Pictured above are cod livers in a bowl.
Vitamin D Experts Defend Cod Liver Oil
In November of 2008, Dr. John Cannell of the Vitamin D Council published a commentary in the journal Annals of Otology, Rhinology & Laryngology attacking cod liver oil because of its high vitamin A content, claiming that vitamin A intakes above the most minimal levels would increase mortality rates, increase vulnerability to infections, cause osteoporosis, and antagonize the beneficial effects of vitamin D. Sixteen scientists signed on to the paper as co-authors. In response, Wise Traditions published my article, “The Cod Liver Oil Debate,” in the Spring, 2009 issue, which defended cod liver oil as an important and balanced source of the fat-soluble vitamins and essential fatty acids. The following November, I expanded on this article in my lecture, “Cod Liver Oil: Our Number One Superfood,” at the Foundation’s annual conference.
We’re not the only ones who responded!
In January 2010, Michael F. Holick, MD PhD, a vitamin D researcher whose work I have cited in previous articles, Linda Linday, a medical doctor whose cod liver oil study formed the starting point for Cannell’s 2008 commentary, and several other colleagues, even including one researcher from the National Institutes of Health, made a direct response to Dr. Cannell and his colleagues in the pages of the same journal. What’s more, they even credited the Weston A. Price Foundation for raising concern about the balance between vitamins A and D!
“Cod liver oil,” they wrote, “available without a prescription for hundreds of years, is a valuable source of vitamins A and D, as well as long-chain omega-3 fatty acids, all of which may be important in the prevention of respiratory tract illnesses in children. In many populations around the world, cod liver oil continues to be a valuable source of these important nutrients. The across-the-board dismissal of cod liver oil as a supplement advocated by [Cannell and colleagues] ignores this reality.”
REDUCED RESPIRATORY INFECTIONS
The authors pointed out that in Dr. Linday’s randomized, controlled trials, cod liver oil supplementation cut doctor’s visits for upper respiratory infections between one-third and one-half. Cannell’s paper called this “less than robust,” but most of us would consider such a reduction meaningful, especially if by taking cod liver oil we got sick less often! The authors, moreover, argued that retinol from animal foods is a more reliable source of vitamin A than carotenes from plant foods since there is such wide variation in people’s ability to convert carotenes to vitamin A—an argument that has appeared in the pages of Wise Traditions many times in the past.
THE IDEAL RATIO
But now to the exciting part.
The authors devoted a section of their paper to the ideal ratio of vitamin A to D. “In the responses to [Cannell and colleagues] from the on-line supplement and nutrition newsletter communities,” they wrote, “the issue of the proper ratio of vitamin A to vitamin D emerged as a major concern.” They gave three references, including one to the Weston A. Price Foundation’s “Cod Liver Oil Update” from December, 2008.
In fact, the importance of balance between vitamins A and D was raised in the pages of Wise Traditions even earlier than 2008. In the spring of 2006, I discussed the issue in my article “Vitamin A on Trial: Does Vitamin A Cause Osteoporosis?” when I argued that vitamin A only contributes to osteoporosis when vitamin D levels are deficient or when the ratio of vitamin A to D is massively out of balance. The following fall, I raised the issue again in my article “From Seafood to Sunshine: A New Understanding of Vitamin D Toxicity,” wherein I presented research showing that vitamin A protects against vitamin D toxicity and introduced the possibility that vitamins A, D, and K2 may be cooperative factors that should all be consumed in proper balance. I more fully developed this concept in my spring 2007 article on vitamin K2, “On the Trail of the Elusive X-Factor: A Sixty-Two-Year- Old Mystery Finally Solved.”
As a result of this research, in December of 2007, I published a hypothesis on the molecular mechanism of vitamin D toxicity in the journal Medical Hypotheses entitled “Vitamin D toxicity redefined: vitamin K and the molecular mechanism,” which emphasized interactions between vitamins A, D, and K2. The following year, researchers from Tufts University published a paper in the Journal of Nutrition supporting this hypothesis, showing that vitamin A protects against vitamin D toxicity in part by helping to properly regulate the production of vitamin K-dependent proteins.
One question I have never been able to answer in any of these articles is the one everyone wants an answer to: what, precisely, is the proper ratio of vitamins A and D?
Dr. Linday and her colleagues offer a suggestion: poultry studies suggest optimal A-to-D ratios between four and eight. Similarly, in her own studies showing that cod liver oil protects against upper respiratory tract infections, Linday supplied her patients with A-to-D ratios between five and eight.
They also point out that rat studies showing that vitamin A is toxic and antagonizes the effects of vitamin D used much higher ratios, ranging from 5,000 to 55,000!
It is refreshing to see a powerful defense of cod liver oil in the scientific literature, and especially refreshing to see the work of the Weston A. Price Foundation cited therein.
We owe a big thank you to Dr. Linda Linday (MD) of St. Luke’s-Roosevelt Hospital Center in NY, NY, Dr. John C. Umhau (MD, MPH) of NIH in Bethesda, MD, Richard D. Shindledecker of New York Downtown Hospital in NY, NY, Dr. Jay N. Dolitsky (MD) of New York Eye and Ear Infirmary in NY, NY and Michael F. Holick (PhD, MD) of Boston University Medical Center in Boston, MA for helping to sort out these important questions about the fat-soluble vitamins.
OPTIMAL VITAMIN D LEVELS
Are some people pushing their vitamin D levels too high? Has science proven that the minimal acceptable blood level of vitamin D, in the form of 25(OH)D, is above 50 ng/mL (125 nmol/L)?
The answer is “No.” If you’ve been trying to maintain your levels this high because you thought this was the case, I’m sorry to break the news. There is, on the contrary, good evidence that 25(OH)D levels should be at least 30-35 ng/ mL (75-88 nmol/L). Much higher levels may be better, or they could start causing harm, especially in the absence of adequate vitamins A and K2. Once we leave the land of 30-35 ng/mL, however, we enter the land of speculation.
The idea that science has proven we need to maintain 50 ng/mL as a minimum comes from Dr. John Cannell of the Vitamin D Council. In his article “Am I Vitamin D Deficient?” he writes the following: “Thanks to Bruce Hollis, Robert Heaney, Neil Binkley, and others, we now know the minimal acceptable level. It is 50 ng/ ml (125 nmol/L). In a recent study, Heaney, et al expanded on Bruce Hollis’s seminal work by analyzing five studies in which both the parent compound (cholecalciferol) and 25(OH)D levels were measured. They found that the body does not reliably begin storing cholecalciferol in fat and muscle tissue until 25(OH)D levels get above 50 ng/ml (125 nmol/L). The average person starts to store cholecalciferol at 40 ng/ml (100 nmol/L), but at 50 ng/ml (125 nmol/L) virtually everyone begins to store it for future use. That is, at levels below 50 ng/ml (125 nmol/L), the body uses up vitamin D as fast as you can make it, or take it, indicating chronic substrate starvation—not a good thing. 25(OH)D levels should be between 50–80 ng/ml (125–200 nmol/L), year-round.”
There are a few problems with this argument. To begin with, Drs. Hollis, Heaney, Binkley, and the other authors of this study rightly made very different conclusions from their own data. In the report they wrote for the American Journal of Clinical Nutrition, they wrote the following: “One could plausibly postulate that the point at which hepatic 25(OH)D production becomes zero-order [this is the point at which the enzymes converting vitamin D to 25(OH) D are saturated with vitamin D] constitutes the definition of the low end of normal status. This value, as suggested in an equation shown in the article, is at a serum 25(OH)D concentration of 88 nmol/L (35.2 ng/mL). It is interesting that this estimate is very close to that produced by previous attempts to define the lower end of the normal range from the relations of serum 25(OH) D to calcium absorption and to serum parathyroid hormone concentration (ie, 75–85 nmol/L, or 30–34 ng/mL).”
According to the authors of this study, then, the point at which the vitamin D enzymes are saturated and vitamin D “accumulates within the body, both in serum and probably in body fat” is not 40 or 50 ng/mL (100 or 125 nmol/L) but rather 35 ng/mL (88 nmol/L).
The authors used a statistical approach that pooled together data from several studies. They presented most of their data in Figure 4, and the data from one other study in Figure 5 (see below). They did not determine the point at which vitamin D starts getting stored in body fat in particular individuals. On the contrary, they used a statistical approach to infer the point at which this occurs in their entire study population. Now, if you compare Figures 4 and 5, looking for the point at which the slope of the line dramatically changes, you will see that it changes at a higher level of 25(OH)D in Figure 5. Dr. Cannell seems to have used the data from Figure 5 to say when vitamin D gets stored in body fat in “virtually everyone” as opposed to “the average person,” but in fact the authors stated that they did not use the data from Figure 5 to determine this point because a different and apparently inferior method of measuring vitamin D levels was used in that data set.
So, we are back to the authors’ original conclusions, that vitamin D saturates its activation enzymes and starts getting stored in body fat when 25(OH)D levels reach 35 ng/mL (88 nmol/L).
The second problem is that this study does not “prove” or “show” or “demonstrate” what the optimal or minimal blood level of vitamin D is. The authors state that one could plausibly postulate that the minimum acceptable blood level is the point at which the enzymes are saturated and vitamin D is stored in body fat, but they never state that “we now know the minimal acceptable level.”
The most definitive way to determine the ideal 25(OH)D level would be to conduct a randomized, controlled trial with different levels of vitamin D supplementation targeted at reaching specific blood levels of 25(OH)D and to test the effects of the different levels of supplementation on clinical outcomes, such as bone mineral density, fracture rate, insulin resistance, glucose tolerance, cancer or heart disease.
We do not yet have this type of data. We do, however, have some strong support for raising 25(OH)D levels to at least 35 ng/mL (88 nmol/L). For example, as the authors of the study we have been looking at pointed out, similar attempts to use statistical approaches to define the 25(OH)D level that maximizes calcium absorption, maximally suppresses parathyroid hormone (which leaches calcium from bone), or maximizes bone mineral density have suggested similar results. A recent randomized, placebo-controlled trial showed that supplementing insulin-resistant women with 4,000 IU of vitamin D per day for six months reduced insulin resistance and had the most powerful effect in women whose 25(OH)D level was raised to over 32 ng/mL (80 nmol/L).
What about higher levels? The evidence is conflicting, and some of it indicates possible harm. For example, a study in the American Journal of Medicine published in 2004 found that in Americans aged over fifty, the maximal bone mineral density (BMD) occurs around 32-40 ng/mL (80- 100 nmol/L). Among Mexican Americans, BMD continues to rise a little after this point, but for whites it plateaus and begins dropping off around 45 ng/mL (110 nmol/L) and for blacks it begins dropping off even before 40 ng/mL (100 nmol/L).
If 50 ng/mL (125 nmol/L) is our minimal acceptable level, this study would seem to suggest that those of us who have “acceptable” levels of 25(OH)D would have lower bone mineral density than those of us who are moderately deficient. And that premise just doesn’t make sense.
Another study published in the European Journal of Epidemiology in 2001 found that South Indians with 25(OH)D levels higher than 89 ng/mL (223 nmol/L) were three times more likely to have suffered from ischemic heart disease than those with lower levels—and of course with such a dramatic elevation of heart disease risk, the risk may have begun increasing at levels substantially lower than 89 ng/mL.
Neither of these studies was designed to show that high levels of 25(OH)D cause decreases in bone mineral density or increases in heart disease risk, but it is possible. As I especially emphasized in my Wise Traditions and Medical Hypotheses articles on vitamin K2, bone resorption and blood vessel calcification are prominent symptoms of vitamin D toxicity in animal experiments. I also emphasized the role of vitamins A and K2 in protecting against vitamin D toxicity. So, even if these levels are in fact harmful, they may only be harmful or may be primarily harmful in the absence of adequate vitamins A and K2. The presence of the other fat-soluble vitamins could even turn these levels from harmful to beneficial.
Nevertheless, what we need in order to show that levels higher than 50 ng/mL are helpful or harmful are vitamin D supplementation trials comparing the effect of different doses resulting in different blood levels on clinical health outcomes, and similar studies examining the interactions between vitamin D and the other fat-soluble vitamins.
Lifeguards in the tropics can reach blood levels in the 50s and 60s naturally from sun exposure, suggesting these levels are “natural,” although lifeguards in Israel have twenty times the rate of kidney stones as the general population.
Kidney stones may be the most sensitive indicator of vitamin D toxicity and are a symptom of vitamin A and K2 deficiency. Thus, I suspect these levels are healthful in the context of a diet rich in vitamins A and K2, and if my levels were to reach this high in the summer sun while I was eating such a diet, I certainly would not worry.
But if you are trying desperately to maintain year-round 25(OH)D status between 50-80 ng/ mL using vitamin D supplements, you have entered the land of speculation. Enter at your own risk.
THE FAT SOLUBLE ACTIVATORS
The key finding of Dr. Weston Price was very high levels of “fat-soluble activators” in traditional diets. No matter what the particulars of the diet—whether in the frozen north, the Alpine highlands or the tropical South Seas—traditional peoples consumed plentiful amounts of vitamins A, D and what Dr. Price referred to as Activator X—now determined to be vitamin K2—from seafood, organ meats and the fat of grass-fed animals. It is difficult to obtain adequate amounts of these activators in Western diets, partly because government agencies have demonized the foods that contain these vitamins, and also because the industrializaton of agriculture has taken most livestock off pasture.
Properly processed cod liver oil is an excellent source of vitamins A and D, and this is why we recommend it for westerners, especially in preparation for conception, during pregnancy and lactation, and for growing children. Unfortunately, while the need for vitamin D has received considerable recognition in recent years, many researchers have spoken out against vitamin A and especially cod liver oil. Chief among the detractors are Dr. John Cannell of the Vitamin D Council, and Dr. Joseph Mercola of mercola.com. This article, which is necessarily technical in parts, serves as part of the ongoing debate on this subject.
For background and more information, see www.westonaprice.org/cod-liver-oil/1622.html. This article combines two recent blog postings by Chris Masterjohn. Visit his blog at www.westonaprice.org/blogs/.
FIGURE 4. Plot of the relation between serum concentrations of vitamin D3 and 25-hydroxyvitamin D after 18–20 weeks of treatment with various doses of vitamin D3. Triangles represent subjects from study B; circles subjects from study C; squares subjects from study F. The regression line is a least-squares fit of the data to a combination exponential and linear function.
FIGURE 5. Plot of the relation between serum vitamin D3 and 25-hydroxyvitamin D in study D only. As in Figure 4, the regression line is a least-squares fit of the data to a combination exponential and linear function.
From the American Journal of Clinical Nutrition, Vol. 87, No. 6, 1738-1742, June 2008. Used with permission.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Summer 2010.
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