Cod Liver Oil: Benefits, Science and Debate

Science Validates the Benefits of Our Number One Superfood

Article Summary

• Mankind has consumed marine liver oils for thousands of years and cod liver oil for at least hundreds of years.
• Several trials conducted before 1940 found that the vitamin A in cod liver oil had powerful anti-infective power, which popularized the oil as a prophylactic and led to its use as a treatment against puerperal fever, measles, and industrial absenteeism.
• Vitamins A and D cooperate with one another. They are not antagonists, but large doses of one may cause harm when not accompanied by the other.
• There is no evidence that vitamin A increases mortality.
• Over a quarter of Americans consume less than half the RDA of vitamin A, which is 3,000 IU per day for adult males. Price’s tooth decay reversal program would have provided over 10,000 IU per day. Sub-optimal intakes of vitamin A may be related to asthma, kidney stones, fatty liver disease, oxidative stress, and susceptibility to environmental toxins.
• During the winter or year-round for people with dark skin, some extra vitamin D from fatty fish or supplements may be necessary for some people.
• High-vitamin cod liver oil is a very useful source of vitamins A and D and omega-3 fatty acids.

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For centuries, cod liver oil has served as a valuable source of vitamins A and D and omega-3 fatty acids. It was a critical component of Weston Price’s program for reversing tooth decay and many practitioners in his day used it to treat eye diseases, rickets, and infections. Along with many other physicians, Dr. Price recommended cod liver oil to promote growth and general health in infants and children. Clinical trials proved that cod liver oil use in adults reduced absenteeism and saved millions of dollars worth of productivity for American industry.

Recently, however, cod liver oil has come under attack. After issuing a series of newsletters criticizing the use of cod liver oil because of its vitamin A content, Dr. John Cannell, through the Vitamin D Council, wrote a commentary entitled “Cod Liver Oil, Vitamin A Toxicity, Frequent Respiratory Infections, and the Vitamin D Deficiency Epidemic” published in the November, 2008 issue of the Journal of Otology, Rhinology, & Laryngology.1 Cannell and co-authors claim that vitamin A intakes above the most minimal levels increase mortality rates, increase vulnerability to infections, cause osteoporosis, and antagonize the beneficial effects of vitamin D.

Cannell concluded that neither children nor adults should use cod liver oil or multivitamins containing true (pre-formed) vitamin A. Sixteen scientists signed on to the paper as co-authors, although this does not mean that each one endorsed every statement in the paper. Cannell quoted this paper extensively and expanded his arguments against vitamin A in his December newsletter,2 while Dr. Joseph Mercola repeated Cannell’s claims on his web site in two articles published this winter.3,4

What the scientific literature shows, however, is that vitamins A and D work as partners rather than antagonists. While there is no solid evidence linking vitamin A to increases in mortality or higher rates of infection, vitamin A does cause adverse effects such as bone loss when it is not provided with its molecular partner, vitamin D. Since cod liver oil provides both partners together, it developed a long and successful history as an important therapeutic and prophylactic supplement. Many modern cod liver oils are deficient in vitamin D and should be avoided, but those providing adequate vitamin D continue to provide an important natural food source of the fat-soluble vitamins.

The Origins of Cod Liver Oil

Hippocrates first recorded the medicinal use of fish oils, and the first century naturalist Pliny the Elder recorded the use of dolphin liver oil as a remedy for chronic skin eruptions.5 In 1848, the British physician John Hughes Bennett observed that cod liver oil had been used from time immemorial by the fishing populations of Scotland, Sweden, and Norway for its general medicinal and strengthening properties.6 For centuries before producing the oil itself, the British used the blackish residue left behind by barreled cod livers as a balm.7 In 1766, a Manchester Infirmary began prescribing ingestion of the oil for rheumatism after a patient cured herself of the disease on two occasions by ingesting her topical treatment.5 The infirmary thereafter used fifty to sixty gallons of cod liver oil per year,6 and after comparing its use to that of a placebo in a number of individual patients, the physician Percival added it to the British Pharmacopoeia in 1771.5

Physicians used cod liver oil to treat the vitamin D deficiency disease rickets at least as far back as 1799, and by the 1820s use of cod liver oil for this purpose was widespread in Germany, Holland and the Netherlands. During the same century, its use expanded to include the treatment of eye diseases and tuberculosis.5 Research between 1920 and 1940 further expanded the use of cod liver oil to prevent or treat measles, industrial absenteeism, and puerperal fever, a fatal infection occurring in women just after giving birth. The advent of sulfa antibiotics and later penicillin mostly eliminated the interest in cod liver oil as an anti-infective agent, but a number of trials conducted before 1940 provided solid evidence of its efficacy. Cod liver oil reduced measles mortality by more than one-half and reduced industrial absenteeism by up to two-thirds in clinical trials. As a prophylactic, it reduced the incidence of puerperal fever by two-thirds, and as a treatment, it reduced mortality from this disease by the same amount.8

Vitam in A as an Anti-Infective

In the 1920s, Edward Mellanby performed a series of experiments at the University of Sheffield showing that vitamin A was the primary anti-infective component of cod liver oil. Mellanby compared the effects of cod liver oil, rich in vitamins A and D, to those of butter, rich in vitamin A only, and to those of olive oil, deficient in both vitamins. Dogs fed butter instead of cod liver oil had soft bones and partially collapsed lungs, but bronchial pneumonia occurred only on the olive oil diet. Mellanby attributed the partial collapse of the lungs to muscular dysfunction induced by vitamin D deficiency and attributed the pneumonia to degeneration of the epithelial lining of the lungs induced by vitamin A deficiency.9

When pure vitamin D2 became commercially available, Mellanby and his colleague Harry Norman Green performed further experiments in rats showing that vitamin A deficiency led to often fatal infections of the tongue, throat, eyes, lungs and gastrointestinal tract in nearly all of the animals. In several hundred vitamin D-deficient rats, by contrast, they observed only two cases of infection. In the vitamin A-deficient rats, moreover, vitamin D supplementation made the infections worse. Green and Mellanby suggested that this was because vitamin D stimulated growth and “thereby made a greater call on the vitamin A stores of the body.” They concluded that while vitamin D was necessary for the calcification of bones and teeth, it did not share the anti-infective properties of vitamin A and it would therefore be dangerous to replace traditional cod liver oil with the newly developed vitamin D supplements. “If a substitute for cod-liver oil is given,” they wrote, “it ought to be at least as powerful as this oil in its content of both vitamins A and D.”9

Vitamins A and D as Molecular Partners

Mellanby was correct when he noted that vitamin D increases the need for vitamin A, but he was probably wrong about the mechanism. Beginning in the 1930s and continuing through the 1960s, research accumulated showing that vitamins A and D each protected against the toxicity of the other.18,19,20,21 This observation held true even when the vitamins were injected into the animals rather than provided in the diet, showing that they did not protect against each other’s toxicity by competing for intestinal absorption.22

To explain the earliest observations of this phenomenon, the German researcher F. Thoenes proposed in 1935 that vitamins A and D cooperated with each other to perform certain functions and that vitamin D caused toxicity by inducing a relative deficiency of vitamin A.23 This concept gained further support in 1998 when Aburto and Britton showed that even moderate doses of vitamin D lower blood levels and liver stores of vitamin A in broiler chickens whether they are provided in the diet or by exposure to ultraviolet light.24

Developments in molecular biology over the last several decades have shown that vitamins A and D carry out most of their actions by binding to specific receptors that will bring them into contact with DNA inside the nucleus of a cell, in order to alter the expression of genes by turning them on or off or by turning them up or down. The receptors for these vitamins, together with those for thyroid hormones, steroid hormones, and other important signaling molecules, are part of a common family of nuclear receptors that interact with one another. Vitamin A is especially involved in these interactions—it not only carries out its own signaling, but forms an essential partnership with most other nuclear hormones, which allows them to carry out their functions. Recent research, described in more detail in the sidebar on page 22, has shown that vitamin D can only effectively control the expression of genes in the presence of vitamin A.

Since vitamin A is required as a signaling partner with vitamin D, vitamin D will increase the turnover of vitamin A. If vitamin A is provided in excess, the results are generally beneficial. Excess vitamin A is stored in the liver. However, when the liver’s storage capacity is exceeded, the overload of vitamin A causes the cells to burst, damaging the liver and releasing storage forms of vitamin A into the systemic circulation that do not belong there. By increasing the utilization of vitamin A, vitamin D can help prevent vitamin A toxicity.

If vitamin A is in short supply, on the other hand, the results can be detrimental. By “stealing” all of the vitamin A needed to use for vitamin D-specific functions, the body will not have enough vitamin A left to support the many other functions for which it is needed—this may partially explain the toxic effects of excess vitamin D.

Vitamin A toxicity is likely due in part to the damage done to liver cells and the release of their contents, including storage forms of vitamin A, into the blood. It may also be the case that there is a natural balance between the many different signaling roles played by vitamin A when all of its signaling partners are present, but that when one of them—such as vitamin D—is absent, this natural balance is thrown off. Thus when vitamin D is provided in adequate amounts, vitamin A does not accumulate excessively in the liver and this natural balance is maintained, but when vitamin D is in short supply, high doses of vitamin A will damage the liver and contribute to an imbalance of cell signaling.

If vitamin D is present in excess, extra vitamin A is needed to fulfill those other functions, while if vitamin D is in short supply, the natural balance of functions in which vitamin A engages may be thrown off.

The current controversies over osteoporosis present a perfect example of how critically important it is to take into account the interactions between these two vitamins. A number of studies have shown that high intakes of vitamin A are associated with reduced bone mineral density and increased risk of hip fracture, but these studies have been conducted in populations with vitamin D intakes as low as 100 IU per day. The only study that mentioned cod liver oil as a source of vitamin A in its population found high levels of vitamin A to be associated with a decreased risk of fracture.25 It may be the case that vitamin A contributes to osteoporosis when vitamin D is deficient, but protects against osteoporosis when vitamin D is adequate.

A review published in 2005 concluded that physicians should explicitly warn their elderly patients to avoid intakes of vitamin A greater than the RDA.26 A large-scale, placebo-controlled trial published in 2006 found that 400 IU of vitamin D plus 1,000 milligrams of calcium increased the risk of kidney stones by 17 percent.27 Kidney stones can be induced by feeding animals vitamin A-deficient diets,9 and prevented in animals by feeding them extra vitamin A.28 Research in the 1930s found that over 90 percent of people with kidney stones were deficient in vitamin A.29 Kidney stones can be induced in animals by feeding doses of vitamin D that are insufficient to cause abnormally high calcium levels,30 suggesting that they are the first and most sensitive marker of vitamin D toxicity. Vitamin A is capable of completely protecting against vitamin D-induced kidney calcification.24 Perhaps such a small amount of vitamin D increased the risk of kidney stones in this elderly population because its members were being advised to avoid vitamin A.

Are Vitamin A Intakes Excessive?

One of the co-authors of the Cannell paper conducted a study, which has not yet been published, showing that four percent of obese Wisconsin adults had blood markers indicating their livers were overloaded with vitamin A.1 Vitamin D mobilizes vitamin A from the liver and increases its utilization,24 so vitamin A overload is most likely to occur in people with low vitamin D status. At least half of all Americans and over 80 percent of African Americans have low vitamin D levels.41 Morbidly obese patients are three times more likely to have low vitamin D levels than non-obese controls.42 Thus, finding markers indicating vitamin A overload is more likely to reflect the poor vitamin D status of most Americans and the exceptionally poor vitamin D status of obese Americans than it is to reflect a supposed excess of vitamin A in the standard American diet.

Vitamin A deficiency has been associated with a number of prevalent diseases, including childhood asthma,43,44 kidney stones formed spontaneously from calcium phosphate,9 and fatty liver disease.45 Vitamin A in doses above those needed to prevent deficiency protects against oxidative stress,46 kidney stones formed from dietary oxalate,28 and exposure to environmental toxins.47

The vitamin A RDA is 3,000 IU for adult males and just over 2,300 IU for adult females. These values are based on studies conducted in the general population, which is now recognized to be largely deficient in vitamin D. Most traditional diets likely supplied more vitamin A than the current RDA. The Greenland Inuit diet in 1953 supplied an average of 30,000 IU per day.48 Other traditional diets where most of the vitamin A came from dairy products likely provided lower levels. Price used three-quarters of a teaspoon of high-vitamin cod liver oil per day and alternated between muscle meats and organ meats in the stews he used for his tooth decay reversal program. Together with whole milk, butter, and carotenes from vegetables, his program probably provided over 10,000 IU of vitamin A per day, although this was to growing children who were recovering from deficiency.

Regardless of whether or not the ideal intake of vitamin A is much higher than the RDA, over a quarter of Americans consume less than half the RDA.49 If people eating diets this low in vitamin A begin supplementing with vitamin D rather than cod liver oil, the danger of such a low intake of vitamin A may be greatly increased.

Cod Liver Oil Supplies a Balance

Cod liver oil should not be seen as a cure-all or as a universal supplement, but neither should cod liver oil be avoided out of fear. It is a valuable and convenient way to obtain vitamins A and D together with omega-3 fatty acids—all nutrients most Americans require in greater levels than they currently obtain through their diets.

Does cod liver oil contain the ideal ratio of vitamins A and D? It is possible that there is an ideal dietary ratio of the two vitamins, but this is not necessarily the case. The body highly regulates its conversion of each vitamin to the active form, and is capable of storing the portion it chooses not to activate at any given time. It is more likely that there is a broad range of acceptable dietary ratios and that harm comes when one or the other vitamin is in unusually short supply.

If there is an ideal ratio, it will vary from person to person and from season to season. People with darker skin may need extra vitamin D from fatty fish or vitamin D supplements year round, and others may need extra vitamin D only in the winter. People should use recommendations as guidelines to help them experiment and find the amount of cod liver oil that works best for them, knowing that it has been a safe and valuable health-promoting food that for centuries has nourished both young and old.

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SIDEBARS

Does Vitamin A Increase the Risk of Infections?

Cannell cites an analysis in his journal article and December newsletter as showing that vitamin A supplements decrease lower respiratory infections “in children with low intake of retinol [vitamin A], as occurs in the Third World” but that “it appears to increase the risk and/or worsen the clinical course in normal children.”1,2 By the time Mercola published the claim, “normal children” became any children living in a developed country. “Unlike third world countries where vitamin A supplementation appears to decrease infections,” Mercola wrote, “vitamin A supplementation in developed countries like the U.S. actually increases infections.”3

The original analysis did not present any findings that separated children into low and normal intakes of vitamin A and did not include any studies conducted in developed countries like the United States.10 It was a meta-analysis that pooled the results of nine studies conducted in India, Ecuador, Indonesia, Brazil, Ghana, Mexico, and the Republic of Congo. Several of these studies have suggested that vitamin A may reduce the incidence of respiratory infection in malnourished children but increase it in well-nourished children. N one of them, however, present evidence that the effect of vitamin A depends on vitamin A status or that vitamin A is helpful in the third world but harmful in the developed world.

An Ecuadorian study of four hundred children under the age of three found that weekly supplements delivering roughly half the RDA for vitamin A reduced the risk of lower respiratory infections among underweight and stunted children but raised the risk among children of normal weight and height.11 An Indonesian study of over 1400 children under the age of four found that three massive doses of vitamin A given over the course of a year, likewise delivering roughly half the RDA, increased lower respiratory illnesses in children of normal height but not in stunted children.12 Although both of these studies measured blood levels of vitamin A, neither of them reported the effect of vitamin A to be dependent on vitamin A status. They were conducted in areas where deficiencies of protein, energy, and multiple vitamins and minerals are common. A child’s status of protein, zinc, vitamin D, and other nutrients will affect his or her metabolism of vitamin A. Growth status itself could affect the metabolism of vitamin A, and adequate growth could deplete other nutrients needed for vitamin A to function properly.

It would also be a mistake to look at lower respiratory infections alone. A number of studies included in the metaanalysis showed vitamin A to have no effect on respiratory infections while nevertheless reducing severe diarrhea by over 20 percent,13 gastrointestinal-associated mortality by over a third,14 infection-associated mortality by half,15 and measles incidence by 95 percent.16,17 The general picture that emerges from the scientific literature is not that vitamin A is helpful only in very small amounts and harmful in larger amounts. The picture that emerges indicates that vitamin A consistently reduces mortality from severe infectious diseases but has a more complicated relationship to lower respiratory infections that we still do not completely understand.

Getting Technical with Vitamins A and D

Vitamins A and D are both precursors to nuclear hormones, which are molecules that bind to receptors, travel into the nucleus, bind to DNA of specific target genes, and control the expression of those genes. Vitamin A is activated in a two-step process in which it is converted first from retinol into retinaldehyde and then from retinaldehyde into all-trans retinoic acid (ATRA). Similarly, vitamin D is activated in a two-step process in which it is converted first from cholecalciferol to calcidiol and then from calcidiol to calcitriol. Retinoic acid binds to several types of retinoic acid receptors (RARs) while calcitriol binds to the vitamin D receptor (VDR).31

In order to bind to DNA and control gene expression, RARs and the VDR must partner up with another receptor called the retinoid X receptor (RXR). These partners bind to each other to form a two-unit receptor complex called a dimer. Since the two receptors that form the dimer are different from one another, the complex is called a heterodimer and the process of binding together is called heterodimerization. The RXR heterodimerizes with many other nuclear receptors as well, such as the thyroid hormone receptor and the steroid hormone receptors. The heterodimers then travel to the nucleus, bind to DNA, and recruit either coactivators that help a gene start making a protein or corepressors that stop the gene from making a protein.31

Researchers agree ATRA must bind RAR and calcitriol must bind VDR for this process to begin, but they debate whether the RXR is simply a “silent partner” or whether it too must be bound by a hormone. A second derivative of vitamin A called 9-cis-retinoic acid (9CRA) is the hormone that binds to and activates the RXR in test tube studies, but some scientists have claimed that 9CRA does not exist in the live animal. In 1992, Heyman and colleagues isolated 9CRA from animal tissues,32 while other researchers using different techniques more recently were unable to find any.33,34 Large doses of vitamin A produce high tissue concentrations of 9-cis-4-oxo-13,14-dihydro-retinoic acid, a probable breakdown product of 9CRA.35 Hormones that bind to the heterodimeric partners of the RXR such as activated vitamin D,24 which binds the VDR, and clofibrate, which binds to PPAR-α,36 decrease levels of vitamin A stored in the liver. Rosiglitazone, which binds to PPAR-γ, another RXR heterodimeric partner, ramps up the activation of retinol to ATRA.37 ATRA spontaneously converts to 9CRA when exposed to the endoplasmic reticulum, one of the organelles present within every cell.38 Taken together, these findings suggest that vitamin D and other signaling compounds whose receptors heterodimerize with the RXR mobilize stored vitamin A from the liver and increase its conversion to 9CRA so that it can be used in cooperative signaling processes.

In 2006, researchers from Spain showed that 9CRA must bind to the RXR in order for the calcitriol-VDR-RXR complex to bind to DNA and control gene expression.39 More recently, the same group showed that when calcitriol binds to the VDR, it recruits corepressors that will cause it to suppress the expression of its target genes, but when 9CRA binds to the complex, the corepressors are released, allowing it to activate the expression of its target genes.40

In plain English, this means that vitamins A and D are not antagonists but actually cooperate with one another to carry out their functions.

Vitamin A and Increased Mortality

Cannell cited a meta-analysis in his journal article and December newsletter showing that “vitamin A supplements” increased the total mortality rate by 16 percent.1,2 While a typical meta-analysis pools together the results of many different studies, this one examined the effects of a large number of antioxidants, and only one section dealt with vitamin A. By the time Mercola published the claim on his web site, “vitamin A supplements” had been expanded to include “vitamin A supplements in cod liver oil.”3 The original meta-analysis, however, obtained this figure by pooling together the results of only two studies on vitamin A given alone,50 neither of which even mentioned cod liver oil.

The first study was a double-blind intervention trial in which researchers administered either 25,000 IU of vitamin A or a placebo to over 2,000 subjects at moderate risk for skin cancer for over four years.51 Vitamin A supplementation did not affect the risk of basal cell carcinoma, but it reduced the occurrence of squamous cell carcinoma by over 25 percent. The median age of the subjects was 63 and over two thirds of them were male; consequently, the majority of the subjects died by the end of the study. After 55 months, 35 percent in the vitamin A group and 36 percent in the placebo group were still alive. The authors did not claim that vitamin A had any effect on mortality.

In the other study the researchers provided either a single dose of 200,000 IU of vitamin A or a placebo to just over 100 elderly nursing home residents.52 They then observed the incidence of respiratory infections over the following 90 days. Vitamin A had no effect. F our patients in the vitamin A group died while only two patients died in the placebo group. The patients in the vitamin A group, however, were on average five years older than those in the placebo group and thus much more likely to die of old age. The authors did not claim that vitamin A had any effect on mortality.

Meta-analyses can often help us see the big picture by examining the totality of the evidence. By pooling together huge amounts of data they often achieve the statistical power necessary to verify associations between different factors that smaller studies would miss. But they also have drawbacks. Studies may be lumped together when they differ in quality or were performed in different contexts. Much of the background information on each study can be lost. In this case, citing a meta-analysis simply serves to obscure the basic facts about two small studies that offered no useful information about the effect of vitamin A on mortality at all.

Potential Dangers of Vitamin D

Dr, John Cannell of the Vitamin D Council argues that humans do not begin storing vitamin D in fat and muscle tissue until blood levels of 25-hydroxyvitamin D (also known as calcidiol and abbreviated 25(OH)D) reach 50 nanograms per milliliter (ng/mL) and that below this amount the enzyme that converts vitamin D to calcidiol for storage in the blood suffers from chronic “starvation.”1 On his Vitamin D Council web site, Cannell now recommends blood levels of calcidiol between 50 and 80 ng/mL53 and supplementation of 1,000 IU for every 25 pounds of bodyweight.2 For someone weighing between 150 and 175 pounds, he thus recommends between 6,000 and 7,000 IU per day from all sources. Cannell and his co-authors consider vitamin D to be perfectly safe for most people in amounts up to 10,000 IU per day—even while simultaneously recommending people avoid supplementing with vitamin A.1 In reality, however, these amounts of vitamin D could be dangerous when combined with low intakes of vitamins A and K2 as occurs in the general population.

Cannell and colleagues cite two studies in their journal article justifying the statement that storage of vitamin D begins at 50 ng/mL.54,55 The first of these was a preliminary report published in 2007, while the second was a much more thorough and consequently more accurate report published in 2008.56 The final report concluded that vitamin D is completely converted to calcidiol when serum calcidiol levels are below 35 ng/mL and inputs from diet and sunshine combined are below 2000 IU per day.55 Above these levels, the conversion of vitamin D to calcidiol drops to an average of 43 percent and much of the remaining vitamin D is stored in body tissues, most likely in adipose tissue. The vitamin D appears to be released from storage as blood levels of calcidiol decline. The authors observed that other studies have shown calcium absorption to be maximized and serum parathyroid hormone (PTH, a promoter of bone resorption) to be maximally suppressed at calcidiol levels of 30-34 ng/mL, in close agreement with their own study.

In support of the contention that daily vitamin D intakes of up to 10,000 IU are perfectly safe for most people, Cannell and colleagues cite a risk assessment published in 2007 that used abnormally high blood and urine calcium levels as its indicator of potential toxicity.57 Clinical vitamin D toxicity, according to these authors, occurs when calcidiol levels exceed 600 ng/mL and is accompanied by pain, conjunctivitis, anorexia, fever, chills, thirst, vomiting and weight loss. If clinical vitamin D toxicity is the only concern, 10,000 IU of vitamin D per day is likely to be harmless. Evidence suggests, however, that vitamin D can begin causing less acute adverse effects at much lower levels when intakes of vitamins A and K2 are inadequate. This is of especial concern because over one quarter of Americans already consume less than half the RDA for vitamin A,49 and blood markers for inadequate vitamin K2 status are universally present in the general population.58

A recent double-blind, placebo-controlled study found that 400 IU of vitamin D and 1,000 mg of calcium increased the risk of kidney stones by 17 percent.27 As described on page 21 of the main text, the vitamin D may have contributed to stone formation by increasing the demand for vitamin A in an elderly population counseled to avoid intakes of vitamin A above the RDA. A 2001 study found that males in South India with calcidiol levels over 89 ng/mL had three times the risk of heart disease as those with lower calcidiol levels.59 Vitamin D increases the demand for vitamin K2 as well as vitamin A, and deficiency of vitamin K2 contributes to calcification of all of the soft tissues, including the kidneys, causing kidney stones, and the arteries and aortic valves, leading to heart disease.60,61 If the association between calcidiol levels and heart disease represents true causation, which it certainly could, it suggests that calcidiol levels begin contributing to soft tissue calcification at levels much lower than 89 ng/mL, at least in the absence of adequate levels of its partner vitamins, A and K2.

In the third National Health and Nutrition Examination Survey, calcidiol levels of 35 ng/mL were associated with high bone mineral density (BMD) among all ages and races. In adults over 50, however, the association above this point was remarkably inconsistent. In whites, it kept increasing until 50 ng/mL and leveled off thereafter. In Mexican Americans, it began declining after about 40 ng/mL. In blacks, BMD began declining after 35 ng/mL and sharply declining after 50 ng/mL. Whether these differences are due to genetics, differential intakes of other fat-soluble vitamins, differential use of anticoagulants or other drugs that interact with fat-soluble vitamin metabolism, or other unknown factors, we do not know. At this stage of the game, however, it makes much more sense to emphasize the importance of obtaining calcidiol levels between 30 and 40 ng/mL, levels where we have the most solid evidence of benefit and the least indication of harm.

Average blood levels of calcidiol in people with abundant exposure to sunshine range from 40 to 65 ng/mL.62 These levels are most likely perfectly safe when intakes of vitamins A and K2 from organ meats and animal fats are just as abundant as the sunshine. The research cited above, moreover, suggests that vitamin D would be stored in adipose tissue at these levels and released when calcidiol levels drop, as they would during the winter in temperate climates—an added bonus for those who wish to obtain their vitamin D from foods like cod liver oil and fatty fish rather than from supplements during the winter. People with dark skin, however, should be careful to make sure that their calcidiol levels stay above 35 ng/mL year-round and use a supplement if necessary. Maintaining levels of 50-80 ng/mL, on the other hand, might be not only unnecessary, but dangerous in the context of a standard diet deficient in the other fat-soluble vitamins.

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References

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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2009.