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Although osteoporosis is a multifactorial disease, vitamin D insufficiency can be an important contributing factor. A multinational (18 different countries with latitudes ranging from 64 degrees north to 38 degrees south) survey of more than 2,600 postmenopausal women with osteoporosis revealed that 64% of subjects had 25(OH)D levels lower than 75 nmol/L (30 ng/mL) (45). Without sufficient vitamin D from sun exposure or dietary intake, intestinal calcium absorption cannot be maximized. This causes PTH secretion by the parathyroid glands; elevated PTH results in increased bone resorption, which may lead to osteoporotic fracture (46). A prospective cohort study that followed more than 72,000 postmenopausal women in the U.S. for 18 years found that those who consumed at least 600 IU/day of vitamin D from diet and supplements had a 37% lower risk of osteoporotic hip fracture than women who consumed less than 140 IU/day of vitamin D (47). The results of most clinical trials suggest that vitamin D supplementation can slow bone density losses or decrease the risk of osteoporotic fracture in men and women who are unlikely to be getting enough vitamin D. However, recent analyses indicate that there is a threshold of vitamin D intake that is necessary to observe reductions in fracture risk. For instance, a recent meta-analysis of randomized controlled trials in older adults found that supplementation with 700 to 800 IU vitamin D daily had a 26% and 23% lower risk of hip fracture and nonvertebral fracture, respectively. In contrast, supplementation with 400 IU of vitamin D daily did not decrease risk of either hip or nonvertebral fracture (48). Additionally, recent results from the Women's Health Initiative trial in 36,282 postmenopausal women showed that daily supplementation with 400 IU of vitamin D3, in combination with 1,000 mg calcium, did not significantly reduce risk of hip fracture compared to a placebo (49). Bischoff-Ferrari et al. suggest that daily intakes of greater than 700 IU of vitamin D may be necessary to optimize serum concentrations of 25(OH)D and thus reduce fracture risk (41).
Support for such a threshold effect of vitamin D on bone health also comes from previous studies. One study in 247 postmenopausal U.S. women reported that supplementation with 500 mg/day of calcium and either 100 IU/day or 700 IU/day of vitamin D3 for two years slowed bone density losses at the hip only in the group taking 700 IU/day (50). Another study found that daily supplementation of elderly men and women with 500 mg/day of calcium and 700 IU/day of vitamin D3 for three years reduced bone density losses at the hip and spine and also reduced the frequency of nonvertebral fractures (51). A subsequent analysis of this cohort revealed that when the calcium and vitamin D3 supplements were discontinued, the bone density benefits were lost within two years (52). Another study found that oral supplementation with 800 IU/day of vitamin D3 and 1,200 mg/day of calcium for three years decreased the incidence of hip fracture in elderly French women (53). Further, oral supplementation of elderly adults in the UK with 100,000 IU of vitamin D3 once every four months (equivalent to about 800 IU/day) for five years reduced the risk of osteoporotic fracture by 33% compared to placebo (54). However, oral supplementation with 400 IU/day of vitamin D3 for more than three years did not affect the incidence of fracture in a study of elderly Dutch men and women (55). All of these studies indicate that at least 700 IU of vitamin D3 daily may be required to observe a beneficial effect on fracture incidence.
However, the Randomised Evaluation of Calcium Or vitamin D (RECORD) trial reported that oral supplemental vitamin D3 (800 IU/day) alone, or in combination with calcium (1,000 mg/day), did not prevent the occurrence of osteoporotic fractures in elderly adults who had already experienced a low-trauma, osteoporotic fracture (56). A lack of an effect could be possibly due to a low compliance in this study or the fact that vitamin D supplementation did not raise serum 25(OH)D levels to a level that would protect against fractures (41).
To date, clinical trials have generally found that vitamin D2 (ergocalciferol) is not effective at preventing fractures (57). Indeed, vitamin D3 (cholecalciferol) is now known to be greater than three times more potent than vitamin D2 (2, 57). Overall, the current evidence suggests that vitamin D3 supplements of at least 800 IU/day may be helpful in reducing bone loss and fracture rates in the elderly. In order for vitamin D supplementation to be effective in preserving bone health, adequate dietary calcium (1,000 to 1,200 mg/day) should also be consumed (see the article on Calcium).
Two characteristics of cancer cells are lack of differentiation (specialization) and rapid growth or proliferation. Many malignant tumors have been found to contain vitamin D receptors (VDR), including breast, lung, skin (melanoma), colon, and bone. Biologically active forms of vitamin D, such as 1,25(OH)2D and its analogs, have been found to induce cell differentiation and/or inhibit proliferation of a number of cancerous and noncancerous cell types maintained in cell culture (58). Results of some, but not all, human epidemiological studies suggest that vitamin D may protect against various cancers. However, it is important to note that epidemiological studies cannot prove such associations.
The geographic distribution of colon cancer mortality resembles the historical geographic distribution of rickets (59), providing circumstantial evidence that decreased sunlight exposure and diminished vitamin D nutritional status may be related to an increased risk of colon cancer. However, prospective cohort studies have not generally found total vitamin D intake to be associated with significant reductions in risk of colorectal cancer when other risk factors are taken into account (60-63). However, some more recent studies have reported that higher vitamin D intakes and serum 25(OH)D levels are associated with reductions in colorectal cancer risk. One five-year study of more than 120,000 people found that men with the highest vitamin D intakes had a risk of colorectal cancer that was 29% lower than men with the lowest vitamin D intakes (64). Vitamin D intake in this study was not significantly associated with colorectal cancer risk in women. Moreover, serum 25(OH)D level, which reflects vitamin D intake and vitamin D synthesis, was inversely associated with the risk of potentially precancerous colorectal polyps (65) and indices of colonic epithelial cell proliferation (66), two biomarkers for colon cancer risk. More recently, a case-control analysis from the Nurses' Health Study cohort reported that plasma 25(OH)D levels were inversely associated with colorectal cancer (67). A randomized, double-blind, placebo-controlled trial in 36,282 postmenopausal women participating in the Women's Health Initiative study found that a combination of supplemental vitamin D (400 IU/day) and calcium (1,000 mg/day) did not lower incidence of colorectal cancer (68). However, it has been suggested that the daily vitamin D dose, 400 IU, was too low to detect any effect on cancer incidence (69). In fact, a recent dose-response analysis estimated that 1,000 IU of oral vitamin D daily would lower one's risk of colorectal cancer by 50% (70).
Although breast cancer mortality follows a similar geographic distribution to that of colon cancer (59, 71), direct evidence of an association between vitamin D nutritional status and breast cancer risk is limited. A prospective study of women who participated in the first National Health and Nutrition Examination Survey (NHANES I) found that several measures of sunlight exposure and dietary vitamin D intake were associated with a reduced risk of breast cancer 20 years later (72). More recently, a 16-year study of more than 88,000 women found that higher intakes of vitamin D were associated with significantly lower breast cancer risk in premenopausal women but not postmenopausal women (73). Garland et al. conducted a pooled, dose-response analysis of two case-control studies in which women with breast cancer had significantly lower plasma 25(OH)D levels compared to controls (74, 75). These authors reported that women with a 25(OH)D level of 52 ng/ml (130 nmol/L) experienced a 50% lower risk of developing breast cancer compared to women with 25(OH)D levels lower than 13 ng/mL (32.5 nmol/L) (76). The authors state that to obtain a 25(OH)D level of 52 ng/mL, around 4,000 IU of vitamin D3 would need to be consumed daily, or 2,000 IU of vitamin D3 daily plus very moderate sun exposure (76). The current tolerable upper limit of intake (UL) for adults, set by the Food and Nutrition Board of the Institute of Medicine, is 2,000 IU/day (see Safety).
Epidemiological studies show correlations between risk factors for prostate cancer and conditions that can result in decreased vitamin D levels (58). Increased age is associated with an increased risk of prostate cancer, as well as with decreased sun exposure and decreased capacity to synthesize vitamin D. The incidence of prostate cancer is higher in African American men than in white American men, and the high melanin content of dark skin is known to reduce the efficiency of vitamin D synthesis. Geographically, mortality from prostate cancer is inversely associated with the availability of sunlight. Findings that prostate cells in culture can synthesize the 25(OH)D3-1-hydroxylase enzyme and that, unlike the renal enzyme, its synthesis is not influenced by PTH or calcium levels also provide support for the idea that increasing 25(OH)D levels may be useful in preventing prostate cancer (77). In contrast, prospective studies have not generally found significant relationships between serum 25(OH)D levels and subsequent risk of developing prostate cancer (78-81). Although a prospective study of Finnish men found that low serum 25(OH)D levels were associated with earlier and more aggressive prostate cancer development (82), another prospective study of men from Finland, Norway and Sweden found a U-shaped relationship between serum 25(OH)D levels and prostate cancer risk. In that study serum 25(OH)D concentrations of 19 nmol/L or lower and 80 nmol/L or higher were associated with higher prostate cancer risk (83). Further research is needed to determine the nature of the relationship between vitamin D nutritional status and prostate cancer risk.
Insulin-dependent diabetes mellitus (IDDM; type 1 diabetes mellitus), multiple sclerosis (MS), and rheumatoid arthritis (RA) are examples of autoimmune diseases. Autoimmune diseases occur when the body mounts an immune response against its own tissue, rather than a foreign pathogen. In IDDM, insulin-producing beta-cells of the pancreas are the target of the inappropriate immune response. In MS, the targets are the myelin-producing cells of the central nervous system, and in RA, the targets are the collagen-producing cells of the joints (84). Autoimmune responses are mediated by immune cells called T cells. The biologically active form of vitamin D, 1,25(OH)2D, has been found to modulate T cell responses, such that the autoimmune responses are diminished. Treatment with 1,25(OH)2D has beneficial effects in animal models of IDDM, MS, and RA. Epidemiological studies have found that the prevalence of IDDM, MS, and RA increases as latitude increases, suggesting that lower exposure to UVB radiation and associated decreases in endogenous vitamin D synthesis may play a role in the pathology of these diseases. The results of several prospective cohort studies also suggest that adequate vitamin D intake may decrease the risk of autoimmune diseases. A prospective cohort study of children born in Finland during the year 1966 and followed for thirty years found that those who received supplemental vitamin D during the first year of life had a significantly lower risk of developing IDDM, while children suspected of developing rickets (severe vitamin D deficiency) during the first year of life had a significantly higher risk of developing IDDM (85). Vitamin D deficiency has also been implicated in MS. A recent case-control study in U.S. military personnel, including 257 cases of diagnosed MS, found that white subjects in the highest quintile of serum 25(OH)D (>99.1 nmol/L) had a 62% lower risk of developing MS (86). A relationship between this indicator of vitamin D status and MS was not observed in blacks or Hispanics, but the power to detect such an association was limited by small sample sizes and overall low serum 25(OH)D concentrations (86). In two large cohorts of U.S. women followed for at least ten years, vitamin D supplement use was associated with a significant reduction in the risk of developing MS (87). Similarly, postmenopausal women with the highest total vitamin D intakes were at significantly lower risk of developing RA after 11 years of follow-up than those with the lowest intakes (88). Thus, evidence from both animal model studies and human epidemiological studies suggests that maintaining sufficient vitamin D levels may help decrease the risk of several autoimmune diseases.
Hypertension (High Blood Pressure)
The results of epidemiological and clinical studies suggest an inverse relationship between serum 1,25(OH)2D levels and blood pressure, which may be explained by recent findings that 1,25(OH)2D decreases the expression of the gene encoding renin (see Function). Data from epidemiological studies suggest that conditions that decrease vitamin D synthesis in the skin, such as having dark-colored skin or living in temperate latitudes, are associated with increased prevalence of hypertension (89). A controlled clinical trial in 18 hypertensive men and women living in the Netherlands found that exposure to UVB radiation three times weekly for six weeks during the winter increased serum 25(OH)D levels and significantly decreased 24-hour ambulatory systolic and diastolic blood pressure measurements by an average of 6 mm Hg (90). In randomized controlled trials of vitamin D supplementation, a combination of 1,600 IU/day of vitamin D and 800 mg/day of calcium for eight weeks significantly decreased systolic blood pressure in elderly women by 9% compared to calcium alone (91), but supplementation with 400 IU of vitamin D daily or a single dose of 100,000 IU of vitamin D did not significantly lower blood pressure in elderly men and women over a two-month period (92, 93). At present, data from controlled clinical trials are too limited to determine whether vitamin D supplementation will be effective in lowering blood pressure or preventing hypertension.
Solar ultraviolet-B radiation (UVB; wavelengths of 290 to 315 nanometers) stimulates the production of vitamin D3 in the epidermis of the skin (94). Sunlight exposure can provide most people with their entire vitamin D requirement. Children and young adults who spend a short time outside two or three times a week will generally synthesize all the vitamin D they need to prevent deficiency. One study reported that serum vitamin D concentrations following exposure to 1 minimal erythemal dose of simulated sunlight (the amount required to cause a slight pinkness of the skin) was equivalent to ingesting approximately 20,000 IU of vitamin D2 (95). People with dark-colored skin synthesize markedly less vitamin D on exposure to sunlight than those with light-colored skin (1). Additionally, the elderly have diminished capacity to synthesize vitamin D from sunlight exposure and frequently use sunscreen or protective clothing in order to prevent skin cancer and sun damage. The application of sunscreen with an SPF factor of 8 reduces production of vitamin D by 95%. In latitudes around 40 degrees north or 40 degrees south (Boston is 42 degrees north), there is insufficient UVB radiation available for vitamin D synthesis from November to early March. Ten degrees farther north or south (Edmonton, Canada) the “vitamin D winter” extends from mid-October to mid-March. According to Dr. Michael Holick, as little as 5-10 minutes of sun exposure on arms and legs or face and arms three times weekly between 11:00 am and 2:00 pm during the spring, summer, and fall at 42 degrees latitude should provide a light-skinned individual with adequate vitamin D and allow for storage of any excess for use during the winter with minimal risk of skin damage (37).
Vitamin D is found naturally in very few foods. Foods containing vitamin D include some fatty fish (mackerel, salmon, sardines), fish liver oils, and eggs from hens that have been fed vitamin D. In the U.S., milk and infant formula are fortified with vitamin D so that they contain 400 IU (10 mcg) per quart. However, other dairy products, such as cheese and yogurt, are not always fortified with vitamin D. Some cereals and breads are also fortified with vitamin D. Recently, orange juice fortified with vitamin D has been made available in the U.S. Accurate estimates of average dietary intakes of vitamin D are difficult because of the high variability of the vitamin D content of fortified foods (30). Vitamin D contents of some vitamin D-rich foods are listed in the table below in both international units (IU) and micrograms (mcg). For more information on the nutrient content of specific foods, search the USDA food composition database.
Most vitamin D supplements available without a prescription contain cholecalciferol (vitamin D3), which is more potent than ergocalciferol (vitamin D2) (2, 57, 96). Multivitamin supplements generally provide 400 IU (10 mcg) of vitamin D. Single ingredient vitamin D supplements may provide 400-2,000 IU of vitamin D, but 400 IU is the most commonly available dose. A number of calcium supplements may also provide vitamin D.
Vitamin D toxicity (hypervitaminosis D) induces abnormally high serum calcium levels (hypercalcemia), which could result in bone loss, kidney stones, and calcification of organs like the heart and kidneys if untreated over a long period of time. Hypercalcemia has been observed following daily doses of greater than 50,000 IU of vitamin D (38). When the Food and Nutrition Board of the Institute of Medicine established the tolerable upper intake level (UL) for vitamin D, published studies that adequately documented the lowest intake levels of vitamin D that induced hypercalcemia were very limited. Because the consequences of hypercalcemia are severe, the Food and Nutrition Board established a very conservative UL of 2,000 IU/day (50 mcg/day) for children and adults (see table below) (30). Research published since 1997 suggests that the UL for adults is likely overly conservative and that vitamin D toxicity is very unlikely in healthy people at intake levels lower than 10,000 IU/day (39, 97, 98). Vitamin D toxicity has not been observed to result from sun exposure (38). Certain medical conditions can increase the risk of hypercalcemia in response to vitamin D, including primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma (39). People with these conditions may develop hypercalcemia in response to any increase in vitamin D nutrition and should thus consult a qualified health care provider regarding any increase in vitamin D intake.
The following medications increase the metabolism of vitamin D and may decrease serum 25(OH)D levels: phenytoin (Dilantin), fosphenytoin (Cerebyx), phenobarbital (Luminal), carbamazepine (Tegretol), and rifampin (Rimactane). The following medications should not be taken at the same time as vitamin D because they can decrease the intestinal absorption of vitamin D: cholestyramine (Questran), colestipol (Colestid), orlistat (Xenical), mineral oil, and the fat substitute Olestra. The oral anti-fungal medication, ketoconazole, inhibits the 25(OH)D3-1-hydroxylase enzyme and has been found to reduce serum levels of 1,25(OH)D in healthy men. The induction of hypercalcemia by toxic levels of vitamin D may precipitate cardiac arrhythmia in patients on digitalis (Digoxin) (99, 100).
The Linus Pauling Institute recommends that generally healthy adults take 2,000 IU (50 mcg) of supplemental vitamin D daily. Most multivitamins contain 400 IU of vitamin D, and single ingredient vitamin D supplements are available for additional supplementation. Sun exposure, diet, skin color, and obesity have variable, substantial impact on body vitamin D levels. To adjust for individual differences and ensure adequate body vitamin D status, the Linus Pauling Institute recommends aiming for a serum 25-hydroxyvitamin D level of at least 80 nmol/L (32 ng/mL). Numerous observational studies have found that serum 25-hydroxyvitamin D levels of 80 nmol/L (32 ng/mL) and above are associated with reduced risk of bone fractures, several cancers, multiple sclerosis, and type 1 (insulin-dependent) diabetes. Infants, children, and adolescents should have a minimum daily intake of 400 IU (10 mcg) of vitamin D, a recommendation set by the American Academy of Pediatrics in 2008.
Older adults (> 50 years)
Daily supplementation with 2,000 IU (50 mcg) of vitamin D is especially important for older adults because aging is associated with a reduced capacity to synthesize vitamin D in the skin upon sun exposure.
Written in March 2004 by:
Updated in January 2008 by:
Reviewed in January 2008 by:
Last updated 11/7/08 Copyright 2000-2009 Linus Pauling Institute
The Linus Pauling Institute Micronutrient Information Center provides scientific information on health aspects of micronutrients and phytochemicals for the general public. The information is made available with the understanding that the author and publisher are not providing medical, psychological, or nutritional counseling services on this site. The information should not be used in place of a consultation with a competent health care or nutrition professional.
The information on micronutrients and phytochemicals contained on this Web site does not cover all possible uses, actions, precautions, side effects, and interactions. It is not intended as medical advice for individual problems. Liability for individual actions or omissions based upon the contents of this sit
Post-Op Duodenal Switch 1 Year Update
on July 2, 2009 7:05 pm
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Back on My Feet - Moving the Homeless Forward One...Browse pages: next >
on June 16, 2009 5:57 am
Back on My Feet - Moving the Homeless Forward One Step at a TimeBe the first to leave a comment.
Please pardon this intrusion asking for donations ... but it's a great cause that I wanted to let you know about! Donations of any size are much appreciated. Short goal total - $200.00 My stretch goal total - $500.00 - All donations are tax deductible - Back On My Feet tax-id number is 26-2109809.
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Thank you for your time and consideration!
How to Search This Site (Or any site) 1) Go to http://www.google.com and click the "Advanced Search" link Tips: Want to see ALL posts by a person (as opposed to only the Latests posts within the current forum)?
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Want to see ALL posts by a person (as opposed to only the Latests posts within the current forum)?
Well I'm almost 40 and have been fighting my weight issues since junior high. I guess it hit home the first time I saw my doctor had checked off morbidly obese on my check up sheet. I've lost large amounts of weight a few times in my life but have never kept anything off more than 6 months.
Being overweight is a family trait. My parents and one sister have also had long time weight issues.
Reasons I chose the Duodenal Switch for my WLS:
I'm an analyst by trade and I did my research. The medical documentation showing the Duodenal Switch surgery was the best overall WLS long term was overwhelming. I then of course had worries about all the things people claim happens if you get the DS.
You smell ... you are in the bathroom all the time ... you will get malnourished etc. etc.
That's where an online community such as the DS board here or a local support group of people who have actually had the surgery and are living with it come into play. I personally met 10-20 people who had the DS prior to getting it. I asked questions, observed them and knew it was the surgery for me.
Fact is most of the bad things people say about the DS were FALSE. I believe now they are mostly the product of people pushed into the RNY because so many docs do it and far fewer have the training needed for the DS procedure.
One other thing I wanted to note here .... DON'T LET YOUR INSURANCE COMPANY DECIDE WHAT IS BEST FOR YOU!
I knew I could lose weight since I'd lost 100lbs a few times in the past. I needed something to help me keep it off long term. The DS malabsorbtion was the key to long term WL for me.
If you think the DS is the procedure for you then fight for it! You have to live with this surgery for the rest of your life. If your insurance covers WLS and has no WLS Exclusion you can usually fight for the DS. Get approved for the RNY then appeal to get it changed to a DS. If they deny you use any external appeal process available to you and it will most likely be overturned due to the documentation available about the success of the DS.
The DS is not only for the super high BMI's. It's for anyone that qualifies for WLS. The DS is actually more customizable since the common channel can be adjusted and the size of the stomach sleeve can be adjusted based on the amount of weight needed to lose.