Vitamin D: the beneficial effects of this sunshine supplement

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1 Vitamin D: the beneficial effects of this sunshine supplement Matriculation date: August 24, 2009 Anticipated graduation date: May 11, 2012 Acknowledgement of grant and assistance: None

2 ABSTRACT The prevalent use of sunscreen, decreased exposure to ultraviolet (UV) sunlight and poor reliable consumption of dietary vitamin D has increased the incidence and risk of vitamin D deficiency in most individuals. Vitamin D deficiency is associated with a higher incidence of morbidity in bone and cardiovascular health as well cancer and hypertension. A lower serum level of vitamin D increases vascular smooth muscle proliferation and calcification and also activates the reninangiotensin-aldosterone-system leading to an increase in arterial hypertension. Further evidence demonstrates an increase in cancer cell apoptosis by 56% (p=0.002). 7 The Institute of Medicine, recommends that individuals consume anywhere between 1,000 IU-4,000 IU of vitamin D in order to maintain adequate serum levels of 50 nmol/ml (>20 ng/ml). Groups at highest risk include the elderly, the obese, exclusively breastfed infants and their lactating mothers and individuals with limited sun exposure (e.g. darker pigmented individuals and those who primarily work indoors). Therefore, it is recommended that vitamin D supplementation be considered for everyone. 1

3 INTRODUCTION When it comes to using vitamin supplements, many individuals and health care providers alike are familiar with the beneficial effects of taking supplements such as fish oil, calcium, vitamin C and a daily multivitamin. However, there is a general lack of knowledge about vitamin D supplements and the increasing evidence of health benefits that vitamin D may provide. These days, the general population is at an increased risk of vitamin D deficiency due to people avoiding skin exposure to sunlight. As more people avoid the amount of daytime sun exposure to decrease their risk of developing skin cancer, there is a lack of natural vitamin D synthesis from the skin. The use of sunscreen and other methods of skin protection from UV light further contribute to vitamin D deficiency. Vitamin D deficiency can lead to an increased risk of pathology such as rickets in children, osteomalacia and osteoporosis in adults, cardiovascular disease, hypertension and even cancer. As healthcare providers, it would be beneficial to consider vitamin D supplementation in our patient population, especially in groups that are at risk for deficiency: the elderly, obese, exclusively breastfed infants and their lactating mothers, darker pigmented individuals and those individuals who may have a chronic disorder which prevents adequate absorption of serum vitamin D levels. BACKGROUND Vitamin D is a fat soluble vitamin that is converted in the liver and kidneys into the active form 1,25 dihydroxyvitamin D (1,25[OH]D2), also know as calcitriol. The active form of vitamin D binds to intracellular vitamin D receptors (VDRs) to activate target gene responses. The most commonly known function of vitamin D is to maintain homeostatic levels of calcium, thus maintaining mineralization of bone. More recently, studies have demonstrated vitamin D 2

4 playing an important role in regulating the immune system, cardiovascular (CV) diseases, hypertension (HTN) and cancer. There are two different forms of vitamin D: ergocalciferol (vitamin D 2 ) found mainly in plant and fungal sources (e.g. mushrooms) and cholecalciferol (vitamin D 3 ), the preferred form of vitamin D that is mainly synthesized endogenously in the skin when exposed to UV sunlight. The amount of vitamin D 3 produced within the body is dependent on multiple factors related to sun exposure: season, time of day, latitude, sunscreen use and the amount of melanin within the skin. Studies have demonstrated that mean concentrations of vitamin D were higher in the spring than in the fall where sunlight exposure is limited. In a study of 107 young adults from diverse ancestries living in Canada during the winter months, more than 93% of the total sample had vitamin D concentrations below optimal levels and there was an inverse relationship between melanin content of skin and vitamin D levels (p=0.033). 1 Other studies have further demonstrated that people living between the 18 and 34 degrees north latitude regions (e.g. Los Angeles) during the wintertime had an increased production of endogenous subcutaneous vitamin D from sunlight than those living in regions further north at 43 degrees north (e.g. Boston). 2 Dietary sources of vitamin D 3 can be found in fatty fishes such as salmon and cod liver oil as well as in foods fortified with vitamin D such as cereals, juices and milk. However, due to low levels of vitamin D available in food sources, combined with the overall limited exposure to sunlight on skin, it is recommended that additional supplementation of vitamin D should be considered. Metabolism of Vitamin D Vitamin D metabolism begins with the ingestion or cutaneous synthesis of vitamin D. Once ingested or synthesized after UV exposure, vitamin D is either stored in fat cells or gets 3

5 converted in the liver by the enzyme 25-hydroxlase into the more active form 25-hydroxyvitamin D (25[OH]D). It is this more active form of vitamin D that circulates in the body and directly correlates to vitamin D obtained from solar and dietary sources. After conversion in the liver, 25[OH]D undergoes another conversion in the kidneys into its active metabolite 1,25[OH]D2. It is in this form (1,25[OH]D2) that the vitamin is in its most active state; circulating in lower concentrations than other forms of vitamin D (e.g. 25[OH]D) due to its greater form of potency. It is also in this form that vitamin D has the highest affinity for VDRs throughout the body. As for regulation, it is the role of phosphorus, calcium and other factors to control the production of 1,25[OH]D2 in the kidneys. Additionally, 1,25[OH]D2 decreases its own production through the process of negative feedback and further acts to decrease the synthesis and secretion of parathyroid hormone (PTH) from the parathyroid glands. Although 1,25[OH]D2 is the most active and potent form of vitamin D within the body, it is actually the serum levels of 25[OH]D that is measured clinically to obtain vitamin D status in individuals (Figure 1). How Vitamin D is Measured in the Body Vitamin D levels are measured by testing serum levels of 25[OH]D, but testing is costly and not routinely indicated as a screening tool. Measurement of vitamin D is recommended in situations where a baseline needs to be established for initiating vitamin D therapy. Testing of vitamin D levels is also recommended in cases where there is an increased risk of deficiency. Some examples of individuals at risk includes those with an overall decreased intake of vitamin D, or those with gastrointestinal (GI) problems preventing adequate absorption of dietary vitamin D (Table 1). Vitamin D level testing may also be indicated in patients who presents with other laboratory or radiologic findings commonly associated with low vitamin D levels such as elevated PTH levels, decreased bone mineral density, or low serum calcium levels (Table 2). 4

6 As for appropriate levels of serum 25[OH]D, there are various levels of concentrations that are currently being discussed. According to the Institute of Medicine (IOM), vitamin D deficiency is defined at serum 25[OH]D concentrations of <30 nmol/l (<12 ng/ml). Vitamin D inadequacy is defined at a range of nmol/l (12-20 ng/ml). Sufficient levels of vitamin D is defined as 50 nmol/ml (>20 ng/ml) with >50 nmol/ml covering for 97.5% of the population needs and serum concentrations >125 nmol/l (>50 ng/ml) are associated with potential adverse effects. ROLE OF VITAMIN D IN HEALTH AND DISEASE PREVENTION Commonly known for its role in bone mineralization, vitamin D is recognized for the prevention of rickets in children and osteomalacia and osteoporosis in adults. In utero, a lack of vitamin D can cause growth retardation and skeletal deformities. In the adult, deficiencies in vitamin D may lead to increased muscle weakness and decreased bone strength which increases the risk of fractures in the deficient individual. Aside from commonly known benefits of vitamin D, new research has demonstrated additional benefits of vitamin D in CV health, blood pressure (BP) and cancer through the activation of VDRs located on tissues throughout the body and through its role in the regulation of PTH. Bone Health Vitamin D is an essential part of bone health, maintaining serum calcium concentrations within the blood. Vitamin D increases the absorption of essential minerals such as calcium and phosphorus from the diet which further aids in supporting bone health. In children, vitamin D prevents the development of rickets and in adults, the development of osteomalacia which could possibly lead to osteoporosis. Rickets, a bone disorder in young children, is rarely seen in 5

7 developed countries due to the addition of vitamin D in food sources. In the adult, deficiency of vitamin D leads to defective mineralization of bone in the skeleton. This in turn leads to osteomalacia and secondary hyperparathyroidism which further induces bone loss and osteoporosis through osteoclastic activity. If there is adequate serum levels of vitamin D, PTH is regulated and calcium stores are maintained within the bones. Studies have demonstrated that decreased levels of vitamin D was associated with decreased bone mineralization, decreased muscle strength, and an increased incidence of falls when compared to women with greater concentrations of serum vitamin D. Cardiovascular health Vitamin D plays an important role in CV health by inhibiting vascular smooth muscle cell (SMC) proliferation. Studies on the effects of vitamin D analogs have demonstrated that activation of VDRs regulates gene expressions involved in SMC proliferation by 46% (p=<0.001). 3 During vascular injury, the activation of SMC increases vascular atherosclerosis and calcification, but by suppressing SMC proliferation and by regulating the genes that express proliferation, vitamin D plays an important role in cardiac myocyte hypertrophy by increasing vascular patency and decreasing vascular stiffness. Vascular calcification is also affected by VDRs that activate genes involved in the prevention of calcification. With low serum vitamin D levels, not enough VDRs are activated in order to prevent calcification. Suppression of vascular calcification is also regulated by PTH. In a study of 107 subjects aged from 25 to 85 years (mean, 62.5 ± 13.8 years), increased serum vitamin D levels had a significant negative correlation in PTH levels (r=-0.24; p<0.001). 4 Results of this study implicates an increased risk of calcification and mortality associated with high PTH levels. In primary hyperparathyroidism (PHPT), elevated PTH levels are linked to an increased risk of 6

8 vascular problems. Studies demonstrated that individuals with increased carotid stiffness had significantly higher PTH levels than those with normal carotid stiffness (141 ± 48 vs ±44 pg/ml; p=0.002) and odds of abnormal stiffness increased 1.91 (CI= ; p=0.024) for every 10 pg/ml increase in PTH. 5 In addition, elderly individuals 65-years-old with low serum vitamin D levels had a higher risk of CV disease mortality (n=1066, Hazard Ratio [H.R] 2.11; CI 95%: ; p=0.007). 6 Hypertension New research demonstrates that vitamin D levels may also contribute to reduction of BP and HTN through the regulation of the renin-angiotensin-aldosterone-system (RAAS). Antihypertensive effects of vitamin D are mainly through the suppression of renin. Vitamin D deficiency activates the RAAS therefore contributing to the arterial hypertension. Vitamin D also impacts the function of endothelial cells and endothelial-cell dependent vasodilation. Studies have demonstrated that an increased dose of vitamin D lowered systolic blood pressure by 14 mmhg (p=0.001). 7 The combination of an up-regulated RAAS and proliferation of SMC can predispose one to hypertension and cardiac cell hypertrophy. However, with regular supplementation of vitamin D, the overall effects of vitamin D deficiency on hypertension can be avoided through the regulation of the RAAS as well as the proliferation of SMC. Cancer Vitamin D has also been implicated in suppression of cancer cell proliferation. Vitamin D regulates the proliferation of cells by binding to VDRs located on body tissues. Binding to VDRs leads to suppression of cancer cell gene expression and transcriptional activity. Studies on the effects of vitamin D and calcium on markers of apoptosis of colorectal cells demonstrated that Bax (an apoptosis promoter) expression increased by 56% (p=0.002) when patients were 7

9 treated to 6 months of vitamin D. 8 These results suggest that vitamin D may enhance apoptosis in colorectal cancer cells and may be used in treatment of colorectal cancer. POPULATIONS AT RISK As healthcare providers, it is important to keep in mind the diverse groups of individuals being treated and to remember that a majority of the population may be at an increased risk of vitamin D deficiency. Those at increased risk of vitamin D deficiency include the elderly, the obese, lactating mothers and their exclusively breastfed infants, as well as those individuals with limited daily sun exposure (e.g. darker pigmented individuals, those who primarily work indoors). Elderly Patients When treating the elderly, it is important to remember that the older adult population is at an increased risk of developing a vitamin D deficiency. The elderly have an increased risk of falls from poor bone and muscle strength as well as an increased risk of morbidity and mortality from low serum vitamin D levels. Several factors contribute to low vitamin D levels in the elderly. As one age, the skin is unable to efficiently synthesize vitamin D and the elderly are more likely to spend their time indoors further contributing to inadequate synthesis of the vitamin. The Obese Another population at risk for deficiency in vitamin D includes the obese individual. Individuals with a body mass index 30 kg/m 2 have significantly lower serum vitamin D levels when compared to their non-obese counterparts due to the increased amount of subcutaneous fat. Increase in subcutaneous fat doesn t necessarily affect the skin s ability to synthesize vitamin D, 8

10 but will cause greater storage of vitamin D within adipose tissue and alters the release of vitamin D into circulation. Individuals who undergo gastric bypass surgery are also at risk of vitamin D depletion over time because vitamin D from food or supplements bypasses a portion of the small intestine where vitamin D is mainly absorbed. Exclusively breastfed infants and their lactating mothers Lactating mothers with exclusively breastfed infants are also at risk of vitamin D deficiency. Vitamin D requirements cannot be met by human milk alone and prenatal vitamin supplements do not contain an adequate amount of vitamin D to achieve normal vitamin D levels. There is an increased risk of vitamin D deficiency in exclusively breastfed infants because their source of vitamin D is primarily through the breastmilk of their mothers. Studies have demonstrated a direct association of vitamin D levels between lactating mothers and their infants. Therefore, it is recommended that lactating mothers who are exclusively breastfeeding their infants take additional supplements of vitamin D. Darker pigmented individuals and those with limited sun exposure Individuals with limited sun exposure (e.g. darker pigmented individuals and those who frequently use sunscreen or religious head coverings), are all at risk of having a lower level of serum vitamin D. Therefore, it is a good idea to consider increasing vitamin D levels in a majority of these patients through supplementation, with or without establishing baseline serum vitamin D levels. VITAMIN D DEFICIENCY IN CHRONIC DISEASES Vitamin D deficiency is found to be prevalent in many chronic disease conditions involving multiple organ systems such as the kidneys, liver and intestines. Chronic disease 9

11 conditions of these organs are associated with an insufficient level of vitamin D in the body because metabolism of vitamin D is dependent on these organs. Individuals with chronic kidney disease (CKD) and other types of renal disorders are at an increased risk of vitamin D deficiency. The kidneys function in converting 25[OH]D into the active metabolite 1,25[OH]D2, therefore it is important to regularly check and follow up on serum vitamin D levels in patients with CKD and other renal insufficiencies. Chronic diseases of the liver affects vitamin D levels because the liver converts vitamin D released from adipose cells into the more active form 25[OH]D (the form that is measured in serum vitamin D levels). It is recommended that vitamin D levels be maintained in these patients. Another group of individuals, those with intestinal fat malabsorption, should also be considered at risk for vitamin D deficiency. Patients diagnosed with intestinal malabsorption problems or inflammatory bowel diseases such as Crohn s or Ulcerative Colitis should be placed on higher doses of vitamin D because of their impaired capability of absorbing fat which is required for the absorption of vitamin D intestinally. RECOMMENDED LEVELS OF SUPPLEMENTATION The Institute of Medicine (IOM) recommended daily allowance (RDA), measured in international units (IU) for vitamin D is as follows: 0 to 12 months, 400 IU; 1 to 70 years, 600 IU; and older than 70 years, 800 IU. Daily upper limits are as follows: 0 to 6 months, 1,000 IU; 6 to 12 months, 1,500 IU; 1 to 3 years, 2,500 IU; 4 to 8 years, 3,000 IU; 9 to 70 years, 4,000 IU; and older than 70 years, 4,000 IU. 10

12 Patients can take vitamin D 2 (ergocalciferol) or vitamin D 3 (cholecalciferol) supplements. Both forms of vitamin D appear to be effective; however vitamin D 3 has a longer half-life and has been shown to be more potent than vitamin D 2. For severe deficiency, a loading dose is often recommended for a short period of time followed by maintenance dosing. Loading doses of 50,000 IU once a week for 2 months, followed by 800 to 1,000 IU daily have also shown to be effective. Ideally, serum vitamin D levels should be 50 nmol/ml (>20 ng/ml) and is expected to increase by about 1 ng/ml for every 100 IU of vitamin D taken each day. Vitamin D Toxicity Although a majority of the population will be deficient in vitamin D, there are rare instances of vitamin D toxicity. Some signs and symptoms of toxicity and overdose include hypercalciuria followed by hypercalcemia. Hypercalcemia has the potential to cause calcification in soft tissues of the body resulting in deposits of calcium in the heart, lungs, or kidneys. Other signs of toxicity may or may not include nausea, vomiting, abdominal cramping, weakness, confusion and heart rhythm abnormalities. Toxicity is shown to occur at an intake of IU (1000 mcg) per day with a toxicity threshold level at 200 to 250 ng/ml. The safe upper limit for serum vitamin D levels are at 100 ng/ml. Fortunately, the risk of toxicity is rare and there is no risk of vitamin D toxicity from sun exposure because the body has a built-in protective mechanism for preventing a level of toxicity from UV sources. CONCLUSION Today, there are many reasons for supplementing vitamin D to our daily regimen. Many individuals are at a risk of vitamin D deficiency due to the increased use of sunscreen, unreliable vitamin D supplementation in the diet, as well as the increased time spent indoors. In addition to 11

13 benefiting bone health, vitamin D can decrease cancer cell proliferation, improve CV health and play a role in the reduction of BP. By inhibiting vascular SMC proliferation, vitamin D improves CV health by decreasing the development of vascular atherosclerosis and hypertrophy. Increasing serum vitamin D levels have also shown to regulate PTH which in turn regulates the concentration of serum calcium. By controlling the amount of calcium circulating in the blood, there is an overall decrease in vascular calcification and stiffness by decreasing the deposition of calcium within tissues. As a consequence, vascular resistance is lowered creating an overall improvement in cardiac function and BP. In addition to decreasing vascular resistance, actions of vitamin D on the body include helping to regulate hypertension through the regulation of the RAAS. Vitamin D affects the body by suppressing the production of renin. By regulating the production of renin combined with decreasing vascular resistance, vitamin D further contributes to controlling HTN through the regulation of BP. It is important as health care providers to consider supplementing most individuals and groups of individuals who may be at an increased risk for deficiency from lack of sun exposure or lack of dietary vitamin D. REFERENCES 1. Gozdizik A, Barta JL, Wu H, et al. Low wintertime vitamin D levels in a sample of healthy young adults of diverse ancestry living in the Toronto area: associations with vitamin D intake and skin pigmentation. BMC Public Health. 2008;26(8):

14 2. Webb A.R., Kline L., Holick M.F. Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin. J Clin Endo Met. 1988;67(2): Wu-Wong JR, Nakane M, Ma J, Ruan X, Kroeger PE. Effects of Vitamin D analogs on gene expression profiling in human coronary artery smooth muscle cells. Atherosclerosis. 2006;186(1): Okazaki R, Sugimoto T, Kaji H, et al. Vitamin D insufficiency defined by serum 25- hydroxyvitamin D and parathyroid hormone before and after oral vitamin D3 load in Japanese subjects. J Bone Miner Metab. 2011;29: Walker MD, Fleischer J, Rundek T, et al. Carotid vascular abnormalities in primary hyperparathyroidism. J Clin Endocrinol Metab. 2009;94(10): Semba RD, Houston DK, Bandinelli S, et al. Relationship of 25-hydroxyvitamin D with all cause and cardiovascular disease mortality in older community-dwelling adults. Eur J Clin Nutr. 2010;64(2): Sugden JA, Davies JI, Witham MD, Morris AD, Struthers AD. Vitamin D improves endothelial function in patients with Type 2 diabetes mellitus and low vitamin D levels. Diabet Med. 2008;25(3): Fedirko V, Bostick RM, Flanders WD, et al. Effects of vitamin D and calcium supplementation on markers of apoptosis in normal colon mucosa: a randomized, doubleblind, placebo-controlled clinical trial. Cancer Prev Res. 2009;2(3):

15 Figure 1: Metabolism of Vitamin D. Circulating vitamin D is converted in the liver via vitamin D-25-hydroxylase into 25- hydroxyvitmain D (25[OH]D), the form that is measured when obtaining serum vitamin D levels. After converting in the liver, 25[OH]D undergoes another conversion in the kidneys into its most active metabolite 1,25 hydroxyvitamin D, circulating at lower concentrations and targeting vitamin D receptors (VDRs) throughout the body. 14

16 Holick MF. Vitamin D Deficiency. N Engl J Med. 2007;357(3):266. Available at Accessed January 15, Table 1: Clinical Risk Factors for Vitamin D Deficiency Kennel KA, Drake MT, Hurley DL. Vitamin D deficiency in adults: when to test and how to treat. Mayo Clin Proc. 2010;85(8): Available at Accessed on January 15,

17 Table 2: Laboratory and Radiographic Findings that Suggest Possible Vitamin D Deficiency Kennel KA, Drake MT, Hurley DL. Vitamin D deficiency in adults: when to test and how to treat. Mayo Clin Proc. 2010;85(8): Available at Accessed January 15,

18 Key Points The prevalent use of sunscreen, as well as the lack of sunlight exposure has contributed to an increase in vitamin D deficiency. It is recommended that the addition of vitamin D supplementation be considered. Vitamin D functions to maintain serum calcium levels. In addition, it has shown to decrease cancer cell production and improve cardiovascular health by inhibiting vascular smooth muscle (SMC) proliferation, suppress vascular calcification and reduce blood pressure. Those at risk of vitamin D deficiency include: the elderly, obese, those with limited sun exposure and exclusively breastfed babies and their mothers. Daily upper limit for supplementation depending on age is up to 4000 IU with ideal serum 25(OH)D levels ranging between nmol/ml. There is no risk of vitamin D toxicity to occur via sunlight, however ingestion of 40,000 IU, may lead to hypercalcemia causing symptoms such as nausea, vomiting and confusion. 17

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