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The Significance of Vitamin D Supplementation
John Claydon D.Hom
The importance of vitamin D is often over-looked. Vitamin D is a hormone like substance that is manufactured in the skin in response to sunlight exposure. Failure to obtain a least a few minutes a day of direct sunlight exposure on the skin (The Sun will not be high enough in the sky to enable UVB rays to get through to generate vitamin D in the skin for several months a year in northern climates such as northern Europe, UK, northern USA) etc will result in a deficiency of vitamin D. Deficiencies have now been linked to a multiple array of diseases and a greatly increased incidence of cancer. These diseases include arthritis, muscle weakness, multiple sclerosis, and other auto-immune disorders. In fact studies have now indicated that mortality from all causes is significantly increased in vitamin D deficient persons. This is not surprising when one considers the multitude of biochemical reactions that cannot complete without vitamin D. Even the failure to integrate calcium and magnesium that was established to be a result of vitamin D deficiency has far reaching implications for getting the health right.
One can take a broad-spectrum of nutrients and be conscientious about ones diet, but failure to address the Vitamin D issue will result in health problems, and is so commonly overlooked. This is especially true of the elderly and persons who already have compromised health, who tend not to venture outside much. This problem has been compounded by false information about the actual amount of vitamin D that we need. There have been warnings by health authorities in the past, not to take more than about 800 IU a day...but that sort of dose is obtained just from partial exposure to the sun when it is high in the sky for a few minutes. Much research has now found that larger supplemental doses are required to overcome vitamin D deficiency syndrome.
The general advice based on this knowledge and client experience, also clinical trails is to supplement initially with around 2000IU-4000IU per day for a few months, thereafter about 2000 IU is usually sufficient. Vitamin D is stored in the body. So for example, if you are exposed to strong sunlight without sunscreen for 30 minutes a day for a few weeks then the body will store enough vitamin D to last possibly a couple months.
Safety Issues (For fuller information see main article below)
In the past there were reports of toxicity of higher doses. Further investigation has found that most or all of these where for Vitamin D2, ergocalciferol. Vitamin D3 or cholecalciferol is the form natural to the body. And is not toxic, in doses below 10,000 IU.
In very rare cases persons can be hypersensitive to Vitamin D, and is usually confined to persons with such conditions are sarcoidosis, oat cell carcinoma of the lung, and non–Hodgkin's lymphoma—although other illness, such as primary hyperparathyroidism, can cause the syndrome. Periodic measurements of 25(OH)D levels and serum calcium will alert the physician to the need to do more tests, such as 1,25(OH)2D3 or PTH. For full details of safety, dose and therapeutic potential see full product information linked below.
Example Directions (for 2,000 IU capsules) Click here for order information
Also for a vitamin D supplement with Boron and colloidal minerals, for arthritis, bone disorders, auto-immune disorders click here
Vitamin D is required on a daily basis unless you expose at least face and bare arms to the sun out of doors, when the sun is at least 50 degrees above the horizon, for at least ten minutes each day, without sunscreen. In Northern countries such as the UK this is not possible for about six months a year. In the absence of the above suggested use is:
Adults Below the age of 50, typically one capsule daily.
Adults over the age of 50, typically two capsules daily
Children under the age of one, if not receiving sunlight as described, typically half a capsule daily. (Capsule may be opened and contents of half mixed with feed) Use proportionally less if Vitamin D is already added to formula feed. Vitamin D supplementation is not needed for babies if the mother is breast feeding and obtaining 4000-6000 IU Vitamin D from all sources, e.g. from sun exposure or taking this supplement.
Children 1 to 4 years old if not receiving the described sunlight typically one capsule every other day.
Children 4 to 10 years one capsules daily.
For housebound individuals with chronic health disorders higher doses are required, eg. 3 capsules daily for the first 6 months then 2 capsules daily.
Do not exceed stated dose, unless under medical supervision, i.e. have blood tested for 25(OH)D, and seeing what you need to do to keep your level around 50 ng/ml. This is a sensible measure for all suffering from long term Chronic health disorders.
Use of vitamin D in clinical practice
Alternative Medicine Review, March, 2008 by John J. Cannell, Bruce W. Hollis
The recent discovery from a meta-analysis of 18 randomized controlled trials that supplemental cholecalciferol (vitamin D) significantly reduces all-cause mortality emphasizes the medical, ethical, and legal implications of promptly diagnosing and adequately treating vitamin D deficiency. Not only are such deficiencies common, and probably the rule, vitamin D deficiency is implicated in most of the diseases of civilization. Vitamin D's final metabolic product is a potent, pleiotropic, repair and maintenance, seco-steroid hormone that targets more than 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. One of the most important genes vitamin D up-regulates is for cathelicidin, a naturally occurring broad-spectrum antibiotic.
Natural vitamin D levels, those found in humans living in a sun-rich environment, are between 40-70 ng/mL, levels obtained by few modern humans. Assessing serum 25-hydroxy-vitamin D (25(OH)D) is the only way to make the diagnosis and to assure treatment is adequate and safe. Three treatment modalities exist for vitamin D deficiency: sunlight, artificial ultraviolet B (UVB) radiation, and vitamin D supplementation. Treatment of vitamin D deficiency in otherwise healthy patients with 2,000-7,000 IU vitamin [D.sub.3] per day should be sufficient to maintain year-round 25(OH)D levels between 40-70 ng/mL. In those with serious illnesses associated with vitamin D deficiency, such as cancer, heart disease, multiple sclerosis, diabetes, autism, and a host of other illnesses, doses should be sufficient to maintain year-round 25(OH)D levels between 55-70 ng/ mL. Vitamin D-deficient patients with serious illness should not only be supplemented more aggressively than the well, they should have more frequent monitoring of serum 25(OH) D and serum calcium. Vitamin D should always be adjuvant treatment in patients with serious illnesses and never replace standard treatment. Theoretically, pharmacological doses of vitamin D (2,000 IU/kg/day for three days) may produce enough of the naturally occurring antibiotic cathelicidin to cure common viral respiratory infections, such as influenza and the common cold, but such a theory awaits further science. (Altern Med Rev 2008; 13(1):6-20)
Introduction
A recent meta-analysis of 18 randomized controlled trials (RCT) found that cholecalciferol (vitamin D) significantly reduced total mortality. (1) This discovery is all the more remarkable because of the relatively low doses of vitamin D used (mean close 528 IU (13 mcg)) and because the finding persisted across a number of subgroup analyses. In spite of the low doses used and the short duration of the trials, vitamin D's mortality reduction was seven percent. (2) Indeed, the recent discovery that statins significantly increase 25-hydroxy-vitamin D (25(OH)D) levels raise the possibility that some--or all--of the mortality reduction of statins may be mediated through increases in vitamin D levels. (3,4)
Lappe et al recently reported the first RCT of vitamin D in preventing internal cancers and found a 60-percent reduction in such cancers by increasing baseline 25(OH)D levels from 29 ng/mL to 38 ng/mL with 1,100 IU (28 mcg) per day. (5) Baseline and treatment-induced serum 25(OH)D levels were strong and independent predictors of cancer risk. Lappe et al's study left open the possibility that higher doses and higher treatment-induced 25(OH)D levels might prevent even more cancers. (Note that 25(OH)D levels are reported in the literature as either ng/mL or nmol/L; 1.0 ng/mL equals 2.5 nmol/L.)
Besides cancer, vitamin D deficiency is associated with cardiovascular disease, hypertension, stroke, diabetes, multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, osteoporosis, periodontal disease, macular degeneration, mental illness, propensity to fall, and chronic pain. (6-10) A recent review presented considerable evidence that influenza epidemics, and perhaps even the common cold, are brought on by seasonal deficiencies in antimicrobial peptides (AMP), such as cathelicidin, secondary to seasonal deficiencies in vitamin D. (11) Results of an RCT support the theory, finding 2,000 IU of vitamin D/day for one year virtually eliminated self-reported incidence of colds and influenza (Figure 1). (12) Even the current triple childhood epidemics of autism (13) (Figure 2), asthma, (14) and type 1 diabetes, (15) all of which blossomed after sun-avoidance advice became widespread, might be the tragic and iatrogenic sequela of gestational or early childhood vitamin D deficiencies brought on by medical advice to avoid the sun. (Most sun screens are absorbed into the skin and blood and are quite likely toxic. Use of coconut oil is ideal, it protects skin from burning and does not block the crucially beneficial ultra-violet A and B. ed)
Claims that vitamin D may help prevent such a wide variety of diseases seem incredible until one realizes vitamin D is not a vitamin; rather, it is the only known substrate for a potent, pleiotropic, repair and maintenance, seco-steroid hormone with a single endocrine function, but multiple autocrine functions. Previously, many practitioners thought vitamin D's activity was principally its endocrine function--the regulation of serum calcium--and was thus mainly involved in bone metabolism. Indeed, the classic endocrine function of vitamin D begins when the kidney hydroxylates 25(OH)D into 1,25[(OH).sub.2]D, which then acts, both directly and indirectly, to maintain serum calcium.
However, in the last ten years, it has become clear the vitamin D steroid hormone system includes more than the classic endocrine pathway used to preserve calcium economy. (16) The enzyme that further hydroxylates 25(OH)D to 1,25[(OH).sub.2]D (activated vitamin D, the steroid hormone) is present in a wide variety of human tissues other than kidney. 1,25[(OH).sub.2]D is autonomously made in tissues and directly affects numerous cells via its autocrine, and presumed paracrine, functions. (17) Most organs show evidence of end organ responsiveness to 1,25[(OH).sub.2]D. (18) Like all steroid hormones, 1,25[(OH).sub.2]D acts as a molecular switch, activating more than 200 target genes, thereby regulating gene expression. Thus, locally produced 1,25[(OH).sub.2]D exists in most tissues of the body, is under autonomous autocrine control, and has as many mechanisms of action as genes it targets. This explains why the same substance may have a role in preventing cancer, influenza, autism, asthma, multiple sclerosis, and cardiovascular disease, not just curing rickets and osteomalacia (Figure 3).
Such claims leave practitioners with understandable skepticism and multiple questions. Is vitamin D a cure-all? When should I recommend vitamin D? How much should I prescribe? What form of vitamin D should I use? How much do children need? How much do pregnant or breastfeeding women need? Is it appropriate to use higher doses of vitamin D as adjuvant treatment for any of the above diseases? How do I interpret vitamin D blood tests and which tests should I order? What is the risk of toxicity?
Another way to ask many of these questions is, "What is an ideal 25(OH)D level?" Levels needed to optimize intestinal calcium absorption (34 ng/mL) (19) are lower than those needed to optimize neuromuscular performance (38 ng/mL). (20) Recent pooled meta-analyses estimate 25(OH)D levels of 52 ng/mL are needed to effect a 50-percent reduction in the incidence of breast cancer. (21) Although some experts believe the lower limit of adequate 25(OH)D levels is in the low 30s, (22,23) others recommend a lower limit of 40 ng/mL; (24,25) there is certainly no scientific consensus.
Ideal levels are unknown but are probably close to levels present when the human genome evolved in sub-equatorial Africa. Natural levels, such as those found at the end of summer in 30 young men who spent the summer working outdoors, were around 50 ng/mL; (26) however, these levels are obtained by only a small fraction of people. (27) Furthermore, despite such summertime levels, at the end of winter 25(OH)D levels in 50 percent of these men dropped to less than 30 ng/mL, indicating a sun-induced level of 50 ng/mL at the end of summer is inadequate to maintain such a level during wintertime.
Another way to ask the "ideal 25(OH)D" question involves understanding vitamin D's unique pharmacokinetics. Unlike any other steroid hormone system, the substrate concentrations for the liver production of 25(OH)D are absolutely rate limiting. This means the liver enzymes that initially hydroxylate vitamin D to form 25(OH)D and the enzyme in tissue that generates 1,25[(OH).sub.2]D operate below their Michaelis-Menten constants throughout the full range of modern human substrate concentrations; i.e., the reactions follow first-order mass action kinetics. (28) The more vitamin D that is ingested, the more is converted into 25(OH)D, and the more is converted into 1,25[(OH).sub.2]D in the tissues. The reaction appears to be uncontrolled; an aberrant, totally unique, and potentially dangerous situation for a steroid hormone system. Imagine, for example, if cortisol, testosterone, progesterone, or estradiol levels were entirely dependent on the intake of their substrate, cholesterol.
Hollis et al recently explained this conundrum and concluded very few humans obtain enough vitamin D even if they take several thousand units per day. (29) Hollis et al studied the pharmacokinetics of the parent compound, vitamin D, and its first metabolic product, 25(OH)D, in two groups; Hawaiians with significant sun exposure and lactating women receiving 6,400 IU of supplemental vitamin D per day. They found 25(OH)D levels had to exceed a minimum of 40 ng/ mL, and often 50 ng/mL, to begin to detect the parent compound in the blood and begin to normalize the kinetics of 25(OH)D production. In other words, when 25(OH)D levels > 40 ng/mL were achieved, the parent compound began to be detectable in the blood, the reactions became saturable and controlled (like other steroid hormone systems), and thus levels above 40 ng/mL appear to represent the lower limit of "normal" 25(OH) D levels.
This implies virtually everyone has a chronic 25(OH)D substrate deficiency, at least in the winter, and the absence of the parent vitamin D compound (cholecalciferol) in the blood means all available vitamin D is used for metabolic needs and none of it is stored. Because of this, most individuals have chronic substrate starvation, functional vitamin D deficiency, and thus, perhaps, higher risk for the "diseases of civilization."
The ideal 25(OH)D level continues to be debated in scientific circles and consensus awaits further science. However, do we wait for science to complete its work with highly seasonal 25(OH)D levels (Figure 4) that reflect sunlight deprivation, levels where vitamin D steroid pharmacokinetics are aberrant, or is it safer to wait with levels normally achieved by humans in a sunrich environment, levels where vitamin D's kinetics are normalized (>40 ng/mL)?
Once a practitioner is comfortable with ideal 25(OH)D levels being above 40 ng/mL, the answers to the questions posed above become fairly simple. Healthy humans should be supplemented with enough vitamin D or exposed to enough ultraviolet B (UVB) radiation to achieve natural 25(OH)D levels (40-70 ng/mL) year-round, whether they are infants, children, pregnant women, lactating women, healthy young adults, or the elderly.
What role vitamin D has in treating--rather than preventing--disease is largely unknown, but given vitamin D's genetic mechanism of action, it may have a significant role. For example, vitamin D reduces cellular proliferation, induces differentiation, induces apoptosis, and prevents angioneogenesis, each a laudable goal in cancer treatment. A simple risk-versus-benefit analysis suggests patients with a potentially fatal cancer (see below) may think it wise to maintain 25(OH)D levels in the high end of natural ranges (55-70 ng/mL), ranges that assure vitamin D's kinetics are normalized. While the RCTs needed to clarify vitamin D's role in the treatment of disease are being conducted, a strong case already exists for adequately diagnosing and aggressively treating vitamin D deficiency. (22,25,30)
Adult vitamin D deficiency is the rule rather than the exception in industrialized nations. (31-33) A high number of otherwise healthy children and adolescents are also vitamin D deficient. (34,35) Rickets, a disease of the industrial revolution, is being diagnosed more frequently, (36) especially in breast-fed infants. (37) Alarmingly, given mounting animal data that gestational vitamin D deficiency causes subtle but irreversible brain damage in mammalian offspring, (38,39) severe deficiencies are common in newborn infants and pregnant women, especially African-Americans. (40) A population-based study of 2,972 U.S. women of childbearing age found 42 percent of African-American women had 25(OH)D levels below 15 ng/mL, and 12 percent had levels below 10 ng/mL. (41)
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Furthermore, the definition of vitamin D deficiency changes almost yearly as research shows the low end of ideal 25(OH)D ranges are higher than were previously thought. The aforementioned prevalence studies used outdated reference values for low-end 25(OH) D ranges and therefore underestimate the incidence of vitamin D deficiency. Obviously, the higher the low end of the 25(OH)D cutoff point, the higher the percentage of the population defined as deficient. Only 10 percent of the subjects in any of the above studies had 25(OH) D levels > 40 ng/mL.
Vitamin D Metabolism and Physiology
Perhaps because the term "vitamin D" contains the word "vitamin" most people wrongly assume they can obtain adequate amounts by eating a healthy diet. The natural diets most humans consume, however, contain minimal vitamin D, unless those diets are rich in wild-caught fatty fish, sun-dried Shitake mushrooms, or wild reindeer meat. Small amounts of vitamin D are contained in fortified foods, such as fortified milk, some orange juices, and cereals, but such sources are minor contributors to vitamin D stores. Traditionally, the human vitamin D system began in the skin, not in the mouth.
Vitamin D normally enters the circulation after UVB from sunlight strikes 7-dehydro-cholesterol in the skin, converting it to vitamin [D.sub.3] or cholecalciferol (vitamin D). When taken by mouth, the body metabolizes vitamin D similarly to that generated in the skin. No matter how it arrives in the circulation, the liver readily hydroxylates vitamin D to 25(OH)D, the circulating form of vitamin D. Hundreds of tissues in the body use 25(OH)D as a substrate to make the end-product, 1,25[(OH).sub.2]D, known as activated vitamin D, a pleiotropic seco-steroid. If enough 25(OH)D substrate is available, multiple tissues are free to autonomously produce and locally regulate the amount of steroid needed for any particular disease state.
The skin's manufacture of vitamin D is extraordinarily rapid and remarkably robust; production after only a few minutes of sunlight easily exceeds dietary sources by an order of magnitude. Incidental sun exposure, not dietary intake, is the principal source of vitamin D stores and is a function of skin surface area exposed. (42,43) For example, when fair-skinned people sunbathe in the summer (one, full-body, minimal erythemal dose of UVB), they produce about 20,000 IU of vitamin D in 30 minutes, (44) the equivalent of drinking 200 glasses of milk (100 IU/8 oz. glass) or taking 50 standard multivitamins (400 IU/tablet) to obtain the same amount orally.
The fact that 20,000 IU vitamin D can be produced in the skin in 30 minutes of sun exposure, combined with vitamin D's basic genomic mechanism of action, raises profound questions. Why did nature develop a system that delivers huge quantities of a steroid precursor after only brief periods of sun exposure? Would natural selection evolve such a system if the remarkably high input that system achieved were unimportant? As humans evolved in a sun-rich environment (sub-equatorial Africa), is modern sunlight deprivation--and the resultant routinely low levels of this repair- and--maintenance steroid in tissues--a possible common cause of the diseases of civilization?
Factors Affecting Vitamin D Levels
Factors that can affect UVB exposure, and thus the skin's production of vitamin D, include latitude, season of the year, time of day, air pollution, cloud cover, melanin content of the skin, use of sunblock, age, and the extent of clothing covering the body. When the sun is low on the horizon, ozone, clouds, and particulate air pollution deflect UVB radiation away from the earth's surface. Therefore, cutaneous vitamin D production is effectively absent early and late in the day and for the entire day during several wintertime months at latitudes above 35 degrees, and impaired anytime the skies are polluted or cloudy.
Thus, vitamin D deficiency is more common the further poleward the population. For example, Boston, Massachusetts (latitude 42 degrees), has a four-month "vitamin D winter" centered around the winter solstice, when insufficient UVB penetrates the atmosphere to trigger skin production. This becomes an even longer period when the fall and late winter months are included, when sufficient UVB only penetrates around solar noon. In northern Europe and Canada, the "vitamin D winter" can extend for six months. Furthermore, properly applied sunblock, common window glass in homes and cars, and clothing all effectively block UVB radiation--even in the summer. Those who avoid sunlight--at any latitude--are at risk of vitamin D deficiency any time of the year. For example, a surprisingly high incidence of vitamin D deficiency exists in Miami, Florida, despite its sunny weather and subtropical latitude. (45)
African-Americans, the elderly, and the obese face added risk. Because melanin in the skin acts as an effective and ever-present sunscreen, dark-skinned people need much longer UVB exposure times to generate the same 25(OH)D stores as fair-skinned individuals. (46) The elderly make much less vitamin D than 20-year-olds after exposure to the same amount of sunlight. (47) Body fat absorbs vitamin D, thus obesity is a major risk factor for deficiency, with obese African-Americans at an even higher risk. (48) Anyone who works indoors, lives at higher latitudes, wears excessive clothing, regularly uses sunblock, is dark-skinned, obese, aged, or who consciously avoids the sun is at high risk for vitamin D deficiency.
In the absence of a metabolic bone disease such as rickets, osteomalacia, or osteoporosis, most practitioners assume vitamin D deficiency is asymptomatic, although that may be changing. Complaints endemic to every practitioner's office, such as muscular weakness, a feeling of heaviness in the legs, chronic musculoskeletal pain, fatigue, or easy tiring may be symptoms of vitamin D deficiency. (49) Such complaints are extremely common, difficult to treat, and easy to dismiss, but they may indicate symptomatic vitamin D deficiency.
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Physical examination is usually unremarkable but may reveal undue pain on sternal or tibial pressure if deficiency is severe. The vast majority of cases appear normal on exam, although frequent infections, autoimmune illness, diabetes, cancer, heart disease, major depression, and a host of other "diseases of civilization" may be warning signs that deficiency has been present for many years. (22,25)
The aged may be wheelchair-bound secondary to vitamin D deficiency-induced myopathy, yet they typically recover mobility after treatment. (50) The recent strong association of low mood and cognitive impairment in the aged with vitamin D deficiency (51) suggests depressed mood and/or impaired cognition may be presenting symptoms. A blinded intervention trial found 4,000 IU vitamin D per day improved the mood of endocrinology outpatients, (52) but there are no interventional studies of its effects on cognition.
Even without physical signs or symptoms, the physician should screen those at risk. Obtaining and properly interpreting a serum 25(OH)D level is the only way to make the diagnosis. A 25(OH)D level should be obtained at least twice yearly on any patient at risk, once in the early spring for the nadir and once in the late summer for a peak level. (53) We recommend 25(OH)D levels be kept above 40 ng/mL year-round (Figure 5).
It is crucial to remember that serum 1,25[(OH).sub.2]D levels play no role in diagnosing vitamin D deficiency. The kidney tightly controls serum 1,25[(OH).sub.2]D levels, which are often normal or even elevated in vitamin D deficiency. Therefore, a patient with normal or high 1,25[(OH).sub.2]D serum levels but low 25(OH)D levels is vitamin D deficient despite high serum levels of the active hormone. Practitioners who rely on serum 1,25[(OH).sub.2]D levels to make the diagnosis of vitamin D deficiency will routinely miss it. (25)
Treatment of Vitamin D Deficiency
Three options exist for treatment of vitamin D deficiency: sunlight, artificial UVB light, and vitamin D supplements. An exposure of 10-15 minutes of full-body summer noon-day sun or artificial UVB radiation (such as tanning beds) will input more than 10,000 IU of vitamin D into the systemic circulation of most light-skinned adults. One or two such exposures per week should maintain 25(OH)D levels in an ideal range, but adequacy should be assured by 25(OH)D blood levels. Those who choose UVB light for vitamin D repletion, from either sunlight or artificial sources, should avoid sunburn, which is associated with malignant melanoma. Furthermore, they should understand that regular UV exposure ages the skin and increases the risk of nonmelanoma skin cancers.
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Information from The Vitamin D council
How Much Vitamin D?
If you refuse to see a physician, or can't find a knowledgeable one, purchase the 1000 IU/day vitamin D3 cholecalciferol pills that are available over-the-counter in North America. Take an average of two pills a day (50 ug or 2,000 IU) year around if you have some sun exposure. If you have little or no sun exposure, you will need to take more than 2,000 IU per day, how much more depends on your latitude of residence, skin pigmentation, and body weight. Generally speaking, the further you live away from the equator, the darker your skin, and the more you weigh, the more you will have to take to maintain healthy blood levels. For example, Dr. Cannell lives at latitude 32 degrees, weighs 220 pounds, and has fair skin. In the late fall and winter he takes 5,000 IU per day, in the early fall and spring he takes 2,000 IU per day, and in the summer he regularly sunbathes for a few minutes most days, and thus takes no vitamin D most days in the summer. The only way you can know how much you vitamin D you need to take is by repeatedly getting your blood tested, called a 25(OH)D test, and seeing what you need to do to keep your level around 50 ng/mL.
Infants and Children
Infants and children under the age of one, should obtain a total of 1,000 IU (25 mcg) per day from their formula, sun exposure, or supplements. As most breast milk contains little or no vitamin D, breast-fed babies should take 1,000 IU per day as a supplement unless they are exposed to sunlight. The only exception to this are lactating mothers who either get enough sun exposure or take enough vitamin D (usually 4,000–6,000 IU per day) to produce breast milk that is rich in vitamin D. Formula fed babies should take an extra 600 IU per day until they are weaned and then take 1,000 IU a day, as advised below.
Children over the age of 1 year, and less than 4 years of age, should take 1,500 IU vitamin D per day, depending on body weight, latitude or residence, skin pigmentation, and sun exposure.
Children over the age of 4, and less than 10 years of age, should take 2,000 IU per day, unless they get significant sun exposure. On the days they are outside in the sun, they do not need to take any; in the winter they will need to take 2,000 IU every day.
Children over the age of 10 years old should follow instructions for adults detailed above.
Vitamin D Upper Limit
If you absolutely avoid the sun, you should have your 25(OH)D level measured and remember that a maximum of two pills a day (50 ug or 2,000 IU) is the upper limit (UL) currently listed by the Food and Nutrition Board as the amount not to exceed unless under the care of a physician. When it comes to vitamin D, the right amount is good, but a lot is not better and can be dangerous. However, 2,000 IU a day is simply not enough for many people to get the full benefit of vitamin D, nor is it enough to keep vitamin D levels around 50 ng/mL, especially in the winter.
Maintaining 25(OH)D Levels
If you are suffering from any of the diseases associated with vitamin D deficiency you need to be under the care of a knowledgeable physician. Your physician needs to replete your vitamin D system with sunlight, artificial light, oral vitamin D, or a combination of the three, while treating your vitamin D deficiency illnesses using conventional means. Regardless of the method used, we believe your physician should be certain your 25(OH)D levels are maintained between 35–65 ng/mL.
For those who do not fear the sun, judiciously expose as much skin as possible to direct midday sunlight for 1/4 the time it takes for one's skin to turn red during those months when the proper ultraviolet light occurs at one's latitude (usually late spring, summer and early fall). Do not get sunburned. Vitamin D production is already maximized before your skin turns pink and further exposure does not increase levels of vitamin D but may increase your risk of skin cancer. Black patients may need five to ten times longer in the sun than white patients, depending on skin type. After several months of judicious sun exposure, a 25(OH)D level should again be obtained to ensure levels between 35–65 ng/mL.
Several artificial light sources are commercially available that provide the proper wavelength for vitamin D production. Sperti makes a good UVB lamp and even has data available on the vitamin D production of its sunlamps.
As far as vitamin D supplements are concerned, we believe cholecalciferol is the preferred oral form of vitamin D, as it is the compound your skin makes naturally when you go in the sun. It is more potent and perhaps even safer than the synthetic analog, ergocalciferol, in more common use. Cholecalciferol is 1.7 times more efficient at raising 25(OH)D levels than is ergocalciferol.
Trang HM, Cole DE, Rubin LA, Pierratos A, Siu S, Vieth R. Evidence that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently than does vitamin D2. Am J Clin Nutr. 1998 Oct;68(4):854–8.
Calcitriol Contraindicated in VDDS (Vitamin D deficiency syndrome)
Ergocalciferol (vit D2) has been used safely by physicians for years (However vitamin D3, is better absorbed are the safest form ed) for a variety of indications. Unfortunately, when doctors don't prescribe ergocalciferol, they sometimes prescribe calcitriol or newer analogs of calcitriol, costing thousands of times more than cholecalciferol. Calcitriol, and its analogs, are contraindicated in vitamin D deficiency because they may cause hypercalcemia and they fail to address the real problem: low stores of 25(OH)D. Cholecalciferol repletes the vitamin D system by filling up your vitamin D tank with 25(OH)D, the vitamin D fuel. Vieth R. The pharmacology of vitamin D, including fortification strategies. In:Feldman D, Glorieux F, eds. Vitamin D, Chapter 61, in press, 2nd ed. Academic Press, San Diego.
Giving calcitriol, or its analogs, for vitamin D deficiency is like shooting ether into your engine to keep your car running. In addition, they pose a significant risk of hypercalcemia (high blood calcium). If you have a simple vitamin D deficiency and your doctor insists on prescribing calcitriol or an expensive analog of vitamin D (other than cholecalciferol or ergocalciferol), find another doctor.
Hypersensitivity Not Toxicity
Vitamin D hypersensitivity syndromes are often mistaken for vitamin D toxicity. This rare syndrome occurs when abnormal tissue subvert the kidney's normal regulation of endocrine 1,25(OH)2D3 (calcitriol) production. Aberrant tissues, usually granulomatous in nature, convert 25(OH)D into 1,25(OH)2D3 causing high blood calcium. The most common of such conditions are sarcoidosis, oat cell carcinoma of the lung, and non–Hodgkin's lymphoma—although other illness, such as primary hyperparathyroidism, can cause the syndrome. Periodic measurements of 25(OH)D levels and serum calcium will alert the physician to the need to do more tests, such as 1,25(OH)2D3 or PTH.
Toxicity is simply not a concern in doses below 10,000 units a day. Restoring physiological serum levels of 25(OH)D will help many more patients than it will hurt.
John Jacob Cannell MD Executive Director. For more information from the Vitamin D council click here
Efficacy and safety of vitamin D3 intake exceeding the lowest observed adverse effect level
Vieth R, Chan PC, MacFarlane GD.
Mount Sinai Hospital, Toronto, Ontario, Canada. rvieth@...
BACKGROUND: The Food and Nutrition Board of the National Academy of Sciences states that 95 microg vitamin D/d is the lowest observed adverse effect level (LOAEL).
OBJECTIVE: Our objective was to assess the efficacy and safety of prolonged vitamin D3 intakes of 25 and 100 microg (1000 and 4000 IU)/d. Efficacy was based on the lowest serum 25-hydroxyvitamin D [25(OH)D] concentration achieved by subjects taking vitamin D3; potential toxicity was monitored by measuring serum calcium concentrations and by calculating urinary calcium-creatinine ratios. DESIGN: Healthy men and women (n = 61) aged 41 +/- 9 y (mean +/- SD) were randomly assigned to receive either 25 or 100 microg vitamin D3/d for 2-5 mo, starting between January and February. Serum 25(OH)D was measured by radioimmunoassay.
RESULTS: Baseline serum 25(OH)D was 40.7 +/- 15.4 nmol/L (mean +/- SD). From 3 mo on, serum 25(OH)D plateaued at 68.7 +/- 16.9 nmol/L in the 25-microg/d group and at 96.4 +/- 14.6 nmol/L in the 100-microg/d group. Summertime serum 25(OH)D concentrations in 25 comparable subjects not taking vitamin D3 were 46.7 +/- 17.8 nmol/L. The minimum and maximum plateau serum 25(OH)D concentrations in subjects taking 25 and 100 microg vitamin D3/d were 40 and 100 nmol/L and 69 and 125 nmol/L, respectively. Serum calcium and urinary calcium excretion did not change significantly at either dosage during the study. CONCLUSIONS: The 100-microg/d dosage of vitamin D3 effectively increased 25(OH)D to high-normal concentrations in practically all adults and serum 25(OH)D remained within the physiologic range; therefore, we consider 100 microg vitamin D3/d to be a safe intake.
For a another full article on vitamin D please see The Healing Power of Sunlight & Vitamin D
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