Issues with Determining Recommendations for Vitamin D Intake - Essay Example

Issues with Determining Recommendations for Vitamin D Intake Issues with Determining Recommendations for Vitamin D Intake Vitamin D is a fat-soluble vitamin obtained from dietary sources, supplements or synthesized in the skin. Upon contact with ultraviolet-B (UVB) radiation from sunlight, the human skin synthesizes Vitamin D3 (cholecalciferol) from 7-dehydrocholesterol. Plants, mushrooms, and yeasts photosynthesis Vitamin D2 (ergocalciferol). Cholecalciferol and ergocalciferol are converted to the biologically active forms in the liver and kidneys. Synthesized cholecalciferol and ingested ergocalciferol enter the circulation and are transported to the liver by the vitamin D-binding protein or albumin (Truesdell et al., 2011). The proceeding process is their hydroxylation to form 25-hydroxyvitamin. The total of 25-hydroxyvitamin D2 together with 25-hydroxyvitamin D3 levels in serum is used as an indicator of vitamin D nutritional status. Studies indicate that this level increases following exposure to sunlight, or dietary intake of vitamin D (Rajakumar et al., 2014). 25-hydroxyvitamin D is hydroxylated to 1,25-dihydroxyvitamin D (calcitriol) in the kidney, a reaction catalyzed by 25-hydroxyvitamin D-1alpha-hydroxylase. Regulation of this reaction is by serum phosphorus, calcium, parathyroid hormone (PTH), fibroblast growth factor 23 and 1,25-dihydroxyvitamin. 1,25-dihydroxyvitamin D production has also been demonstrated in the skin, parathyroid gland, breast, colon, prostate, and immune system and bone cells. 1,25-dihydroxyvitamin D then binds to a receptor of vitamin D in the nucleus of a cell and recruits retinoic acid X receptor. This VDR/RXR complex binds small sequences of DNA called vitamin D response elements (VDREs) (Battault et al., 2013). It then initiates a cascade of molecular interactions that modulate the transcription of specific genes. Vitamin D regulates calcium and phosphorus homeostasis that are necessary for the maintenance of bone mineralization (Vieth, 2012). In the endocrine system Vitamin D regulates insulin secretion. Investigation shows that it is a potent immune system modulator. It also exhibits effects in the cardiovascular system regulating blood pressure. Severe vitamin D deficiency results in a condition known as rickets in children and osteomalacia in adults since it is important for development and maintenance of the bone structure (Persson et al., 2013). Osteoporosis has been linked to secondary hyperthyroidism caused by vitamin D deficiency. Increased PTH secretion by the parathyroid glands result in increased bone resorption increasing the bone breakdown and precipitate osteoporosis. Cancer, particularly colorectal and breast cancer risk has been associated with vitamin D deficiency (Anık et al., 2014). By binding to VDR, 1,25-dihydroxyvitamin D inhibits proliferation and stimulates the differentiation of cells preventing the uncontrolled proliferation of cells and hence cancer. Vitamin D deficiency also has a connection with autoimmune diseases, including type 1 diabetes mellitus, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematous. Prevalence of type 2 diabetes show association with suboptimal levels of serum 25-hydroxyvitamin D (Greer, 2004). Deficiency of vitamin D has been associated with glucose homeostasis and impaired glucose tolerance and insulin resistance (Ghanizadeh et al., 2014). Neurodegenerative diseases such as Cognitive impairment and Alzheimers disease have been linked to vitamin D abnormalities in the cerebral parts of the hippocampus and cortex. A deficiency in pregnant women has been linked with several adverse effects for the mother and newborn including small-for-gestational-age and low-birth-weight infants. Vitamin D Nutritional Status and Recommended Dietary Allowance Serum 25-hydroxyvitamin D concentration is measured to indicate vitamin D status. Cutoff values defining states of insufficiency and deficiency require further investigation. Laboratory reference values for sufficient levels of vitamin D are based on serum 25-hydroxyvitamin D levels of healthy individuals. Studies, however, suggested that health-based cutoff values should be higher to prevent secondary hyperparathyroidism and bone loss (Drewnowski and Rehm, 2015). Concentration below 20-25 nmol/L has been associated with rickets and osteomalacia. It has however shown that levels below 80 nmol/L do not optimize PTH levels and calcium absorption. The threshold values of serum 25-hydroxyvitamin D concentrations in relation to PTH suppression and optimal calcium absorption are yet to be determined. Studies with well-fitted curve displaying the inverse association between paired measurements of serum PTH and 25-hydroxyvitamin D have not found evidence of a threshold for PTH suppression even with 25-hydroxyvitamin D concentrations beyond 175 nmol/L. Mild hyperparathyroidism has been observed with serum 25-hydroxyvitamin D levels beyond 50 nmol/L indicating that PTH is an inefficient indicator of vitamin D insufficiency. The proposed cutoffs by the Institute of Medicine are as follows: deficiency as serum 25-hydroxyvitamin D values ≤ 30 nmol/L; insufficiency as serum 25-hydroxyvitamin D values of 30-49 nmol/L; and sufficiency as serum 25-hydroxyvitamin D values of 50-125 nmol/L (Looker, 2011). Institute of Medicine aims at achieving circulating 25-hydroxyvitamin D concentrations 50-125 nmol/L that are sufficient to sustain bone health and optimal calcium absorption with the dietary reference intakes. The proposed cutoffs by the US Endocrine Society are as follows: deficiency as serum 25-hydroxyvitamin D values ≤ 50 nmol/L; insufficiency as serum 25-hydroxyvitamin D values of 51-74 nmol/L; sufficiency as serum 25-hydroxyvitamin D values of 75-250 nmol/L. This is based on the consideration of the potential role of circulating levels lower than 75 nmol/L in the burden of many chronic diseases (Holick, 2011). Institute of Medicine Food and Nutrition Board set a Recommended Dietary Allowance (RDA) of vitamin D to maintain bone integrity. This 2010 RDA of vitamin D was increased from the adequate intake set in 1997. The RDA are as follows: Infants 10 mcg; children 15 mcg; adolescent and adults 14-70 years 15 mcg; adults above 71years 20 mcg; and pregnant and breastfeeding female 15 mcg. Factors Influencing Vitamin D Status Vitamin D status varies depending on environmental factors, cultural practices, and biological factors. Therefore, dietary reference intervals boards should take these factors into consideration when establishing Recommended Dietary Allowance. This is because the RDA may vary from population to population. Vitamin D status varies depending on environmental conditions. These conditions influence the intensity of UVB radiation that reaches the ground and hence the synthesis of cholecalciferol (LeFevre, 2015). Therefore, geographical locations, including latitude and altitudes, and atmospheric conditions such air pollution are important factors to consider in determining vitamin D status. Quality and quantity of UVB rays are also affected by seasonal changes and these changes, therefore, affect vitamin D synthesis (Cashman, 2014). Some cultures and religions require concealed clothing style especially for the female population. Study of Middle Eastern women who wore a headscarf or covered all skin for religious or cultural reasons found that 96% had serum 25-hydroxyvitamin D levels less than 50 nmol/mL. 60% had vitamin D levels below 30 nmol/mL (Nichols 2012). This is because the concealed clothes limit skin contact with UVB radiation and hence the synthesis of cholecalciferol. Rickets and osteomalacia are commonly observed in such populations. Sun safety measures limit contact of the skin with UVB radiation and hence the synthesis of cholecalciferol. These measures include limiting sun exposure, wearing protective clothing and hats, and applying sunscreens that are now commonly practiced in the modern world (Brown et al., 2013). It has been shown that the application of 2 mg/cm2 sunscreen 2 mg/cm2 having a sun protection factor (SPF) of 10 decreases UVB radiation by 90% significantly affecting the synthesis of vitamin D. Infants who are completely breastfed do not receive vitamin D supplementation since human milk provides 10-80 IU of vitamin D per liter (L) and therefore about an average of 0.2-1.5 mcg/day to an infant (Xinqing Deng et al., 2013). Thus, it is recommended that the infant receive vitamin D supplementation to reach the Recommended Dietary Allowance. Breastfeeding women are advised to adopt vitamin D supplementation to improve the vitamin D status of the breastfed infant. Vitamin D synthesis, absorption, and metabolism that determine vitamin D status are affected by several of biological factors. Skin pigmentation influences the synthesis of cholecalciferol. Studies show that individuals with a dark complexion synthesize less vitamin D on exposure to sunlight when compared to their counterparts with light-colored skin (Gallagher et al., 2012). A survey of the population of women aged 20 to 39 years old in US found the average 25-hydroxyvitamin D serum levels as; 70 nmol/mL Caucasian, 50 nmol/mL Mexican American, and 35 nmol/mL African American (Ginde, 2009). Genetic variations mainly in the levels of vitamin D- binding protein influences the vitamin D status. The levels of vitamin D-binding protein influence the bioavailability of vitamin D (Pfeiffer et al., 2012). These levels vary from individual and are influenced by genetic polymorphism. 25-hydroxyvitamin D not bound to DBP is readily bioavailable D, and the level of this bioavailable 25-hydroxyvitamin D will depend on the level of DBP. The old have reduced capacity to synthesize vitamin D in skin when exposed to UVB radiation. It is, therefore, paramount that their diet is supplemented to reach the RDA. The RDA for individuals above 71 years is20 mcg (Anık et al., 2014). Several diseases cause increased risk of vitamin D deficiency. Chronic kidney disease (CKD) affects the process by which 25-hydroxyvitamin D is hydroxylated to 1,25-dihydroxyvitamin D (calcitriol) in the kidney, the reaction catalyzed by 25-hydroxyvitamin D-1alpha-hydroxylase. It also causes an increased loss of 25-hydroxyvitamin D in urine, therefore, affecting the vitamin D status. Fat malabsorption syndromes cause decreased absorption of dietary vitamin D and impaired conversion of vitamin D to 25-hydroxyvitamin D in the liver (Demi̇rel et al., 2014). Cystic fibrosis and both non-cholestatic and cholestatic liver diseases, therefore, affect the vitamin D status. Another disease affecting vitamin D status is inflammatory bowel disease like Crohns disease. In obese individuals, vitamin D is synthesized in the skin or ingested can be sequestered in body fat stores, making it less bioavailable. Magnesium controls the action of critical enzymes in vitamin D metabolism and hence its deficiency negatively affects vitamin D status. Studies show that high magnesium intake reduces the likelihood of vitamin D deficiency. These factors influencing variations in vitamin D status should be taken into consideration to develop recommendations for vitamin D intake. Recommended Dietary Allowance should be population specific to be effective. Measures to prevent deficiency and hence the associated diseases such fortification of food with vitamin D should also consider these factors. Bibliography Anık, A., Çatlı, G., Makay, B., Abacı, A., Küme, T., Ünsal, E., Böber, E., 2014. Decreased vitamin D levels in children with familial Mediterranean fever. Int. J. Rheum. Dis. 17, 321–326. doi:10.1111/1756-185X.12253 Balk SJ, Council on Environmental Health, Section on Dermatology. Ultraviolet radiation: a hazard to children and adolescents. Pediatrics. 2011;127(3):e791-817. (PubMed) Battault, S., Whiting, S., Peltier, S., Sadrin, S., Gerber, G., Maixent, J., 2013. Vitamin D metabolism, functions and needs: from science to health claims. Eur. J. Nutr. 52, 429–441. doi:10.1007/s00394-012-0430-5 Binkley, N, & Wiebe, D 2013, Special Section on Bone and Nutrition: Clinical Controversies in Vitamin D: 25(OH)D Measurement, Target Concentration, and Supplementation, Journal of Clinical Densitometry, 16, pp. 402-408, Science Direct, EBSCOhost, viewed 14 April 2015 Brickley, M, Moffat, T, & Watamaniuk, L 2014, Biocultural perspectives of vitamin D deficiency in the past, Journal of Anthropological Archaeology, 36, pp. 48-59, Science Direct, EBSCOhost, viewed 14 April 2015 Brown, J., Sandmann, A., Ignatius, A., Amling, M., Barvencik, F., 2013. New perspectives on vitamin D food fortification based on a modeling of 25(OH)D concentrations. Nutr. J. 12, 1–21. doi:10.1186/1475-2891-12-151 Cashman, K, Hayes, A, ODonovan, S, Zhang, J, Kinsella, M, Galvin, K, Kiely, M, & Seamans, K 2014, Dietary calcium does not interact with vitamin D3 in terms of determining the response and catabolism of serum 25-hydroxyvitamin D during winter in older adults, American Journal Of Clinical Nutrition, 6, p. 1414, Academic OneFile, EBSCOhost, viewed 15 April 2015. Cashman, KD 2015, Review: Vitamin D: dietary requirements and food fortification as a means of helping achieve adequate vitamin D status, Journal of Steroid Biochemistry and Molecular Biology, 148, 17th Vitamin D Workshop, pp. 19-26, Science Direct, EBSCOhost, viewed 14 April 2015 Catharine R., Christine L. Taylor, Ann L. Yaktine, and Heather B. Del Valle. IOM (Institute of Medicine). 2011. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: The National Academies Press. Demi̇rel, F., Kara, Ö., Tepe, D., Esen, İ., 2014. Bone mineral density and vitamin D status in children and adolescents with congenital adrenal hyperplasia. Turk. J. Med. Sci. 44, 109–114. doi:10.3906/sag-1301-114 Drewnowski, A., Rehm, C.D., 2015. Socioeconomic gradient in consumption of whole fruit and 100% fruit juice among US children and adults. Nutr. J. 14, 1–9. doi:10.1186/1475-2891-14-3 Eserian, JK 2013, Regular article: Vitamin D as an effective treatment approach for drug abuse and addiction, Journal of Medical Hypotheses and Ideas, 7, pp. 35-39, Science Direct, EBSCOhost, viewed 14 April 2015 Gallagher, J.C., Sai, A., Templin II, T., Smith, L., 2012. Dose Response to Vitamin D Supplementation in Postmenopausal Women. Ann. Intern. Med. 156, 425–W–131. Ghanizadeh, G., Babaei, M., Naghii, M.R., Mofid, M., Torkaman, G., Hedayati, M., 2014. The effect of supplementation of calcium, vitamin D, boron, and increased fluoride intake on bone mechanical properties and metabolic hormones in rat. Toxicol. Ind. Health 30, 211–217. doi:10.1177/0748233712452775 Ginde AA, Liu MC, Camargo CA, Jr. Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Arch Intern Med. 2009;169(6):626-632. Greer, F.R., 2004. ‘Issues in establishing vitamin D recommendations for infants and children. Am. J. Clin. Nutr. 80, 1759S–1762S. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011;96(7):1911-1930. Hossein-nezhad, A, & Holick, M 2013, Review: Vitamin D for Health: A Global Perspective, Mayo Clinic Proceedings, 88, pp. 720-755, Science Direct, EBSCOhost, viewed 14 April 2015 LeFevre, M.L., 2015. Screening for Vitamin D Deficiency in Adults: U.S. Preventive Services Task Force Recommendation Statement. Ann. Intern. Med. 162, 133–140. doi:10.7326/M14-2450 Looker AC, Johnson CL, Lacher DA, Pfeiffer CM, Schleicher RL, Sempos CT. Vitamin D status: United States, 2001-2006. NCHS Data Brief. 2011(59):1-8. (PubMed) Nichols EK, Khatib IM, Aburto NJ, et al. Vitamin D status and determinants of deficiency among non-pregnant Jordanian women of reproductive age. Eur J Clin Nutr. 2012;66(6):751-756. Persson, K., Öhlund, I., Nordström, L., Winberg, A., Rönmark, E., West, C.E., 2013. Vitamin D deficiency at the Arctic Circle - a study in food-allergic adolescents and controls. Acta Paediatr. 102, 644–649. doi:10.1111/apa.12172 Pfeiffer, C.M., Schleicher, R.L., Johnson, C.L., Coates, P.M., 2012. Assessing vitamin status in large population surveys by measuring biomarkers and dietary intake - two case studies: folate and vitamin D. Food Nutr. Res. 56, 1–10. doi:10.3402/fnr.v56i0.5944 Rajakumar, K., Holick, M.F., Moore, C.G., Cohen, E., Olabopo, F., Haralam, M.A., Bogusz, J., Nucci, A., Greenspan, S.L., 2014. Impact of seasonal flux on 25-hydroxyvitamin D and bone turnover in pre- and early pubertal youth. Pediatr. Int. 56, 35–42. doi:10.1111/ped.12210 Spiro, A, & Buttriss, J 2014, Vitamin D: An overview of vitamin D status and intake in Europe, Nutrition Bulletin, 39, 4, pp. 322-350, Academic Search Premier, EBSCOhost, viewed 14 April 2015. Truesdell, D., Shin, H., Liu, P.-Y., Ilich, J.Z., 2011. Vitamin D Status and Framingham Risk Score in Overweight Postmenopausal Women. J. Womens Health 15409996 20, 1341–1348. doi:10.1089/jwh.2010.2599 Vieth, R., 2012. Implications for 25-Hydroxyvitamin D testing of public health policies about the benefits and risks of Vitamin D fortification and supplementation. Scand. J. Clin. Lab. Invest. 72, 144–153. doi:10.3109/00365513.2012.682893 Xinqing Deng, Yiqing Song, Manson, J.E., Signorello, L.B., Zhang, S.M., Shrubsole, M.J., Ness, R.M., Seidner, D.L., Qi Dai, 2013. Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III. BMC Med. 11, 1–14. doi:10.1186/1741-7015-11-187 Yawn, J, Lawrence, L, Carroll, W, & Mulligan, J 2015, Review: Vitamin D for the treatment of respiratory diseases: Is it the end or just the beginning?, Journal of Steroid Biochemistry and Molecular Biology, 148, 17th Vitamin D Workshop, pp. 326-337, Science Direct, EBSCOhost, viewed 14 April 2015 Read More