天涯小站 2.0

 找回密码
 注册
搜索
查看: 1775|回复: 1

The Miracle of Vitamin D (ZT)

[复制链接]
发表于 2009-5-21 00:14:30 | 显示全部楼层 |阅读模式
这一篇里有很多有用的信息。由于篇幅较长,所以单开一线贴出。建议大家耐心读完全文。
AF

-----------------------------------------------------------------------------------------

The Miracle of Vitamin D (ZT)

By Krispin Sullivan, CN
NOTE: Be sure to read the Winter           2000 and Fall 2002 updates to this article,           at the end of the original article.
        Contents
        
         
        The Miracle of Vitamin D         In April of 2000 a clinical observation published in Archives of           Internal Medicine caught my attention. Dr. Anu Prabhala and his           colleagues reported on the treatment of five patients confined to wheelchairs           with severe weakness and fatigue. Blood tests revealed that all suffered           from severe vitamin D deficiency. The patients received 50,000 IU vitamin           D per week and all became mobile within six weeks.1
         Dr. Prabhala's research sparked my interest and led to a search for           current information on vitamin D, how it works, how much we really need           and how we get it. The following is a small part of the important information           that I found.
         Any discussion of vitamin D must begin with the discoveries of the           Canadian-born dentist Weston A. Price. In his masterpiece Nutrition           and Physical Degeneration, Dr. Price noted that the diet of isolated,           so-called "primitive" peoples contained "at least ten times" the amount           of "fat-soluble vitamins" as the standard American diet of his day.2           Dr. Price determined that it was the presence of plentiful amounts of           fat-soluble vitamins A and D in the diet, along with calcium, phosphorus           and other minerals, that conferred such high immunity to tooth decay           and resistance to disease in nonindustrialized population groups.
         Today another Canadian researcher, Dr. Reinhold Vieth, argues convincingly           that current vitamin D recommendations are woefully inadequate. The           recommended dose of 200-400 international units (IU) will prevent rickets           in children but does not come close to the optimum amount necessary           for vibrant health.3 According to Dr. Vieth, the minimal           daily requirement of vitamin D should be in the range of 4,000 IU from           all sources, rather than the 200-400 currently suggested, or ten times           the Recommended Daily Allowance (RDA). Dr. Vieth's research perfectly           matches Dr. Price's observations of sixty years ago!
        Vitamin D From Sunlight          Pick up any popular book on vitamins and you will read that ten minutes           of daily exposure of the arms and legs to sunlight will supply us with           all the vitamin D that we need. Humans do indeed manufacture vitamin           D from cholesterol by the action of sunlight on the skin but it is actually           very difficult to obtain even a minimal amount of vitamin D with a brief           foray into the sunlight.4,5
         Ultraviolet (UV) light is divided into 3 bands or wavelength ranges,           which are referred to as UV-C, UV-B and UV-A.6 UV-C is the           most energetic and shortest of the UV bands. It will burn human skin           rapidly in extremely small doses. Fortunately, it is completely absorbed           by the ozone layer. However, UV-C is present in some lights. For this           reason, fluorescent and halogen and other specialty lights may contribute           to skin cancer.
         UV-A, known as the "tanning ray," is primarily responsible for darkening           the pigment in our skin. Most tanning bulbs have a high UV-A output,           with a small percentage of UV-B. UV-A is less energetic than UV-B, so           exposure to UV-A will not result in a burn, unless the skin is photosensitive           or excessive doses are used. UV-A penetrates more deeply into the skin           than UV-B, due to its longer wavelength. Until recently, UV-A was not           blocked by sunscreens. It is now considered to be a major contributor           to the high incidence of non-melanoma skin cancers.7 Seventy-eight           percent of UV-A penetrates glass so windows do not offer protection.         
         The ultraviolet wavelength that stimulates our bodies to produce vitamin           D is UV-B. It is sometimes called the "burning ray" because it is the           primary cause of sunburn (erythema). However, UV-B initiates beneficial           responses, stimulating the production of vitamin D that the body uses           in many important processes. Although UV-B causes sunburn, it also causes           special skin cells called melanocytes to produce melanin, which is protective.           UV-B also stimulates the production of Melanocyte Stimulating Hormone           (MSH), an important hormone in weight loss and energy production.8
         The reason it is difficult to get adequate vitamin D from sunlight           is that while UV-A is present throughout the day, the amount of UV-B           present has to do with the angle of the sun's rays. Thus, UV-B is present           only during midday hours at higher latitudes, and only with significant           intensity in temperate or tropical latitudes. Only 5 percent of the           UV-B light range goes through glass and it does not penetrate clouds,           smog or fog.
         Sun exposure at higher latitudes before 10 am or after 2 pm will cause           burning from UV-A before it will supply adequate vitamin D from UV-B.           This finding may surprise you, as it did the researchers. It means that           sunning must occur between the hours we have been told to avoid. Only           sunning between 10 am and 2 pm during summer months (or winter months           in southern latitudes) for 20-120 minutes, depending on skin type and           color, will form adequate vitamin D before burning occurs.9
         It takes about 24 hours for UV-B-stimulated vitamin D to show up as           maximum levels of vitamin D in the blood. Cholesterol-containing body           oils are critical to this absorption process.10 Because the           body needs 30-60 minutes to absorb these vitamin-D-containing oils,           it is best to delay showering or bathing for one hour after exposure.           The skin oils in which vitamin D is produced can also be removed by           chlorine in swimming pools.
         The current suggested exposure of hands, face and arms for 10-20 minutes,           three times a week, provides only 200-400 IU of vitamin D each time           or an average of 100-200 IU per day during the summer months. In order           to achieve optimal levels of vitamin D, 85 percent of body surface needs           exposure to prime midday sun. (About 100-200 IU of vitamin D is produced           for each 5 percent of body surface exposed, we want 4,000 iu.) Light           skinned people need 10-20 minutes of exposure while dark skinned people           need 90-120 minutes.11
         Latitude and altitude determine the intensity of UV light. UV-B is           stronger at higher altitudes. Latitudes higher than 30° (both north           and south) have insufficient UV-B sunlight two to six months of the           year, even at midday.12 Latitudes higher than 40° have insufficient           sunlight to achieve optimum levels of D during six to eight months of           the year. In much of the US, which is between 30° and 45° latitude,           six months or more during each year have insufficient UV-B sunlight           to produce optimal D levels. In far northern or southern locations,           latitudes 45° and higher, even summer sun is too weak to provide optimum           levels of vitamin D.13-15 A simple meter is available to           determine UV-B levels where you live.
         Vitamin D From Food          What the research on vitamin D tells us is that unless you are a fisherman,           farmer, or otherwise outdoors and exposed regularly to sunlight, living           in your ancestral latitude (more on this later), you are unlikely to           obtain adequate amounts of vitamin D from the sun. Historically the           balance of one's daily need was provided by food. Primitive peoples           instinctively chose vitamin-D-rich foods including the intestines, organ           meats, skin and fat from certain land animals, as well as shellfish,           oily fish and insects. Many of these foods are unacceptable to the modern           palate.
        For food sources to provide us with D the source must be sunlight exposed.           With exposure to UV-B sunlight, vitamin D is produced from fat in the           fur, feathers, and skin of animals, birds and reptiles. Carnivores get           additional D from the tissues and organs of their prey. Lichen contains           vitamin D and may provide a source of vitamin D in the UV-B sunlight-poor           northern latitudes.16 Vitamin D content will vary in the           organs and tissues of animals, pigs, cows, and sheep, depending on the           amount of time spent in UV-B containing sunlight and/or how much D is           given as a supplement. Poultry and eggs contain varying amounts of vitamin           D obtained from insects, fishmeal, and sunlight containing UV-B or supplements.           Fish, unlike mammals, birds and reptiles, do not respond to sunlight           and rely on vitamin D found in phytoplankton and other fish. Salmon           must feed on phytoplankton and fish in order to obtain and store significant           vitamin D in their fat, flesh, skin, and organs. Thus, modern farm-raised           salmon, unless artificially supplemented, may be a poor source of this           essential nutrient.
        Modern diets usually do not provide adequate amounts of vitamin D;17           partly because of the trend to low fat foods and partly because we no           longer eat vitamin-D-rich foods like naturally reared poultry and fatty           fish such as kippers, and herring. Often we are advised to consume the           egg white while the D is in the yolk or we eat the flesh of the fish           avoiding the D containing skin, organs and fat. Sun avoidance combined           with reduction in food sources contribute to escalating D deficiencies.           Vegetarian and vegan diets are exceptionally poor or completely lacking           in vitamin D predisposing to an absolute need for UV-B sunlight. Using           food as one's primary source of D is difficult to impossible.
        Vitamin D Miracles         Sunlight and vitamin D are critical to all life forms. Standard textbooks           state that the principal function of vitamin D is to promote calcium           absorption in the gut and calcium transfer across cell membranes, thus           contributing to strong bones and a calm, contented nervous system. It           is also well recognized that vitamin D aids in the absorption of magnesium,           iron and zinc, as well as calcium.
         Actually, vitamin D does not in itself promote healthy bone. Vitamin           D controls the levels of calcium in the blood. If there is not enough           calcium in the diet, then it will be drawn from the bone. High levels           of vitamin D (from the diet or from sunlight) will actually demineralize           bone if sufficient calcium is not present.
         Vitamin D will also enhance the uptake of toxic metals like lead,           cadmium, aluminum and strontium if calcium, magnesium and phosphorus           are not present in adequate amounts.18 Vitamin D supplementation           should never be suggested unless calcium intake is sufficient or supplemented           at the same time.
         Receptors for vitamin D are found in most of the cells in the body           and research during the 1980s suggested that vitamin D contributed to           a healthy immune system, promoted muscle strength, regulated the maturation           process and contributed to hormone production.
         During the last ten years, researchers have made a number of exciting           discoveries about vitamin D. They have ascertained, for example, that           vitamin D is an antioxidant that is a more effective antioxidant than           vitamin E in reducing lipid peroxidation and increasing enzymes that           protect against oxidation.19;20
         Vitamin D deficiency decreases biosynthesis and release of insulin.21           Glucose intolerance has been inversely associated with the concentration           of vitamin D in the blood. Thus, vitamin D may protect against both           Type I and Type II diabetes.22
         The risk of senile cataract is reduced in persons with optimal levels           of D and carotenoids.23
         PCOS (Polycystic Ovarian Syndrome) has been corrected by supplementation           of D and calcium.24
         Vitamin D plays a role in regulation of both the "infectious" immune           system and the "inflammatory" immune system.25
         Low vitamin D is associated with several autoimmune diseases including           multiple sclerosis, Sjogren's Syndrome, rheumatoid arthritis, thyroiditis           and Crohn's disease.26;27
         Osteoporosis is strongly associated with low vitamin D. Postmenopausal           women with osteoporosis respond favorably (and rapidly) to higher levels           of D plus calcium and magnesium.28
         D deficiency has been mistaken for fibromyalgia, chronic fatigue or           peripheral neuropathy.1;28-30
         Infertility is associated with low vitamin D.31 Vitamin           D supports production of estrogen in men and women.32 PMS           has been completely reversed by addition of calcium, magnesium and vitamin           D.33 Menstrual migraine is associated with low levels of           vitamin D and calcium.81
         Breast, prostate, skin and colon cancer have a strong association           with low levels of D and lack of sunlight.34-38
         Activated vitamin D in the adrenal gland regulates tyrosine hydroxylase,           the rate limiting enzyme necessary for the production of dopamine, epinephrine           and norepinephrine. Low D may contribute to chronic fatigue and depression.39
         Seasonal Affective Disorder has been treated successfully with vitamin           D. In a recent study covering 30 days of treatment comparing vitamin           D supplementation with two-hour daily use of light boxes, depression           completely resolved in the D group but not in the light box group.40
         High stress may increase the need for vitamin D or UV-B sunlight and           calcium.41
         People with Parkinsons and Alzheimers have been found to have lower           levels of vitamin D.42;43
         Low levels of D, and perhaps calcium, in a pregnant mother and later           in the child may be the contributing cause of "crooked teeth" and myopia.           When these conditions are found in succeeding generations it means the           genetics require higher levels of one or both nutrients to optimize           health.44-47
         Behavior and learning disorders respond well to D and/or calcium combined           with an adequate diet and trace minerals.48;49
        Vitamin D and Heart Disease         Research suggests that low levels of vitamin D may contribute to or           be a cause of syndrome X with associated hypertension, obesity, diabetes           and heart disease.50 Vitamin D regulates vitamin-D-binding           proteins and some calcium-binding proteins, which are responsible for           carrying calcium to the "right location" and protecting cells from damage           by free calcium.51 Thus, high dietary levels of calcium,           when D is insufficient, may contribute to calcification of the arteries,           joints, kidney and perhaps even the brain.52-54
         Many researchers have postulated that vitamin D deficiency leads to           the deposition of calcium in the arteries and hence atherosclerosis,           noting that northern countries have higher levels of cardiovascular           disease and that more heart attacks occur in winter months.55-56
         Scottish researchers found that calcium levels in the hair inversely           correlated with arterial calcium-the more calcium or plaque in the arteries,           the less calcium in the hair. Ninety percent of men experiencing myocardial           infarction had low hair calcium. When vitamin D was administered, the           amount of calcium in the beard went up and this rise continued as long           as vitamin D was consumed. Almost immediately after stopping supplementation,           however, beard calcium fell to pre-supplement levels.27
         Administration of dietary vitamin D or UV-B treatment has been shown           to lower blood pressure, restore insulin sensitivity and lower cholesterol.58-60
         The Battle of the Bulge         Did you ever wonder why some people can eat all they want and not           get fat, while others are constantly battling extra pounds? The answer           may have to do with vitamin D and calcium status. Sunlight, UV-B, and           vitamin D normalize food intake and normalize blood sugar. Weight normalization           is associated with higher levels of vitamin D and adequate calcium.61           Obesity is associated with vitamin-D deficiency.62-64 In           fact, obese persons have impaired production of UV-B-stimulated D and           impaired absorption of food source and supplemental D.65
         When the diet lacks calcium, whether from D or calcium deficiency,           there is an increase in fatty acid synthase, an enzyme that converts           calories into fat. Higher levels of calcium with adequate vitamin D           inhibit fatty acid synthase while diets low in calcium increase fatty           acid synthase by as much as five-fold. In one study, genetically obese           rats lost 60 percent of their body fat in six weeks on a diet that had           moderate calorie reduction but was high in calcium. All rats supplemented           with calcium showed increased body temperature indicating a shift from           calorie storage to calorie burning (thermogenesis).61
         The Right Fats         The assimilation and utilization of vitamin D is influenced by the           kinds of fats we consume. Increasing levels of both polyunsaturated           and monounsaturated fatty acids in the diet decrease the binding of           vitamin D to D-binding proteins. Saturated fats, the kind found in butter,           tallow and coconut oil, do not have this effect. Nor do the omega-3           fats.66 D-binding proteins are key to local and peripheral           actions of vitamin D. This is an important consideration as Americans           have dramatically increased their intake of polyunsaturated oils (from           commercial vegetable oils) and monounsaturated oils (from olive oil           and canola oil) and decreased their intake of saturated fats over the           past 100 years.
         In traditional diets, saturated fats supplied varying amounts of vitamin           D. Thus, both reduction of saturated fats and increase of polyunsaturated           and monounsaturated fats contribute to the current widespread D deficiency.
         Trans fatty acids, found in margarine and shortenings used           in most commercial baked goods, should always be avoided. There is evidence           that these fats can interfere with the enzyme systems the body uses           to convert vitamin D in the liver.80
        Vitamin D Therapy         In my clinical practice, I test for vitamin-D status first. If D is           needed, I try to combine sunlight exposure with vitamin D and mineral           supplements.
         Single, infrequent, intense, skin exposure to UV-B light not only           causes sunburn but also suppresses the immune system. On the other hand,           frequent low-level exposure normalizes immune function, enhancing NK-cell           and T-cell production, reducing abnormal inflammatory responses typical           of autoimmune disorders, and reducing occurrences of infectious disease.26;67;68-71           Thus it is important to sunbathe frequently for short periods of time,           when UV-B is present, rather than spend long hours in the sun at infrequent           intervals. Adequate UV-B exposure and vitamin-D production can be achieved           in less time than it takes to cause any redness in the skin. It is never           necessary to burn or tan to obtain sufficient vitamin D.
         If sunlight is not available in your area because of latitude or season,           sunlamps made by Sperti can be used to provide a natural balance of           UV-B and UV-A. Used according to instructions, these lamps provide a           safe equivalent of sunlight and will not cause burning or even heavy           tanning. Tanning beds, on the other hand, are not acceptable as a means           of getting your daily dose of vitamin D because they provide high levels           of UV-A and very little UV-B.
         If you have symptoms of vitamin-D insufficiency or are unable to spend           time in the sun, due to season or lifestyle or prior skin cancer, consider           adding a supplement of 1,000 IU daily. Higher levels may be needed but           should be recommended and monitored by your health care practitioner           after testing serum 25(OH)D. 1,000 iu can be obtained from a concentrated           supplement or from 2 teaspoons of high quality cod liver oil. Both Carlson           Labs and Solgar make a 1,000 IU vitamin-D supplement naturally derived           from fish oil. (Do not attempt to obtain large amounts of vitamin D           from cod liver oil alone, as this would supply vitamin A in excessive           and possibly toxic amounts.)
         Supplementation is safe as long as sarcoidosis, liver or kidney           disease is not present and the diet contains adequate calcium, magnesium           and other minerals.
         Adequate calcium and magnesium, as well as other minerals,           are critical parts of vitamin D therapy. Without calcium and magnesium           in sufficient quantities, vitamin-D supplementation will withdraw calcium           from the bone and will allow the uptake of toxic minerals. Do not supplement           vitamin D and do not sunbathe unless you are sure you have sufficient           calcium and magnesium to meet your daily needs. Weston Price suggested           a minimum of 1,200-2,400 mg of calcium daily. Research suggests that           1,200-1,500 mg is adequate as a supplement for most adults, both men           and women. (Magnesium intake should be half that of calcium.)
         Two excellent sources of calcium in the human diet are dairy products           and bone broths.2 If the diet does not contain sufficient           amounts, you will need to add supplements. Bone meal, dolomite powder           or calcium and magnesium tablets (Solgar or Kal), or calcium carbonate           or lactate (Solgar, Kal, Now or Twinlab) are good calcium sources, inexpensive           and safe.74 All of these brands have been tested and found           to be free of lead and other heavy metals.
         In my experience, the forms of calcium given in supplements should           be equivalent to those found in food-bone meal as in the broth, calcium           lactate as in milk products and dolomite as in lime used to process           cornmeal products. These forms work most efficiently and with the least           cost for bone repletion and general repletion of serum calcium status.75           If your diet is high in protein, calcium lactate or carbonate is probably           a better source of calcium.
         Read the label carefully to see how much elemental calcium is contained           in each dose or tablet and make sure to take the right amount. If the           label says a serving size is three tablets and contains 1,000 mg of           calcium, you must take the full serving size to get that amount.
         Higher amounts of calcium are important for anyone diagnosed with           bone loss. Total daily calcium as a supplement may range from 1,500           mg to 2,000 mg depending on current bone status and your body size.           Make the effort to split up your daily dose. Do not take all your calcium           and magnesium once a day. A higher percentage of the calcium dose is           absorbed if delivered in smaller, more frequent amounts.82
         Expensive "chelated" calciums are not necessary if vitamin-D status           is adequate. Taking calcium without sufficient D may cause other problems.           Vitamin D controls the production of some calcium binding proteins,           which are critical to normal calcium utilization.
         Patients on vitamin-D therapy report a wide range of beneficial results           including increased energy and strength, resolution of hormonal problems,           weight loss, an end to sugar cravings, blood sugar normalization and           improvement of nervous system disorders.
         A paradoxical transient and non-complicating hypercalciuria (more           calcium in the urine) may occur when the program is first initiated.           This resolves quickly when adequate calcium and other minerals are consumed.           Two other temporary side effects may occur during the first several           months of treatment. One is daytime sleepiness after calcium is taken.           This usually resolves itself after about one week. The other condition           is the reappearance of pain and discomfort at the site of old injuries,           a sign of injury remodeling or proper healing, which may take some time           to clear up.
         Toxicity Issues        Vitamin programs usually omit vitamin D because of concerns about toxicity.           These concerns are valid because vitamin D in all forms can be toxic           in pharmacological (drug-like) doses. The dangers of toxicity have not           been exaggerated, but the doses needed to result in toxicity have been           ill defined with the unfortunate result that many people currently suffer           from vitamin-D deficiency or insufficiency.
         Abnormally high levels of vitamin D are indicated by blood levels           exceeding 65 ng/ml or 162 nmol/l for extended periods of time and may           be associated with chronic toxicity. Levels of 200-300 nmol/l or higher           have been seen in several studies using supplementation and quickly           resolve when supplementation is stopped. In such cases no long-term           problems have been found. Long-term supplementation, without monitoring,           may have serious consequences.
         Before 1993, there was no affordable and available blood test for           vitamin D. Now there is. To avoid problems, anyone engaging in levels           of vitamin-D supplementation above 1,000 iu daily should have periodic           blood tests. Don't forget to calculate your total vitamin-D intake from           all sources-sunlight, food (including vitamin D in milk) and supplements,           including cod liver oil.
         Dr. Vieth suggests that critical toxicity may occur at doses of 20,000           IU daily and that the Upper Limit (UL) of safety be set at 10,000 IU,           rather than the current 2,000 IU. While this may or may not be the definitive           marker for safety in healthy persons with no active liver or kidney           disease, there is no clinical evidence that long-term supplementation           needs to be greater than 4,000 IU for optimal daily maintenance. This           level would be somewhat lower when combined with exposure to UV-B.3;76
         Doses used in clinical studies range from as little as 400 IU daily           to 10,000-500,000 IU, given either as a single onetime dose or daily,           weekly or monthly. Such large doses are given either as a prophylactic           or because compliance is considered a problem. There seems to be some           evidence that vitamin D works better, without toxicity, when given in           lower, more physiologic doses of 2,000-4,000 IU daily rather than as           100,000 IU once a month. However, a single monthly dose of 100,000 IU           did replete low levels of vitamin D in adolescents during winter.77
         In my experience and that of other researchers, high, infrequent dosing           can lead to problems. In one recent study, blood levels rose from low           to extremely high, (more than 300 nmol/l) 2 to 4 hours after a 50,000           IU oral dose,65 and then slowly returned to pretreatment           suboptimal levels. Clearly this must disrupt normal feedback mechanisms           in D and calcium regulation.
         Vitamin A can be administered in large, infrequent doses from consumption           of animal or fish liver (or injections, used in third world countries           to prevent blindness) because we have storage capacity for vitamin A           in our livers. Vitamin D is different. It has only a small storage pool           in the liver and peripheral fat. Our ancestors most definitely did not           get vitamin D in large, infrequent doses. While vitamin D is stored           in body fat, storage is not sufficient to maintain optimum blood levels           during winter months.78 A single exposure to UV-B light will           raise levels of vitamin D over the next 24 hours and then return to           baseline or slightly higher within 7 days. Historically our requirements           for D were satisfied by daily exposure to sunlight and/or daily intake           from food. Lowfat diets and lack of seafood in the diet further contribute           to the current worldwide insufficiency of vitamin D.
         Sunlight on the Inside         If any nutrient incorporates the properties of sunlight, it is vitamin           D. The healthy "primitive" peoples that Dr. Price observed not only           had broad, round, "sunny" faces, they also had sunny dispositions and           optimistic attitudes towards life in spite of many hardships. Typical           food intakes for peoples who have not been "civilized" range from 3,000           IU-6,000 IU. Modern intakes are paltry in comparison. The standard American           diet provides vitamin D only in very low quantities.
         The first step towards redressing some of the ills of civilized life-from           depression to road rage, from cavities to osteoporosis-would be to get           more light, inside or outside. Vitamin D adds sunlight to life from           childhood through the golden years. In nonagenarians and centagenarians           high levels of vitamin D in the blood and normal thyroid function were           the strongest markers of health and longevity.79
         Whether in the form of sunlight or dietary vitamin D from food and           fish oils, optimal levels of the sunshine vitamin allow your body and           mind to thrive, even during periods of stress.
         About the Author
         

         Krispin Sullivan, CN is a researcher and clinical nutritionist in practice in Woodacre, California. She is currently working on a book, Naked at Noon: The Importance of Sunlight and Vitamin D, to be published in 2001.
Instructions for physician monitoring of vitamin D, calcium and magnesium           repletion are available from www.sunlightandvitamind.com           or by contacting Krispin at krispin@krispin.com           or 1-415-488-9636.
         References
        Sidebar Articles         
Food Sources of Vitamin D         USDA databases compiled in the 1980s list the following foods as rich           in vitamin D. The amounts given are for 100 grams or about 3 1/2 ounces.           These figures demonstrate the difficulty in obtaining 4,000 IU vitamin           D per day from ordinary foods in the American diet. Three servings of           herring, oysters, catfish, mackerel or sardines plus generous amounts           of butter, egg yolk, lard or bacon fat and 2 teaspoons cod liver oil           (500 iu per teaspoon) yield about 4,000 IU vitamin D-a very rich diet           indeed!
        
Cod Liver Oil
              Lard (Pork Fat)
              Atlantic Herring (Pickled)
              Eastern Oysters (Steamed)
              Catfish (Steamed/Poached)
              Skinless Sardines (Water Packed)
              Mackerel (Canned/Drained)
              Smoked Chinook Salmon
              Sturgeon Roe
              Shrimp (Canned/Drained)
              Egg Yolk (Fresh)
              (One yolk contains about 24 IU)
              Butter
              Lamb Liver (Braised)
              Beef Tallow
              Pork Liver (Braised)
              Beef Liver (Fried)
              Beef Tripe (Raw)
              Beef Kidney (Simmered)
              Chicken Livers (Simmered)
              Small Clams (Steamed/Cooked Moist)
              Blue Crab (Steamed)
              Crayfish/Crawdads (Steamed)
              Northern Lobster (Steamed)
10,000
              2,800
              680
              642
              500
              480
              450
              320
              232
              172
              148

              56
              20
              19
              12
              12
              12
              12
              12
              8
              4
              4
              4
        The Many Forms of Vitamin D         There are two types of vitamin D found in nature. Vitamin D2           is formed by the action of UV-B on the plant precursor ergosterol. It           is found in plants and in was formerly added to irradiated cows milk.           Most milk today contains D3. Vitamin D3 or cholecalciferol           is found in animal foods. Both forms of vitamin D have been used successfully           to treat rickets and other diseases related to vitamin D insufficiency.         
         Many consider D3 the preferred vitamin, having more biologic           activity. Vitamin D3 as found in food or in human skin always           comes with various metabolites or isomers that may have biological benefit.           Dr. Price believed that there were as many as 12 metabolites or isomers           in the vitamin D found in animal foods. When vitamin D is taken in the           form of fish oil, or eaten in foods such as eggs or fish, these metabolites           will be present. Both D2 and D3 can be toxic when           taken inappropriately in large amounts.
         When humans take in vitamin D from food or sunlight, it is converted           first in the liver to the form 25(OH)D and then in the kidney to 1,25(OH)D.           These active forms of vitamin D are available by prescription and are           given to patients with liver or kidney failure or those with an hereditary           metabolic defect in vitamin-D conversion.
         
Assessing Vitamin D Status         Blood Testing: Currently there are two tests available for physicians           to assess vitamin-D status. One is for the somewhat biologically active           precursor 25(OH)D and another for 1,25(OH)D, the most active form, which           is converted in the kidney and other organs. The latter is often normal           in the blood even when the precursor 25(OH)D is low or deficient. The           precursor is a better marker of vitamin-D status (or reserves) than           the most active 1,25(OH)D form. It is the optimum level of 25(OH)D that           is most strongly associated with general good health. (The test values           given in this article are for 25(OH)D.) For many years the acceptable           level of 25(OH)D has been at least 9 ng/ml (23 nmol/l). Some researchers           believe that 20 ng/ml (50 nmol/l) should be the lower acceptable limit72           but Dr. Vieth presents a large amount of data to support his claim that           this is far from optimal.3 Optimal levels are certainly at least 32           ng/ml (80 nmol/l) and preferably closer to 40 ng/ml (100 nmol/l).
         Salivary pH Testing for calcium sufficiency: A method of assessing           ionized calcium levels has been used by Weston Price, DDS and Carl Reich,           MD and has confirmation in current research.73 After determining           your serum-D status (testing) and undertaking a program of supplementation           with vitamin D, calcium and magnesium, morning salivary pH should read           6.8-7.2. Lower values may indicate insufficient vitamin D (retest),           or low levels of calcium in the diet. Look for pH paper with a range           of 5.5-8.0 and increments of 0.2. PH papers with 0.5-degree increments           are not sensitive enough to monitor progress. (Note: Do not take more           than 1,000 IU of vitamin D without testing and supervision by a knowledgeable           healthcare practitioner. Calcium can be adjusted within the ranges suggested.           Several months of supplementation may be required to show positive results           if the deficiency is severe and prolonged.)
        Sources         
        
        References
         1. Prabhala A, Garg R, Dandona P. Severe myopathy           associated with vitamin D deficiency in western New York. Arch.Intern.Med.           2000;160:1199-203.         
2. Price, Weston A. Characteristics of Primitive and           Modernized Dietaries. Nutrition and Physical Degeneration.           New Canaan, Connecticut: Keats Publishing, Inc 1989:256-81.         
3. Vieth R. Vitamin D supplementation, 25-hydroxyvitamin           D concentrations, and safety [see comments]. Am.J.Clin.Nutr.           1999;69:842-56.         
4. Glerup H, Mikkelsen K, Poulsen L et al. Commonly           recommended daily intake of vitamin D is not sufficient if sunlight           exposure is limited. J.Intern.Med. 2000;247:260-8.         
5. Glerup H, Eriksen EF. [Vitamin D deficiency. Easy           to diagnose, often overlooked (see comments)]. Ugeskr.Laeger 1999;161:2515-21.           6. Diffey BL. Solar ultraviolet radiation effects on biological systems.           Phys.Med.Biol. 1991;36:299-328.         
7. Moan J, Dahlback A, Setlow RB. Epidemiological support           for an hypothesis for melanoma induction indicating a role for UVA radiation.           Photochem.Photobiol. 1999;70:243-7.         
8. Ranson M, Posen S, Mason RS. Human melanocytes as           a target tissue for hormones: in vitro studies with 1 alpha-25, dihydroxyvitamin           D3, alpha-melanocyte stimulating hormone, and beta-estradiol. J.Invest           Dermatol.1988;91:593-8.         
9. Sayre, R. M., Dowdy, J. C., Shepherd, J., Sadig,           I., Bager, A., and Kollias, N. Vitamin D Production by Natural and Artificial           Sources. 1998. Orlando, Florida, Photo Medical Society Meeting. 3-1-1998.           Ref Type: Conference Proceeding         
10. Holick MF. The cutaneous photosynthesis of previtamin           D3: a unique photoendocrine system. J.Invest Dermatol. 1981;77:51-8.         
11. Matsuoka LY, Wortsman J, Haddad JG, Kolm P, Hollis           BW. Racial pigmentation and the cutaneous synthesis of vitamin D [see           comments]. Arch.Dermatol. 1991;127:536-8.         
12. Matsuoka LY, Wortsman J, Haddad JG, Hollis BW. In           vivo threshold for cutaneous synthesis of vitamin D3. J.Lab Clin.Med.           1989;114:301-5.         
13. Season, latitude, and ability of sunlight to promote           synthesis of vitamin D3 in skin. Nutr.Rev. 1989;47:252-3.         
14. Pettifor JM, Moodley GP, Hough FS et al. The effect           of season and latitude on in vitro vitamin D formation by sunlight in           South Africa. S.Afr.Med.J. 1996;86:1270-2.         
15. Webb AR, Kline L, Holick MF. 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.Endocrinol.Metab 1988;67:373-8.         
16. Bjorn LO, Wang T. Vitamin D in an ecological context.           Int.J.Circumpolar.Health 2000;59:26-32.         
17. Xue L, Lipkin M, Newmark H, Wang J. Influence of           dietary calcium and vitamin D on diet-induced epithelial cell hyperproliferation           in mice. J.Natl.Cancer Inst. 1999;91:176-81.         
18. Moon J. The role of vitamin D in toxic metal absorption:           a review. J.Am.Coll.Nutr. 1994;13:559-64.         
19. Sardar S, Chakraborty A, Chatterjee M. Comparative           effectiveness of vitamin D3 and dietary vitamin E on peroxidation of           lipids and enzymes of the hepatic antioxidant system in Sprague-Dawley           rats. Int.J.Vitam.Nutr.Res. 1996;66:39-45.         
20. Wiseman H. Vitamin D is a membrane antioxidant.           Ability to inhibit iron-dependent lipid peroxidation in liposomes compared           to cholesterol, ergosterol and tamoxifen and relevance to anticancer           action. FEBS Lett. 1993;326:285-8.         
21. Bourlon PM, Billaudel B, Faure-Dussert A. Influence           of vitamin D3 deficiency and 1,25 dihydroxyvitamin D3 on de novo insulin           biosynthesis in the islets of the rat endocrine pancreas. J.Endocrinol.           1999;160:87-95.         
22. Baynes KC, Boucher BJ, Feskens EJ, Kromhout D. Vitamin           D, glucose tolerance and insulinaemia in elderly men [published erratum           appears in Diabetologia 1997 Jul;40(7):870]. Diabetologia 1997;40:344-7.         
23. Jacques PF, Hartz SC, Chylack LT, Jr., McGandy RB,           Sadowski JA. Nutritional status in persons with and without senile cataract:           blood vitamin and mineral levels. Am.J.Clin.Nutr. 1988;48:152-8.         
24. Thys-Jacobs S, Donovan D, Papadopoulos A, Sarrel           P, Bilezikian JP. Vitamin D and calcium dysregulation in the polycystic           ovarian syndrome. Steroids 1999;64:430-5.         
25. Abu-Amer Y, Bar-Shavit Z. Regulation of TNF-alpha           release from bone marrow-derived macrophages by vitamin D [published           erratum appears in J Cell Biochem 1994 Nov;56(3):426]. J.Cell Biochem.           1994;55:435-44.         
26. Cantorna MT. Vitamin D and autoimmunity: is vitamin           D status an environmental factor affecting autoimmune disease prevalence?           Proc.Soc.Exp.Biol.Med. 2000;223:230-3.         
27. Vogelsang H, Ferenci P, Woloszczuk W et al. Bone           disease in vitamin D-deficient patients with Crohn's disease. Dig.Dis.Sci.           1989;34:1094-9.         
28. Bettica P, Bevilacqua M, Vago T, Norbiato G. High           prevalence of hypovitaminosis D among free-living postmenopausal women           referred to an osteoporosis outpatient clinic in northern Italy for           initial screening. Osteoporos.Int. 1999;9:226-9.         
29. Glerup H, Mikkelsen K, Poulsen L et al. Hypovitaminosis           D myopathy without biochemical signs of osteomalacic bone involvement.           Calcif.Tissue Int. 2000;66:419-24.         
30. Kyriakidou-Himonas M, Aloia JF, Yeh JK. Vitamin           D supplementation in postmenopausal black women. J.Clin.Endocrinol.Metab           1999;84:3988-90.         
31. Uhland AM, Kwiecinski GG, DeLuca HF. Normalization           of serum calcium restores fertility in vitamin D-deficient male rats.           J.Nutr. 1992;122:1338-44.         
32. Kinuta K, Tanaka H, Moriwake T, Aya K, Kato S, Seino           Y. Vitamin D is an important factor in estrogen biosynthesis of both           female and male gonads. Endocrinology 2000;141:1317-24.         
33. Thys-Jacobs S. Micronutrients and the premenstrual           syndrome: the case for calcium. J.Am.Coll.Nutr. 2000;19:220-7.         
34. Garland CF, Garland FC, Gorham ED. Calcium and vitamin           D. Their potential roles in colon and breast cancer prevention. Ann.N.Y.Acad.Sci.           1999;889:107-19.         
35. John EM, Schwartz GG, Dreon DM, Koo J. Vitamin D           and breast cancer risk: the NHANES I Epidemiologic follow-up study,           1971-1975 to 1992. National Health and Nutrition Examination Survey.           Cancer Epidemiol.Biomarkers Prev. 1999;8:399-406.         
36. Miller GJ. Vitamin D and prostate cancer: biologic           interactions and clinical potentials. Cancer Metastasis Rev.           1998;17:353-60.         
37. Gorham ED, Garland CF, Garland FC. Acid haze air           pollution and breast and colon cancer mortality in 20 Canadian cities.           Can.J.Public Health 1989;80:96-100.         
38. Kleibeuker JH, Van der MR, de Vries EG. Calcium           and vitamin D: possible protective agents against colorectal cancer?           Eur.J.Cancer 1995;31A:1081-4.         
39. Puchacz E, Stumpf WE, Stachowiak EK, Stachowiak           MK. Vitamin D increases expression of the tyrosine hydroxylase gene           in adrenal medullary cells. Brain Res.Mol.Brain Res. 1996;36:193-6.         
40. Gloth FM, III, Alam W, Hollis B. Vitamin D vs broad           spectrum phototherapy in the treatment of seasonal affective disorder.           J.Nutr.Health Aging 1999;3:5-7.         
41. Fujita T, Ohgitani S, Nomura M. Fall of blood ionized           calcium on watching a provocative TV program and its prevention by active           absorbable algal calcium (AAA Ca). J.Bone Miner.Metab 1999;17:131-6.         
42. Sato Y, Kikuyama M, Oizumi K. High prevalence of           vitamin D deficiency and reduced bone mass in Parkinson's disease. Neurology           1997;49:1273-8.         
43. Sato Y, Asoh T, Oizumi K. High prevalence of vitamin           D deficiency and reduced bone mass in elderly women with Alzheimer's           disease. Bone 1998;23:555-7.         
44. Nikiforuk G, Fraser D. The etiology of enamel hypoplasia:           a unifying concept. J.Pediatr. 1981;98:888-93.         
45. Taylor AN. Tooth formation and the 28,000-dalton           vitamin D-dependent calcium- binding protein: an immunocytochemical           study. J.Histochem.Cytochem. 1984;32:159-64.         
46. Price, Weston A. Primitive Control of Dental Caries.           Nutrition and Physical Degeneration. New Canaan, Connecticut:           Keats Publishing, Inc 1989:326-52.         
47. Price, Weston A. Prenatal Nutritional Deformities           and Disease Types. Nutrition and Physical Degeneration. New           Canaan, Connecticut: Keats Publishing, Inc 1989:326-52.         
48. Kozielec T, Starobrat-Hermelin B, Kotkowiak L. [Deficiency           of certain trace elements in children with hyperactivity]. Psychiatr.Pol.           1994;28:345-53.         
49. Starobrat-Hermelin B. [The effect of deficiency           of selected bioelements on hyperactivity in children with certain specified           mental disorders]. Ann.Acad.Med.Stetin. 1998;44:297-314.         
50. Boucher BJ. Inadequate vitamin D status: does it           contribute to the disorders comprising syndrome 'X'? [published erratum           appears in Br J Nutr 1998 Dec;80(6):585]. Br.J.Nutr. 1998;79:315-27.         
51. Schilli MB, Paus R, Czarnetzki BM, Reichrath J.           [Vitamin D3 and its analogs as multifunctional steroid hormones. Molecular           and clinical aspects from the dermatologic viewpoint]. Hautarzt           1994;45:445-52.         
52. Fujita T, Okamoto Y, Sakagami Y, Ota K, Ohata M.           Bone changes and aortic calcification in aging inhabitants of mountain           versus seacoast communities in the Kii Peninsula. J.Am.Geriatr.Soc.           1984;32:124-8.         
53. Watson KE, Abrolat ML, Malone LL et al. Active serum           vitamin D levels are inversely correlated with coronary calcification.           Circulation 1997;96:1755-60.         
54. Sugihara N, Matsuzaki M, Kato Y. [Assessment of           the relation between bone mineral metabolism and mitral annular calcification           or aortic valve sclerosis-the relation between mitral annular calcification           and post menopausal osteoporosis in elderly patients]. Nippon Ronen           Igakkai Zasshi 1990;27:605-15.         
55. Segall JJ. Latitude and ischaemic heart disease           [letter]. Lancet 1989;1:1146.         
56. Williams FL, Lloyd OL. Latitude and heart disease           [letter]. Lancet 1989;1:1072-3.         
57. MacPherson A, Balint J, Bacso J. Beard calcium concentration           as a marker for coronary heart disease as affected by supplementation           with micronutrients including selenium. Analyst 1995;120:871-5.         
58. Krause R, Buhring M, Hopfenmuller W, Holick MF,           Sharma AM. Ultraviolet B and blood pressure [letter]. Lancet           1998;352:709-10.         
59. Jorde R, Bonaa KH. Calcium from dairy products,           vitamin D intake, and blood pressure: the Tromso Study. Am.J.Clin.Nutr.           2000;71:1530-5.         
60. Rostand SG. Ultraviolet light may contribute to           geographic and racial blood pressure differences [see comments]. Hypertension           1997;30:150-6.         
61. Zemel MB, Shi H, Greer B, Dirienzo D, Zemel PC.           Regulation of adiposity by dietary calcium. FASEB J. 2000;14:1132-8.         
62. Bell NH, Epstein S, Greene A, Shary J, Oexmann MJ,           Shaw S. Evidence for alteration of the vitamin D-endocrine system in           obese subjects. J.Clin.Invest 1985;76:370-3.         
63. Buffington C, Walker B, Cowan GS, Jr., Scruggs D.           Vitamin D Deficiency in the Morbidly Obese. Obes.Surg. 1993;3:421-4.         
64. Liel Y, Ulmer E, Shary J, Hollis BW, Bell NH. Low           circulating vitamin D in obesity. Calcif.Tissue Int. 1988;43:199-201.         
65. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF.           Decreased bioavailability of vitamin D in obesity. Am.J.Clin.Nutr.           2000;72:690-3.         
66. Bouillon R, Xiang DZ, Convents R, Van Baelen H.           Polyunsaturated fatty acids decrease the apparent affinity of vitamin           D metabolites for human vitamin D-binding protein. J.Steroid Biochem.Mol.Biol.           1992;42:855-61.         
67. Garssen J, Norval M, el Ghorr A et al. Estimation           of the effect of increasing UVB exposure on the human immune system           and related resistance to infectious diseases and tumours. J.Photochem.Photobiol.B           1998;42:167-79.         
68. Amento EP, Bhalla AK, Kurnick JT et al. 1 alpha,25-dihydroxyvitamin           D3 induces maturation of the human monocyte cell line U937, and, in           association with a factor from human T lymphocytes, augments production           of the monokine, mononuclear cell factor. J.Clin.Invest 1984;73:731-9.         
69. Aslam SM, Garlich JD, Qureshi MA. Vitamin D deficiency           alters the immune responses of broiler chicks. Poult.Sci. 1998;77:842-9.         
70. Corman LC. Effects of specific nutrients on the           immune response. Selected clinical applications. Med.Clin.North           Am. 1985;69:759-91.         
71. Muller K, Bendtzen K. 1,25-Dihydroxyvitamin D3 as           a natural regulator of human immune functions. J.Investig.Dermatol.Symp.Proc.           1996;1:68-71.         
72. Barger-Lux MJ, Heaney RP, Dowell S, Chen TC, Holick           MF. Vitamin D and its major metabolites: serum levels after graded oral           dosing in healthy men. Osteoporos.Int. 1998;8:222-30.         
73. Rehak NN, Cecco SA, Csako G. Biochemical composition           and electrolyte balance of "unstimulated" whole human saliva [In Process           Citation]. Clin.Chem.Lab Med. 2000;38:335-43.         
74. Talbot JR, Guardo P, Seccia S et al. Calcium bioavailability           and parathyroid hormone acute changes after oral intake of dairy and           nondairy products in healthy volunteers. Osteoporos.Int. 1999;10:137-42.         
75. Heaney RP, Dowell MS, Barger-Lux MJ. Absorption           of calcium as the carbonate and citrate salts, with some observations           on method. Osteoporos.Int. 1999;9:19-23.         
76. Chesney RW. Vitamin D: can an upper limit be defined?           J.Nutr. 1989;119:1825-8.         
77. Duhamel JF, Zeghoud F, Sempe M et al. [Prevention           of vitamin D deficiency in adolescents and pre-adolescents. An interventional           multicenter study on the biological effect of repeated doses of 100,000           IU of vitamin D3 (see comments)]. Arch.Pediatr. 2000;7:148-53.         
78. Davies PS, Bates CJ, Cole TJ, Prentice A, Clarke           PC. Vitamin D: seasonal and regional differences in preschool children           in Great Britain [published erratum appears in Eur J Clin Nutr 1999           Jul;53(7):584]. Eur.J.Clin.Nutr. 1999;53:195-8.         
79. Mariani E, Ravaglia G, Forti P et al. Vitamin D,           thyroid hormones and muscle mass influence natural killer (NK) innate           immunity in healthy nonagenarians and centenarians [published erratum           appears in Clin Exp Immunol 1999 Jul;117(1):206]. Clin.Exp.Immunol.                    
80. Enig, Mary G. Modification of Membrane Lipid Composition           and Mixed-Function Oxidases in Mouse Liver Microsomes by Dietary Trans           Fatty Acids. 1984. University Microfilms International. Ann           Arbor, Michigan.         
81. Thys-Jacobs S. Vitamin D and calcium in menstrual           migraine. Headache 1994;34:544-6.         
82. Heaney, RP et al. J of Bone and Mineral Research,           5:11;1990 p. 1135-1137.
回复

使用道具 举报

 楼主| 发表于 2009-5-21 00:35:38 | 显示全部楼层
Vitamin D Update, Winter 2000

by Krispin Sullivan, CN

Note: This update appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Winter 2000.

Since the publication of "The Miracle of Vitamin D" in the last issue of Wise Traditions, some clarification is necessary. The action of vitamin D, whether from food, supplements or sunlight conversion, is that of a "pro-hormone," rather than of a vitamin.

According to the dictionaries, a hormone is a substance, usually a peptide or steroid, produced by one tissue and conveyed by the bloodstream to another. Hormones affect physiological activity, such as growth or metabolism. More generally, a hormone is one of various similar substances found in plants and insects that regulate development. By contrast, vitamins are various fat-soluble or water-soluble organic substances essential in minute amounts for normal growth and activity of the body. They are obtained naturally from plant and animal foods.

Hormones are powerful regulators that can have both good and bad effects. With progesterone, DHEA, estrogen, thyroid or any other hormone, including vitamin D, there can be a profound cellular response when levels are altered by supplementation. Vitamins and minerals are elements used by the body to make enzymes, bone, immune fractions and other substances in the human body, but they are not regulators.

As a pro-hormone, vitamin D can be dangerous because too much has the potential for great harm as does too little. That is why testing is important for those on vitamin-D therapy. When you take thyroid hormones, you are instructed to test first and retest to make sure the amount you are taking is correct. So, too, with vitamin D. The rule is test, treat (if necessary) and retest until you find the right amount to meet your daily need. According to our current levels of knowledge, there are no obvious symptoms of vitamin D overdose until the overdose is nonreversible. Testing can alert us not only to deficiency but also toxicity. Fortunately, we now have tests for vitamin D status that are not expensive.

In my practice, I am discovering that some people may need upwards of 4,000 IU daily to maintain optimal blood levels. Others may find that anything over 200-400 IU puts them in a situation of overdose. This is a problem of genetics. Some people utilize vitamin D better than others. Before the days of travel and great population migrations, the process of natural selection created population groups that best responded to the levels of vitamin D available through exposure to sunlight and in the diet. Migration, immigration and intermarriage make it impossible to determine needs without testing.

Once you test and determine the level of D from sunlight, food and supplements that maintains optimum levels of vitamin D in your blood, then you know the "dose" that you will need as long as you live at that altitude and latitude. You should test twice a year as in many locations the need for D may vary greatly from summer to winter.

For detailed information visit my website sunlightandvitamind.com

VITAMIN D UPDATE-A WARNING, Fall 2002

By Krispin Sullivan, CN

I have reported in this magazine on the substantial benefits that can be gained from vitamin D therapy (Wise Traditions, Fall 2000). However, my own clinical experience and the research of others is clearly showing chronic subclinical vitamin D toxicity is possible, from both supplements or tropical sunlight. Elevated levels of serum vitamin D can cause significant bone loss and calcification of soft tissues.

If you are using supplements of vitamin D (natural or synthetic) or are light skinned and have had significant sun exposure in tropical or subtropical areas and haven't done so before, it is very important to test your blood levels of D.

Optimal values of 25(OH)D are 40-50 ng/ml
Acceptable values of 25(OH)D are 35-55 ng/ml
Levels above 55 ng/ml will be toxic for some individuals.

There is no good reason to maintain levels of D in this higher range and strong evidence showing potential harm.

You need to TEST. The correct test to order is 25(OH)D, also called 25-hydroxyvitamin D. Make sure this is the test you get. Labs often give the test for 1,25-dihydroxyvitamin D, the active hormone. This test is the wrong test as it offers no meaningful data regarding D status.

Lab One offers the least expensive testing I have found nationwide and is available in most states. Your physician can reach them at 1-800-646-7788. The test is 25-hydroxyvitamin D. The Lab One test number, just to be sure you get the right test, is #3247. Rarely does insurance cover the cost for this test, which is about $60 including lab fees. Other labs I have queried charge $100-180 for the same test.

The important thing to remember if you are doing vitamin D therapy, or spending lots of time in the sun, is to TEST!
回复 支持 反对

使用道具 举报

手机版|天涯小站

GMT-5, 2025-12-2 05:52 PM

Powered by Discuz! X3.4

© 2001-2017 Comsenz Inc.

快速回复 返回顶部 返回列表