Here's an excerpt from Nutrition and Physical Degeneration, about traditional and modernized Swiss groups. Keep in mind these are Europeans we're talking about (although he found the same thing in all the races he studied):
The reader will scarcely believe it possible that such marked differences in facial form, in the shape of the dental arches, and in the health condition of the teeth as are to be noted when passing from the highly modernized lower valleys and plains country in Switzerland to the isolated high valleys can exist. Fig. 3 shows four girls with typically broad dental arches and regular arrangement of the teeth. They have been born and raised in the Loetschental Valley or other isolated valleys of Switzerland which provide the excellent nutrition that we have been reviewing.Price attributed this physical change to a lack of minerals and the fat-soluble vitamins necessary to make good use of them: vitamin A, vitamin D and what he called "activator X"-- now known to be vitamin K2 MK-4. The healthy cultures he studied all had an adequate source of vitamin K2, but many ate very little K1 (which comes mostly from vegetables). Inhabitants of the Loetschental valley ate green vegetables only in summer, due to the valley's harsh climate. The rest of the year, the diet was limited chiefly to whole grain sourdough rye bread and pastured dairy products.
Another change that is seen in passing from the isolated groups with their more nearly normal facial developments, to the groups of the lower valleys, is the marked irregularity of the teeth with narrowing of the arches and other facial features... While in the isolated groups not a single case of a typical mouth breather was found, many were seen among the children of the lower-plains group. The children studied were from ten to sixteen years of age.
The dietary transitions Price observed were typically from mineral- and vitamin-rich whole foods to refined modern foods, predominantly white flour and sugar. The villagers of the Loetschental valley obtained their fat-soluble vitamins from pastured dairy, which is particularly rich in vitamin K2 MK-4.
In a modern society like the U.S., most people exhibit signs of poor cranial development. How many people do you know with perfectly straight teeth who never required braces? How many people do you know whose wisdom teeth erupted normally?
The archaeological record shows that our hunter-gatherer ancestors generally didn't have crooked teeth. Humans evolved to have dental arches in proportion to their tooth size, like all animals. Take a look at these chompers. That skull is from an archaeological site in the Sahara desert that predates agriculture in the region. Those beautiful teeth are typical of paleolithic humans and modern hunter-gatherers. Crooked teeth and impacted wisdom teeth are only as old as agriculture. However, Price found that with care, certain traditional cultures were able to build well-formed skulls on an agricultural diet.
So was Price on to something, or was he just cherry picking individuals that supported his hypothesis? It turns out there's a developmental syndrome in the literature that might shed some light on this. It's called Binder's syndrome. Here's a description from a review paper about Binder's syndrome (emphasis mine):
Allow me to translate: in Binder's patients, the middle third of the face is underdeveloped, they have narrow dental arches and crowded teeth, small nostrils and abnormally small sinuses (sometimes resulting in mouth breathing). Sound familiar? So what causes Binder's syndrome? I'll give you a hint: it can be caused by prenatal exposure to warfarin (coumadin).
The essential features of maxillo-nasal dysplasia were initially described by Noyes in 1939, although it was Binder who first defined it as a distinct clinical syndrome. He reported on three cases and recorded six specific characteristics:5
Individuals with Binder's syndrome have a characteristic appearance that is easily recognizable.6 The mid-face profile is hypoplastic, the nose is flattened, the upper lip is convex with a broad philtrum, the nostrils are typically crescent or semi-lunar in shape due to the short collumela, and a deep fold or fossa occurs between the upper lip and the nose, resulting in an acute nasolabial angle.
- Arhinoid face.
- Abnormal position of nasal bones.
- Inter-maxillary hypoplasia with associated malocclusion.
- Reduced or absent anterior nasal spine.
- Atrophy of nasal mucosa.
- Absence of frontal sinus (not obligatory).
Warfarin is rat poison. It kills rats by causing them to lose their ability to form blood clots, resulting in massive hemmorhage. It does this by depleting vitamin K, which is necessary for the proper functioning of blood clotting factors. It's used (in small doses) in humans to thin the blood as a treatment for abnormal blood clots. As it turns out, Binder's syndrome can be caused by a number of things that interfere with vitamin K metabolism. The sensitive period for humans is the first trimester. I think we're getting warmer...
Another name for Binder's syndrome is "warfarin embryopathy". There happens to be a rat model of it. Dr. Bill Webster's group at the University of Sydney injected rats daily with warfarin for up to 12 weeks, beginning on the day they were born (rats have a different developmental timeline than humans). They also administered large doses of vitamin K1 along with it. This is to ensure the rats continue to clot normally, rather than hemorrhaging. Another notable property of warfarin that I've mentioned before is its ability to inhibit the conversion of vitamin K1 to vitamin K2 MK-4. Here's what they had to say about the rats:
The warfarin-treated rats developed a marked maxillonasal hypoplasia associated with a 11-13% reduction in the length of the nasal bones compared with controls... It is proposed that (1) the facial features of the human warfarin embryopathy are caused by reduced growth of the embryonic nasal septum, and (2) the septal growth retardation occurs because the warfarin-induced extrahepatic vitamin K deficiency prevents the normal formation of the vitamin K-dependent matrix gla protein in the embryo."Maxillonasal hypoplasia" means underdevelopment of the jaws and nasal region. Proper development of this region requires fully active matrix gla protein (MGP), which I've written about before in the context of vascular calcification. MGP requires vitamin K to activate it, and it seems to prefer K2 MK-4 to K1, at least in the vasculature. Administering K2 MK-4 along with warfarin prevents warfarin's ability to cause arterial calcification (thought to be an MGP-dependent mechanism), whereas administering K1 does not.
Here are a few quotes from a review paper by Dr. Webster's group. I have to post the whole abstract because it's a gem:
The normal vitamin K status of the human embryo appears to be close to deficiency [I would argue in most cases the embryo is actually deficient, as are most adults in industrial societies]. Maternal dietary deficiency or use of a number of therapeutic drugs during pregnancy, may result in frank vitamin K deficiency in the embryo. First trimester deficiency results in maxillonasal hypoplasia in the neonate with subsequent facial and orthodontic implications. A rat model of the vitamin K deficiency embryopathy shows that the facial dysmorphology is preceded by uncontrolled calcification in the normally uncalcified nasal septal cartilage, and decreased longitudinal growth of the cartilage, resulting in maxillonasal hypoplasia. The developing septal cartilage is normally rich in the vitamin K-dependent protein matrix gla protein (MGP). It is proposed that functional MGP is necessary to maintain growing cartilage in a non-calcified state. Developing teeth contain both MGP and a second vitamin K-dependent protein, bone gla protein (BGP). It has been postulated that these proteins have a functional role in tooth mineralization. As yet this function has not been established and abnormalities in tooth formation have not been observed under conditions where BGP and MGP should be formed in a non-functional form.I think there's a good case to be made that most people in modern societies exhibit some degree of "Binder's syndrome" due to subclinical vitamin K2 deficiency during growth. I believe the evidence suggests that prenatal vitamin K2 MK-4 deficiency is behind narrow dental arches, crooked teeth, underdevelopment of the face and jaw, underdevelopment of the sinuses with mouth breathing in some cases, and poor tooth development resulting in a high susceptibility to dental cavities.
These symptoms are so common they are viewed as normal in industrial societies. There is no other single factor that so elegantly explains these characteristic changes in cranial form. Rickets (vitamin D deficiency during growth) also causes cranial malformations, but they are distinct from those caused by K2 deficiency.
Humans do not efficiently convert K1 into K2 MK-4 (unlike rats), so we require a ready source of K2 in the diet. Our hunter-gatherer ancestors had a relatively high intake of K2 MK-4 from the organs of wild animals (particularly brain, pancreas, and marrow), insects and seafood. Our food supply today is depleted of K2, due to our avoidance of organ meats and poor animal husbandry practices. K2 MK-4 is found only in animal products. Pastured dairy is the most convenient source of K2 MK-4 in the modern diet, just as it was for the villagers of the Loetschental valley when Dr. Price visited them. Dairy from grain-fed cows contains much less K2.
Price felt that to ensure the proper development of their children, mothers should eat a diet rich in fat-soluble vitamins both before and during pregnancy. This makes sense in light of what we now know. There is a pool of vitamin K2 MK-4 in the organs that turns over very slowly, in addition to a pool in the blood that turns over rapidly. Entering pregnancy with a full store means a greater chance of having enough of the vitamin for the growing fetus. Healthy traditional cultures often fed special foods rich in fat-soluble vitamins to women of childbearing age and expectant mothers, thus ensuring beautiful and robust progeny.