This is the second 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.” In part one, I described Price’s “study design” as the observation of a series of “natural experiments” where he compared isolated and modernized subgroups of each of a series of “primitive racial stocks,” so he could evaluate the effect of modernization while controlling for hereditary, cultural, and geographic factors. In this post, I’d like to explain why comparing one “primitive racial stock” to another is a far less valuable and far more confounded approach, using apparent adaptations in vitamin D metabolism among the Inuit as an illustrative example.
Suppose we picked two groups, the Inuit and the Gaelics. On page 441 of Nutrition and Physical Degeneration, we see that the “primitive” Inuit had only 0.09 percent of teeth attacked by cavities while the “primitive” Gaelics had 1.2 percent of teeth attacked. We might conclude from this that the traditional Inuit diet is superior to the traditional Gaelic diet, perhaps because it wasn’t full of oats. After all, even on their traditional diets the Gaelics had thirteen times more tooth decay than the Inuit.
Such a conclusion would ignore the fact that the Inuit and Gaelics might have hereditary differences that affect skeletal and dental health. In fact, there are good reasons to believe that the Inuit have specific adaptations related to vitamin D metabolism that protect their skeletal health at the expense of other measures of health, particularly the nervous system.
In “The Pursuit of Happiness,” my 2008 Wise Traditions conference lecture, “The Fat-Soluble Vitamins and Mental Health,” and in a previous post of mine, “Vitamin D — Problems With the Latitude Hypothesis” I described a phenomenon called pibloktoq, a form of hysteria documented among the Inuit of the Thule District of northern Greenland. In a chapter he contributed to Psychological Anthropology (Hsu, 1972), Anthony FC Wallace reviewed evidence suggesting the phenomenon results from hypocalcemia secondary to low intakes of vitamin D and calcium. Here are some key points he made:
- The disorder involves a period of hours or days in which the person seems irritable or withdrawn, followed by sudden, wild excitement with irrational, offensive, and dangerous behavior. It ends with convulsions and stupor. Finally, the person recovers but cannot remember the experience.
- It certainly occurs in northwest Greenland, probably occurs elsewhere in Greenland, and might occur anywhere in the world. The degree to which it is a specifically Inuit disorder is unclear.
- It occurs most often in the late winter and early spring, and least often in the summer.
- It can reach epidemic proportions in the Thule district.
- It resembles tetany, a condition caused by low concentrations of calcium in the blood, which involves involuntary muscle spasms and sometimes severe convulsions, and is often complicated by emotional and cognitive disorganization.
- Medical reports have often noted a tendency towards signs of tetany, such as convulsions in infants and leg cramps in adults, among the Inuit.
- In certain regions of Alaska and Greenland where the fishing is poor, access to calcium from dried whole fish and vitamin D from marine oils is often scarce. Combined with lower availability of vitamin D from sunlight, whether because of latitude or clothing, Inuit dwelling in these regions could easily become deficient in vitamin D and calcium, especially during the winter.
- Wallace suggested that in someone already suffering from low total calcium, prolonged deep breathing, or hyperventilation from emotional stress, could lower the concentration of carbon dioxide in the blood, which would in turn alter the acid-base balance and thereby reduce the concentration of ionized calcium in the blood. Thus, the ionized calcium would transiently become low enough to cause an attack.
Wallace had one major fact standing in the way of his argument, however: if the Inuit are vulnerable to tetany caused by vitamin D and calcium deficiency, why have rickets and osteomalacia been so rare among them? He suggested that the physically difficult arctic environment led to adaptations in vitamin D metabolism that spare the skeleton at the expense of the nervous system. This passage is worth quoting in full:
One fact, however, militates against a simple dietary calcium deficiency hypothesis: the reported extreme rarity of rickets in Eskimo infants and of osteomalacia in Eskimo adults (for example, in pregnant and lactating women). These are diseases in which, as a consequence of inadequate calcium intake or utilization, or both, the bones yield their calcium to the blood and, eventually, to the urine, with the sufferer thus gradually losing calcium from the body at the expense of bony tissue.
In temperate latitudes, rickets and osteomalacia are normally forestalled by milk, sunlight, and supplementary vitamin D3 preparations in cod liver oil and vitamin pills. If one hypothesizes that the Eskimo diet is low in calcium, and perhaps in sun-formed vitamin D3, how is it that rickets is not evident? The answer to this question requires another hypothesis concerning hormonal function.
It would seem that if calcium and/or vitamin D3 intake is chronically low in the high arctic environment, then the Eskimo physiology must for generations have been forced to “choose” between tetany and rickets — and, unlike more southerly populations, it has “chosen” tetany as the lesser of two evils. (More precisely, of course, it is the environment which has selected the better-fitted physiological alternative.)
Rickets and osteomalacia would in a primitive Eskimo economy be fatal because they are physically crippling. Sporadic attacks of tetany, even if occasionally damaging or even fatal, would be by comparison merely an annoyance. Hence the hypocalcemia hypothesis requires the corollary that the Polar and perhaps other Eskimo tend to be mildly hypoparathyroid (or, more exactly, again, that in this cultural-ecological matrix, optimum parathyroid function requires a lower activity than does optimum function under the conditions familiar to European and American medical practice). Such a mild “hypoparathyroidism” would be conceived as a product of natural selection for primitive life in an arctic environment, yielding a type of hormonal balance which retains calcium in the bones even if calcium levels in serum fall occasionally.
There is, as a matter of fact, some evidence to support this hypothesis. The doomed medieval Norsemen, not preadapted to high arctic environment, who settled along the west coast of Greenland, and who finally died out and were replaced by ricketless Eskimo, did suffer from rickets and osteomalacia (Maxwell, 1930:20).
Wallace thus argued that the Inuit are adapted to a lower “normal” level of parathyroid hormone. Calcitriol, the active form of vitamin D, will increase the amount of calcium we absorb from food all by its own, but it needs the help of parathyroid hormone to leach calcium from the bones so that it will enter the blood and be available to the nervous system. As a result, parathyroid hormone helps spare calcium for the nervous system at the expense of the skeletal system. Thus, a lower level of parathyroid hormone would alter the function of calcitriol in a way that spares calcium for the skeletal system at the expense of the nervous system.
A 2004 paper published in Calcified Tissue International supports this idea (1). Inuits consuming “western fare” and living in Denmark had lower 25(OH)D, higher calcitriol, and lower parathyroid hormone compared to Danes. Inuits consuming “traditional fare” had 25(OH)D levels comparable to Danes, but had even higher calcitriol and even lower parathyroid hormone. “Traditional fare” was defined loosely in this paper as containing “seal and or whale at least once a week.”
Let’s quickly review normal vitamin D physiology before interpreting these results. Parathyroid hormone causes the activation of 25(OH)D, the semi-activated form of vitamin D, to calcitriol. Greater intakes of vitamin D increase the amount of 25(OH)D. When more 25(OH)D is available to the enzyme that performs the final activation step, that enzyme can make calcitriol more easily without the help of parathyroid hormone. Thus, greater vitamin D intakes suppress parathyroid hormone.
Nevertheless, when Inuit and Danes are consuming similar diets, the Inuit paradoxically have less parathyroid hormone circulating, and yet have a greater rate of activation of 25(OH)D to calcitriol. To my knowledge, no one has yet demonstrated the hereditary basis for this, but the results suggest to me that the Inuit have a genetic polymorphism that increases the rate of the final activation step independently of parathyroid hormone. When they eat their traditional diet, the Inuit achieve normal levels of 25(OH)D, yet have even greater calcitriol and even lower parathyroid hormone. Thus, the Inuit should be best off with a traditional diet, but for likely genetic reasons, their skeletal systems will be better off than those of Danes regardless of diet. On a modern diet or in times of scarcity, this benefit to the skeletal system likely comes at the expense of the nervous system.
Price’s data is consistent with this hypothesis. The Inuit not only had one of the lowest rates of tooth decay on their traditional diet; they also had one of the lowest rates of tooth decay on a modernized diet: only 13 percent, compared to thirty percent among the Gaelics and Swiss.
This is just one illustrative example of hereditary differences in skeletal metabolism that could exist between the different “primitive racial stocks” that Price studied. There are likely many others, making it important to emphasize Price’s intentional study design — comparing isolated and modernized subgroups of each “racial stock” — over the many other much more confounded observations we could casually make when reading his work.
Read more about the author, Chris Masterjohn, PhD, here.
1. Rejnmark L, Jorgensen ME, Pedersen MB, Hansen JC, Heickendorff L, Lauridsen AL, Mulvad G, Siggaard C, Skjoldborg H, Sorensen TB, Pedersen EB, Mosekilde L. Vitamin D insufficiency in Greenlanders on a westernized fare: ethnic differences in calcitropic hormones between Greenlanders and Danes. Calcif Tissue Int. 2004;74(3):255-63.