Vitamin D: Its Role and Management in the Bariatric Patient March 2011 Nazy Zarshenas, BSc, MND, APD Ms. Zarshenas is a Senior Clinical Dietician at St. George Private Hospital, St. George Upper GI Unit, Sydney, Australia Bariatric Times. 2011;8(3):22–23 Introduction Research over the past 20 years has associated vitamin D with a wide range of health benefits including prevention of cancer, cardiovascular disease, hypertension, pre-eclampsia (a medical condition in which hypertension arises in pregnancy), diabetes, and metabolic syndrome.[1–3] Adequate vitamin D intake has also been associated with improved immune response, neuropsychological functioning, and physical performance.[1–3] A recent review by the Institute of Medicine (IOM) found that the strongest benefits of vitamin D and calcium are in bone health.[14] Calcium and vitamin D are essential nutrients for promoting bone growth and maintenance.4 Vitamin D’s role is to maintain normal serum calcium concentration in order to preserve the process of bone mineralization. It does this by stimulating calcium and phosphate absorption through the intestine by working in parallel with parathyroid hormone (PTH) to enhance distal tubule calcium reabsorption, and by increasing bone reabsorption. This installment of “Nutritional Considerations in the Bariatric Patient” will discuss the health benefits associated with proper vitamin D intake in the bariatric surgery patient. Screening for and treating vitamin D deficiency Bariatric surgery procedures often result in nutritional deficiencies, with vitamin D being the most common.[5–12] In fact, the prevalence of vitamin D deficiency in the bariatric surgery population has been reported to be as high as 84 percent.[13] To prevent exacerbation of nutritional deficiencies, it is imperative to screen for and treat any deficiencies preoperatively. Vitamin D is a prohormone, as it can be synthesised endogenously. The sources of vitamin D are as follows: 1. Exposure to sunlight. Cholecalciferol (i.e., vitamin D3) is formed in the skin through the action of ultraviolet (UV) light on 7-dehydrocholesterol to produce cholecalciferol. 2. Diet. Ergocalciferol (vitamin D2) is the dietary source of vitamin D. It is found in small quantities in fatty fish (e.g., North Sea salmon, herring, and mackerel), liver, eggs, and fortified foods (e.g., dairy products, cereals). Ergocalciferol is also used as the major source of supplementation.[4] The Dietary Reference Intakes (DRIs) for calcium and vitamin D have recently been updated. The DRIs for calcium and vitamin D for healthy adults are 1,000 to 1,300mg per day and 600IU per day, respectively. A total of 800IU per day of vitamin D has been recommended for individuals above the age of 70, with a general upper (safe) level of 4000 IU.[14] These DRIs are devised for the general public and should not be applied to population groups at high risk of developing vitamin D deficiency, which includes individuals with obesity. Also, patients with medical conditions that predispose them to vitamin D deficiency, such as inflammatory bowel disease, celiac disease, and pancreatic insufficiency are also at higher risk and need close monitoring.[5,15] To diagnose vitamin D deficiency, 25 hydroxy vitamin D (25-OHD), iPTH, calcium, albumin, and creatinine levels should be evaluated.[4,15] There is much debate as to the optimal level of 25-OHD. Some sources consider 20µg/mL to be adequate and other sources suggest >30µg/mL to be the optimal level.[16] Most recently, the IOM has reported that there is not enough evidence to support the benefit of achieving levels 30µg/L.[14] The current recommendations for treating moderate-to-severe vitamin D deficiency in the nonbariatric patient are 3000 to 5000 IU per day for at least 6 to 12 weeks, followed by 1000 IU.[15] The two most common vitamin D preparations are Cholecalciferol (D3) and ergocalciferol (D2). Some studies[23,24,25] have shown that D3 has a greater potency than D2 in treating vitamin D deficiency. However this is not consistent throughout the literature.[26] Furthermore the efficacy of these two preparation needs further investigation in obese patients. One small pilot study[27] comparing the these two forms of vitamin D preparations found a better suppression of PTH with D3 than D2. However, as different doses of the two forms of vitamin D were used we can not draw any direct comparison from this study. Alternatively, a higher dose vitamin D2 50,000 IU once per month for 3 to 6 months may be prescribed (compounded high-dose Vitamin D can be prescribed if high-dose Vitamin D is not available). A 300,000 to 600,000 IU vitamin D3 given intramuscularly, once or twice per year, has also shown to be effective.[17]
Adiposity has been inversely associated with vitamin D status. There are several hypotheses for this. There is likely vitamin D deposition in body fat compartments and, therefore, decreased bioavailability of D3 from cutaneous and dietary sources.[18] Vitamin D is a fat-soluble vitamin, and the theory is that the vitamin is sequestered or stuck in the excessive and large fat cells of individuals with obesity where it is not available to the rest of the body. Underexposure to solar ultraviolet radiation, as well as vitamin D malabsorption, which may occur due to its more rapid transit through the GI tract following operations that shorten the GI tract, could also be factors.[19–22] Poor vitamin D levels preoperatively and the malabsorption effect of some bariatric procedures may necessitate higher-dose vitamin D supplementation for correction of the deficiencies. The treatment dose suggested is 50,000 IU once per week, orally or intramuscularly for eight weeks.[23] Conclusion Candidates for weight loss surgery should have vitamin D screening and treatment for deficiency preoperatively. Furthermore, prospective, long-term studies on vitamin D and calcium in the bariatric population are greatly needed in order to create appropriate prevention and treatment strategies for the metabolic bone disease that may follow these procedures. References 1. Bischoff-Ferrari HA, Giovannucci E, Willett WC et al. Estimation of optimal serum concentration of 25hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006; 84(1): 18–28. 2. Grant WB, Holick MF. Benefits and requirements of vitamin D for optimal health: a review. Altern Med Rev. 2005;10(2): 94–111. 3. Schwalfenberg G. Not enough vitamin D: health consequences for Canadians. Can Fam Physician. 2007;53(5):841–854. 4. Nowson CA, Diamind TH, Passco JA, et al. Vitamin D in Australia: issues and recommendations. Aust Fam Physician. 2004; 33(3): 133–138. 5. Bhan A, Rao AD, Rao DS. Osteomalacia as a result of vitamin D deficiency. Endocrinol Metab Clin North Am. 2010; 39(2):321-31. 6. Strohmayer E, Via MA, Yanagisawa R. Metabolic management following bariatric surgery. Mt Sinai J Med. 2010; 77(5):431–445. 7. Khandalavala BN, Hibma PP, Fang X. Prevalence and persistence of vitamin D deficiency in biliopancreatic diversion patients: a retrospective study. Obes Surg. 2010; 20(7):881–884. 8. Ziegler O, Sirveaux MA, Brunaud L, et al. Medical follow up after bariatric surgery: nutritional and drug issues. General recommendations for the prevention and treatment of nutritional deficiencies. Diabetes Metab. 2009; 35(6 Pt 2): 554–557. 9. John S, Hoegeri C. Nutritional deficiencies after gastric bypass surgery. J Am Osteopath Assoc. 2009; 109(11):601–604. 10. Xanthakos SA. Nutritional deficiencies in obesity and after bariatric surgery. Pediatric Clin North Am. 2009; 56(5):1105–1121. 11. Al-Shoha A, Quin S, Palniktar S, et al. Osteomalacia with bone marrow fibrosis due to severe vitamin D deficiency after a gastrointestinal bypass operation for severe obesity. Endocr Pract. 2009; 15(6): 528–533. 12. Kaidar-Person O, Rosenthal RJ. Malnutrition in morbidly obese patients: fact or fiction? Minerva Chir. 2009;64(3):297–302. 13. Fish E, Beverstein G, Olson D, Reinhart S, et al. Vitamin D status of the morbidly obese bariatric surgery patient. J Surg Res. 2010 Sept 8. Epub ahead of print. 14. The advisory committee. Dietary reference intakes for calcium and vitamin D. Institute of Medicine. 2010 Nov. www.iom.edu/vitamind Accessed December 13, 2010. 15. Working Group of the Australian and New Zealand Bone and Mineral Society, Endocrine Society of Australia and Osteoporosis Australia. Vitamin D and adult bone health in Australia and New Zealand: a position statement. MJA 2005; 182(6): 281-285. 16. Hollis WB. Circulating 25-hydroxyvitamin D levels indicative of vitamin D deficiency: implications for establishing a a new effective dietary intake recommendation for vitamin D. J Nutr. 2005; 135(2):317–322. 17. Lips P. Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications. Endocr Rev. 2001; 22:477–4501. 18. Wortsman J, Matsuoka LY, Chen TC et al. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr. 2000;72:690–693. 19. Bell NH, Epstein S, Shary J, et al. Evidence for the alteration of the vitamin D-endocrine system in obese subjects. J Clin Invest. 1985;76:7370–7373. 20. Compston JE, Vedi S, Ledger JE, et al. Vitamin D status and bone histomorphometry in gross obesity. Am J Nutr. 1981;34:2359–63. 21. Wortsman J Matsuka LY, Chen TC, et al. Decreased bioavailability of vitamin D in obesity Am J Nutr. 2000; 35:290–304. 22. Aills L, Blankenship J, Buffington C, et al. ASMBS allied health nutritional guidelines for the surgical weight loss
patient. Surg Obes Relat Dis. 2008;4(5 Suppl):S73–S108. Epub 2008 May 19. 23. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89:5387–5391. 24. Trang HM, Cole DE, Rubin LA, et al. Evidence that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently than does vitamin D2. Am J Clin Nutr. 1998;68:854–858. 25. Romagnoli E, Mascia ML, Cipriani C, et al. Short- and long-term variations in serum calciotropic hormones after a single very large dose of ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3) in the elderly. J Clin Endocrinol Metab. 2008;93:3015–3020. 26. Holick MF, Biancuzzo RM, Chen TC, et al. Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D. J Clin Endocrinol Metab. 2008;93:677–681. 27. Stein EM, Strain G, Sinha N, et al. Clin Endocrinol (Oxf). 2009;71(2):176–183