Examining overly simple models: Vitamin D Status

The default model of nutritional deficiency looks something like this:

  • Marker for nutritional status is low
  • Recommendation/treatment is to increase intake of that nutrient

The problem is that both of these points may be incomplete, to the point of leading to ineffective remedies.

As Chris Masterjohn writes about 25(OH)D, the primary marker for Vitamin D status:

Although commonly used as one, 25(OH)D is not a specific marker of vitamin D status. 25(OH)D is a compound that we make from vitamin D in our liver. Vitamin D will indeed dose-dependently increase 25(OH)D, but many other factors affect the rate at which 25(OH)D is synthesized, used, or degraded. These include variations in the genetics of vitamin D metabolism, intakes of other nutrients, crisis states such as inflammation, and disease states such as cancer.

Some of the factors that cause low 25(OH)D are bad and some of them are good. While there is likely some critical threshold below which low 25(OH)D almost certainly indicates a major problem, this is not necessarily the case with moderately low 25(OH)D. In order to determine whether moderately low 25(OH)D is a good thing or a bad thing, and in order to understand what, if anything, to do about it, we need to understand why it’s low.

An Ancestral Perspective on Vitamin D Status, Part 2: Why Low 25(OH)D Could Indicate a Deficiency of Calcium Instead of Vitamin D | Mother Nature Obeyed – Weston A Price Foundation

That last sentence is key, not just for Vitamin D but for every aspect of health. There may be many reasons for certain markers being used to assess nutritional status to be high or low and understanding that reason is critical to resolving the underlying issue. This article then goes on to make the case that low serum calcium could result in low 25(OH)D I conclusion with which I agree.

Where I part ways a bit with the article relates to the 2nd point I listed above, that increased intake of a nutrient will improve the nutritional status. The article suggests that if serum calcium levels are low that increasing consumption of foods rich in calcium will help. I would say that could be true but I’m not convinced that low calcium intake is much of a problem in the United States. More likely, in my opinion, a person may have issues with suboptimal assimilation and/or utilization of calcium, which may include the effect of reducing serum 25(OH)D, among many other effects. These issues may be the result of suboptimal organ function or toxins.

At the risk of repeating myself, overly simplistic models of human health and nutrition are often inadequate in determining a course of action that restores health beyond just symptom management. People would be better off if they understood that there may be several reasons for a particular health marker to be outside of a normal range. And when the presence of a nutritional deficiency is suspected, people should consider that increasing the intake of that nutrient may not be sufficient to resolve the underlying problem.

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