In the first post in this series, I critiqued the “naked ape hypothesis of optimal serum 25(OH)D,” which I believe influences many researchers to interpret uncertainties in the scientific literature in a way that is biased towards recommendations for high intakes of vitamin D that could be harmful to some people, especially without appropriate attention to the nutrient density and balance of the diet, and to the overall context of a healthy diet and lifestyle.

Now I would like to begin critiquing the use of low 25(OH)D on its own to determine vitamin D status. As the series progresses, I will discuss numerous explanations for low 25(OH)D besides vitamin D deficiency. In this post, I will discuss why a deficient intake of calcium can probably cause low 25(OH)D.

I’ve explained the gist of this post and its bottom line over at the Daily Lipid Video Blog. The details follow.

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It has become increasingly common for health enthusiasts and now even typical patients in the doctor’s office to have a lab estimate their vitamin D status by measuring serum 25-hydroxyvitamin D, abbreviated 25(OH)D, and use vitamin D supplements to bring this value into the “sufficient” range. While even this basic practice is problematic, the extraordinary influence of what I like to call the “naked ape hypothesis of optimal serum 25(OH)D” has created a paradigm wherein “deficiency” and “insufficiency” are together seen as the norm, and 25(OH)D levels that may actually be quite dangerous — especially when not adequately balanced by other nutrients in the diet — are specifically sought out as a panacea.

Indeed, this paradigm heavily influenced some of my early articles on the fat-soluble vitamins, such as my 2006 article “From Seafood to Sunshine: A New Understanding of Vitamin D Safety,” where I contributed original ideas about the interactions between the fat-soluble vitamins, but essentially took the popular ideas advocating high levels of serum 25(OH)D for granted. I now believe my rush to embrace the latter paradigm was quite hasty and that it deserves the same critical attention that I have put into my ideas about vitamin interactions.

In this series, I will argue that we should emphasize serum 25(OH)D much less and emphasize the nutrient density and nutrient balance of the overall diet and lifestyle much more. I will also offer some practical guidelines for interpreting 25(OH)D in a more nuanced and sophisticated way.

I’d like to begin by pointing out some not-so-obvious and yet profound problems with the “naked ape hypothesis of serum 25(OH)D.” For simplicity, I may refer to this hypothesis simply as the “naked ape hypothesis” through the remainder of this post.

If you’re anxious for the bottom line, you can watch the video summary. If you’d like to head straight into meat of the post, you can find it below.

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Osteocalcin is a vitamin K-dependent protein that our bones produce. The job of vitamin K is to activate this protein by adding carbon dioxide to it, which in scientific jargon we call “carboxylation.” Vitamin K researchers widely regard the ratio of undercarboxylated to carboxylated or total osteocalcin as a marker of inadequate vitamin K status. Evidence has accumulated over the last half decade, however, that undercarboxylated osteocalcin may stimulate the production of insulin and testosterone, while simultaneously enhancing insulin sensitivity, and by doing so, make us lean and fertile.

Is undercarboxylated osteocalcin a good thing or a bad thing? Could this represent a downside to getting enough vitamin K, particularly vitamin K2, the form that most effectively reaches our bones? I’ll tackle these questions in this post as I critically review the literature on undercarboxylated osteocalcin’s role as an insulin- and testosterone-boosting hormone.
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This is the seventh and final installment in a series of posts in which I am laying out the most salient points from my 2012 Real Food Summit talk, “Weston Price on Primitive Wisdom.” See these links for part 1, part 2part 3, part 4, part 5, and part 6.

How are we to place Price’s work in its appropriate context? How are we to respect and embrace the wisdom of our ancestors, while using modern science and our personal experience to refine and enrich the pool of accumulated wisdom? I will explore these questions in this final post.

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In April of 2011, I posted a rebuttal of a Nature paper from Stanley Hazen’s group at the Cleveland Clinic arguing that choline from animal foods causes heart disease:

Does Dietary Choline Contribute to Heart Disease?

Their argument was that our intestinal bacterial convert choline to trimethylamine, which our livers then convert to trimethylamine oxide (TMAO), which causes atherosclerosis in mice, and thus, by extension, probably in humans. I pointed out that previous studies have shown that supplements with salts of free choline do in fact generate TMAO, but uncontaminated phosphatidylcholine, the main form of choline found in food, does not. Moreover, choline-rich foods like liver and eggs did not produce more TMAO than a control breakfast, but seafood, which is generally contaminated with some trimethylamine or TMAO, did.

In a new paper in Nature Medicine, these authors have expanded their argument to claim that the carnitine in red meat contributes to heart disease through the same pathway. Put on your seat belts, folks, and let’s take a look!

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I recently came across several papers published in The Veterinary Record in the 1960s documenting the efficacy and risks of injecting cows with a mega-dose of vitamin D just before calving to prevent “milk fever,” which isn’t a fever at all, but is a mix of clinical symptoms including weakness, loss of appetite, and in the extreme case heart failure. It results from low blood levels of calcium, which sometimes occur in the first few days of lactation, before the cow can adequately adjust its calcium balance to meet the new demands for this mineral. It may be a relatively recent disease resulting from the excessive demand for lactation placed on modern dairy cows. In this post, I will review these papers, which provide evidence that thyroid hormone and vitamin A protect against the harmful effects of the vitamin D injections.

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This is the sixth installment in a series of posts in which I am laying out the most salient points from my 2012 Real Food Summit talk, “Weston Price on Primitive Wisdom.” See these links for part 1, part 2part 3, part 4, and part 5. This post will cover Price’s support for what we could call “real food,” and why he considered alternative approaches to be based on the accumulation of knowledge at the expense of wisdom.

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This is the fifth installment in a series of posts in which I am laying out the most salient points from my 2012 Real Food Summit talk, “Weston Price on Primitive Wisdom.” See these links for part 1, part 2part 3, and part 4.

One of the major sections of my talk was on Price’s theory of primitive wisdom. Since this section was based on my June, 2011 blog post, “Understanding Weston Price on Primitive Wisdom — Ancient Doesn’t Cut It,” it makes little sense to write another post about it in this series. In brief, Price concluded that the groups he studied maintained good health not simply because they were limited to a more primitive environment and lacked industrial foods, but because they had accumulated wisdom about how to select important nutrient-dense foods and possessed the strength of character necessary to procure those foods even when doing so proved difficult. In this post, I’d like to focus on what Price found and concluded regarding wheat and other cereal grains.

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This is the fourth installment in a series of posts in which I am laying out the most salient points from my 2012 Real Food Summit talk, “Weston Price on Primitive Wisdom.” See these links for part 1, part 2, and part 3.

At the first annual Ancestral Health Symposium in 2011, I had the great honor of meeting “Paleo” contributor Loren Cordain. Dr. Cordain told me that he considered Weston Price “the grandfather of the Paleo movement,” and said the only thing Price lacked was an “evolutionary approach.” In fact Price did retrospectively offer an “evolutionary approach” in the 1945 edition of Nutrition and Physical Degeneration, which many would have missed if they read the free online version of the book, but this approach is very different from that generally invoked by the Paleo movement and is absent from the 1939 edition, where Price laid out the intentions behind his study design. In this post, I will explore these approaches.

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This is the third installment in a series of posts in which I will lay out the most salient points from my 2012 Real Food Summit talk, “Weston Price on Primitive Wisdom.” See these links for part 1 and part 2.

In this post, I’ll address the scope of Price’s work. Although his most rigorous findings were that tooth decay and dental deformities consistently showed dramatic increases with modernization when modernized subgroups of each “racial stock” were compared to their traditionally living counterparts, the full extent of Price’s work is broader than this.

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