone turnover in elderly blacks and whites. J Clin Endocrinol Metab. 2001;86:3801–4.
29. Aloia JF, Talwar SA, Pollack S, Yeh J. A randomized controlled trial of vitamin D3 supplementation in African American women. Arch Intern Med. 2005;165:1618–23.
30. Bouillon R, Verstuyf A, Branisteanu D, Waer M, Mathieu C. [Immune modulation by vitamin D analogs in the prevention of autoimmune diseases]. [Dutch] Verh K Acad Geneeskd Belg. 1995;57:371–85.
31. DeLuca HF, Cantorna MT. Vitamin D: its role and uses in immunology. FASEB J. 2001;15:2579–85.
32. Timms PM, Mannan N, Hitman GA, Noonan K, Mills PG, Syndercombe-Court D, Aganna E, Price CP, Boucher BJ. Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders? QJM. 2002;95:787–96.
33. Reichel H, Norman AW. Systemic effects of vitamin D. Annu Rev Med. 1989;40:71–8.[Medline]
34. Dietrich T, Joshipura KJ, Dawson-Hughes B, Bischoff-Ferrari HA. Association between serum concentrations of 25-hydroxyvitamin D3 and periodontal disease in the US population. Am J Clin Nutr. 2004;80:108–13.
35. Bang B, Asmussen K, Sorensen OH, Oxholm P. Reduced 25-hydroxyvitamin D levels in primary Sjogren's syndrome. Correlations to disease manifestations. Scand J Rheumatol. 1999;28:180–3.[Medline]
36. Harris SS. Vitamin D in type 1 diabetes prevention. J Nutr. 2005;135:323–5.
37. Scragg ., Sowers M, Bell C, Third National Health and Nutrition Examination Survey. Serum 25-hydroxyvitamin D, diabetes, and ethnicity in the Third National Health and Nutrition Examination Survey. Diab Care. 2004;27:2813–18.
38. Scragg R, Holdaway I, Singh V, Metcalf P, Baker J, Dryson E. Serum 25-hydroxyvitamin D3 levels decreased in impaired glucose tolerance and diabetes mellitus. Diab Res Clin Prac. 1995;27:181–8.
39. Munger KL, Zhang SM, O'Reilly E, Hernan MA, Olek MJ, Willett WC, Ascherio A. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004;62:60–5.
40. VanAmerongen BM, Dijkstra CD, Lips P, Polman CH. Multiple sclerosis and vitamin D: an update. Eur J Clin Nutr. 2004;31:1–5.
41. Merlino LA, Curtis J, Mikuls TR, Cerhan JR, Criswell LA, Saag KG, Iowa Women's, Health Study. Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women's Health Study. Arthr Rheum. 2004;50:72–7.[Medline]
42. Knox EG. Ischaemic-heart-disease mortality and dietary intake of calcium. Lancet. 1973;1:1465–7.[Medline]
43. McCarron DA, Morris CD. The calcium deficiency hypothesis of hypertension. Ann Intern Med. 1987;107:919–22.
44. Scragg R, Jackson R, Holdaway IM, Lim T, Beaglehole R. Myocardial infarction is inversely associated with plasma 25-hydroxyvitamin D3 levels: a community-based study. Int J Epidemiol. 1990;19:559–63.
45. Scragg R, Khaw KT, Murphy S. Effect of winter oral vitamin D3 supplementation on cardiovascular risk factors in elderly adults. Eur J Clin Nutr. 1995;49:640–6.[Medline]
46. Sato Y, Kaji M, Metoki N, Satoh K, Iwamoto J. Does compensatory hyperparathyroidism predispose to ischemic stroke? Neurology. 2003;60:626–9.
47. Zittermann A, Schleithoff SS, Tenderich G, Berthold HK, Korfer R, Stehle P. Low vitamin D status: a contributing factor in the pathogenesis of congestive heart failure? J Am Coll Cardiol. 2003;41:105–12.
48. Grant WB, Garland CF. A critical review of studies on vitamin D in relation to colorectal cancer. Nutr Cancer. 2004;48:115–23.[Medline]
49. Cross HS, Bises G, Lechner D, Manhardt T, Kallay E. The vitamin D endocrine system of the gut—its possible role in colorectal cancer prevention. J Steroid Biochem Mol Biol 2005;97:121–8.[Medline]
50. Garland CF, Garland FC, Gorham ED. Calcium and vitamin D. Their potential roles in colon and breast cancer prevention. Ann NY Acad Sci. 1999;889:107–19.[Medline]
51. Janowsky EC, Lester GE, Weinberg CR, Millikan RC, Schildkraut JM, Garrett PA, Hulka BS. Association between low levels of 1,25-dihydroxyvitamin D and breast cancer risk. Pub Health Nutr. 1999;2:283–91.
52. Welsh J, Wietzke JA, Zinser GM, Byrne B, Smith K, Narvaez CJ. Vitamin D-3 receptor as a target for breast cancer prevention. J Nutr. 2003;133:2425S–33S.
53. Stewart LV, Weigel NL. Vitamin D and prostate cancer. Exp Biol Med. 2004;229:277–84.
54. Ahonen MH, Tenkanen L, Teppo L, Hakama M, Tuohimaa P. Prostate cancer risk and prediagnostic serum 25-hydroxyvitamin D levels. Cancer Cause Control. 2000;11:847–52.[Medline]
55. Schwartz GG. Vitamin D and the epidemiology of prostate cancer. Semin Dial. 2005;18:276–89.[Medline]
56. Reichel H, Koeffler HP, Norman AW. The role of the vitamin D endocrine system in health and disease. N Engl J Med. 1989;320:980–91.[Medline]
57. Barreto AM, Schwartz GG, Woodruff R, Cramer SD. 25-Hydroxyvitamin D3, the prohormone of 1,25-dihydroxyvitamin D3, inhibits the proliferation of primary prostatic epithelial cells. Cancer Epi Biom Prev. 2000;9:265–70.
58. Peehl DM, Krishnan AV, Feldman D. Pathways mediating the growth-inhibitory actions of vitamin D in prostate cancer. J Nutr. 2003;133:2461S–9S.
59. National Center for Health Statistics. Natl Vital Stat Rep. 2005;53:9.
60. Weisberg P, Scanlon KS, Li R, Cogswell ME. Nutritional rickets among children in the United States: review of cases reported between 1986 and 2003. Am J Clin Nutr. 2004;80:1697S–705S.
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