Vitamin A/CLO debate - Weston Price response

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http://www.westonaprice.org/The-Cod-Liver-Oil-Debate.html

The Cod Liver Oil Debate Print E-mail

Health Topics - Cod Liver Oil

Written by Masterjohn

2009-Apr-30

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.

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. 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.

ph 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

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, 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.â€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

Dspecific 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.

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 Worldâ€

but that “it appears to increase the risk and/or worsen the clinical course in

normal children.â€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.â€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 W hile 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.â€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, 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.â€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.

References

1. Cannell JJ, Vieth R, Willet W, et al. Cod Liver Oil, Vitamin A Toxicity,

Frequent Respiratory Infections, and the Vitamin D Deficiency Epidemic. Ann Otol

Rhinol Laryngol. 2008;117(11):864-70.

2. Cannell JJ. The Vitamin D Newsletter: Vitamin A Toxicity. December, 2008.

Now archived at http://www.vitamindcouncil.org/newsletter/2008-december.shtml.

3. Mercola J. Important Cod Liver Oil Update.

http://articles.mercola.com/sites/articles/archive/2008/12/23/important-cod-live\

r-oil-update.aspx. Published December 23, 2008. Accessed January 21, 2009.

4. Mercola J. Why Vitamin A May Not Be as Useful or Harmless as You Thought.

http://articles.mercola.com/sites/articles/archive/2009/01/03/why-vitamin-a-may-\

not-be-as-useful-or-harmlessas-you-thought.aspx. Published January 3, 2009.

Accessed January 21, 2009.

5. Guy RA. The History of Cod Liver Oil As a Remedy. Am J Dis Child.

1923;26:112-6.

6. JH. Treatise on the Oleum Jecoris Aselli or Cod Liver Oil.

ton, SC: BiblioBazaar LLC, 2008.

7. Kurlansky M. Cod: A Biography of the Fish That Changed the World. New

York, NY: and Company, 1997.

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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.

About the Author

MasterjohnMasterjohn is the author of several Wise Traditions

articles and the creator and maintainer of Cholesterol-And-Health.Com, a website

dedicated to extolling the virtues of cholesterol and cholesterol-rich foods. He

has authored two items accepted for publication in peer-reviewed journals: a

letter in an upcoming issue of the Journal of the American College of Cardiology

criticizing the conclusions of a recent study on saturated fat and a full-length

feature in an upcoming issue of Medical Hypotheses proposing a molecular

mechanism of vitamin D toxicity. Masterjohn holds a Bachelor's degree in History

and is preparing to pursue a PhD in Molecular and Cellular Biology. He is also a

Weston A. Price Foundation Local Chapter Leader in West Brookfield,

Massachusetts.