The data suggests that the answer is yes. The first four of these health foods are rich sources of vitamin K2 and the last food item is packed with Vitamins A and D. The proposed mechanism for their protective effect rests in a wonderful biological quartet. The instruments of this quartet include the fat soluble vitamins D, K2, and A playing harmoniously with a ubiquitous human protein called Matrix gla protein (MGP).
The basic science is exquisite. Vitamins D and A acting together enhance the expression of MGP. In other words, these two fat-soluble vitamins cause our bodies to increase the production of MGP. MGP resides throughout our bodies including the walls of our arteries. Vitamin K2 then activates the MGP which in turn regulates (prevents) the calcification of plaque in the walls of our arteries. MGP masterfully plays this role in many arteries and it’s artistry is particularly effective in the coronary arteries that supply blood and oxygen to heart muscle.
Heavily calcified coronary plaque (the nasty stuff that produces atherosclerosis) as compared to un-calcified plaque is much more likely to rupture and create an acute blockage, thereby causing a heart attack. By inhibiting calcification of coronary plaque activated MGP decreases the risk of a heart attack. The biochemistry and physiology of this process are well accepted and discussed in the opening of several papers that address this topic. (1,2,3)
The data that support this theory includes a lot of basic science that describes the interaction between the four players as well as nutritional studies in humans and rodents.
The first major human study was the Rotterdam study published in the Journal of the American Society for Nutritional Sciences, 2004. Here is a quote from the summary.
“Vitamin K-dependent proteins, including matrix Gla-protein, have been shown to inhibit vascular calcification. Activation of these proteins via carboxylation depends on the availability of vitamin K. We examined whether dietary intake of phylloquinone (vitamin K-1) and menaquinone (vitamin K-2) were related to aortic calcification and coronary heart disease (CHD) in the population-based Rotterdam Study.”
The study followed 4801 adults for over 7 years and analyzed the relationship between Vitamin K intake and incidence of heart attacks, (fatal and non-fatal), death from all causes, and atherosclerosis in the aorta (the major artery of the body). The results were impressive. The analysis divided the 4801 people into three equal groups, 1/3 with the highest consumption of Vitamin K, 1/3 with the lowest consumption, and 1/3 in the middle. The higher and middle groups compared to the group with the lowest consumption had:
- significantly fewer non-fatal heart attacks,
- significantly fewer deaths from heart attack,
- significantly fewer deaths from all causes.
In addition, the group with the highest consumption of Vitamin K2 had significantly less calcified plaque in the walls of their aortas.
Comparing the group of the highest intake of vitamin K2 to the group with the lowest intake, the highest intake group had 41% less risk of non-fatal heart attack, 57% lower risk of death from heart attack and 26% lower risk of death from all causes after adjusting for multiple factors that are believed to play a role in heart attack risk. (Those other factors included age, gender, total energy intake, BMI, smoking status, pack-years smoking, diabetes, education, alcohol consumption. consumption of saturated fat, poly unsaturated fat, flavonoids (anti-oxidants) and calcium.)
Vitamin K2 consumption showed these significant associations whereas Vitamin K1 did not. Vitamin K2 is found most abundantly in animal foods that contain erroneously demonized saturated fat, Vitamin K1 is found in plants that do not contain much if any saturated fat. So this represents not only a strong statistical signal for the health benefit of Vitamin K2, but also supports the health benefit of consuming animal foods with saturated fat. The individuals who consumed more meat and more full fat fermented cheese (the two major sources of vitamin K2 in this study) had dramatically reduced risk of heart attack (both fatal and non-fatal), reduced risk of death from all causes, and less calcified plaque in the major artery of the body, the aorta. Vitamin K2 is a fat soluble vitamin which means it comes with the fat in these foods. Eating low fat foods misses this healthy opportunity.
Five years after the Rotterdam study was published, another study demonstrated similar findings. The title tells the story.
“A high menaquinone (vitamin K2) intake reduces the incidence of coronary heart disease.”
This study followed 16,057 women aged 49-70 years for 8 years. The study participants had no known heart disease at the start of the study. The results:
“After adjustment for traditional risk factors and (other) dietary factors, we observed an inverse association between vitamin K(2) and risk of CHD with a Hazard Ratio (HR) of 0.91 [95% CI 0.85-1.00] per 10 microg/d vitamin K(2) intake.”
Translation: for every increase in daily consumption of vitamin K2 by 10 micrograms per day, there was an average 9% reduction in risk of coronary disease events.
Let’s look at how much Vitamin K2 was consumed in the three groups described in the first study. Going from the lowest to the highest daily consumption the groups averaged 15.1, 26.9 and 40.9 micrograms per day. To put this in perspective, you can view a table of the Vitamin K2 content of various foods produced by Chris Masterjohn, a portion of which appears below. Before you do that, let me explain some facts about Vitamin K2.
Vitamin K2 actually represents a group of very similar vitamins that differ chemically only in the number of specific chemical side chains. The number of these side chains varies from 4 to 10, so these are referred to as MK-4 through MK-10. From Wikepedia:
All K vitamins are similar in structure: they share a “quinone” ring, but differ in the length and degree of saturation of the carbon tail and the number of “side chains”. The number of side chains is indicated in the name of the particular menaquinone (e.g., MK-4 means that four molecular units – called isoprene units – are attached to the carbon tail) and this influences the transport to different target tissues.
MK-4 is made in the tissue of grass-eating mammals that convert Vitamin K1 (from the green plants) to Vitamin K2 (MK-4). This can be obtained from animal muscle, organ meats, or the milk and milk products of mammals, including human breast milk.
The other forms of Vitamin K-2 (side-chain length > 4) are made by bacteria during the fermentation of foods (such as cheese, sauerkraut, kim chee and Natto). Here is the table from Chris Masterjohn. Go here for the original table.
The percentage of vitamin K2 present as MK-4 represents that synthesized by animal tissues, while the remainder represents that synthesized by bacteria during fermentation.
|FOOD||VITAMIN K2 (MCG/100G)|
|Goose Liver Paste||369.0||(100% MK-4)|
|Hard Cheeses||76.3||(6% MK-4)|
|Soft Cheeses||56.5||(6.5% MK-4)|
|Egg Yolk (Netherlands)||32.1||(98% MK-4)|
|Goose Leg||31.0||(100% MK-4)|
|Curd Cheeses||24.8||(1.6% MK-4)|
|Egg Yolk (United States)||15.5||(100% MK-4)|
|Chicken Liver||14.1||(100% MK-4)|
|Chicken Breast||8.9||(100% MK-4)|
|Chicken Leg||8.5||(100% MK-4)|
|Ground Beef (Medium Fat)||8.1||(100% MK-4)|
|Calf Liver||5.0||(100% MK-4)|
|Whole Milk||1.0||(100% MK-4)|
Where did our paleolithic hunter-gatherer ancestors get their Vitamin K2? They did not consume dairy products. Vitamin K2 is heavily concentrated in the pancreas, brain and liver of humans and animals. Hunter-gatherers do not waste these valuable fatty organs, in fact offal was deemed the most treasured part of a successful hunt among many hunter-gatherer societies studied during the 19th and 20th centuries.
Not many Americans eat offal such as pancreas, brain and liver so similar to Holland (where these studies were conducted) most Vitamin K2 in the American diet probably comes from hard cheese and egg yolks.
But what is the weakness in drawing conclusions from these two studies?
First they were epidemiological studies, the data was obtained from FFQs (food frequency questionnaires). They were not randomized controlled clinical trials (RCTs). There have been no RCTs that have looked specifically at Vitamin K2 relative to coronary artery disease and deaths. Having said that, you should be aware that most nutrition studies that have been published (in particular those that demonize saturated fat ) fall into the same category, they are epidemiological studies based upon food frequency questionnaires (FFQs) and such studies have been criticized with regards to reliability of data and for lack of controlling the multiple dietary and non-dietary factors that can influence health outcomes.(4)
Unlike the two studies discussed here that statistically adjusted for multiple known or argued risk factors, the epidemiologic studies that are alleged to suggest potential harm from saturated fat did not control or adjust for other statistical “con-founders”. In addition, the review papers that have so overwhelmed our society causing fat-phobia have ignored the large body of evidence that demonstrates the health benefits of consuming animal foods that contain fat soluble vitamins as well as many other vital nutrients. (4)
Regarding randomized controlled trials, there have been many convincing RCTs in rodents that demonstrate not only prevention of calcified plaques in arterial walls but actual reversal of atherosclerosis in rodents with high doses of vitamin K2. (5) Furthermore, a certain breed of experimental rodent that completely lacks MGP suffers from early death caused by severe atherosclerosis further supporting the fundamental role of activated MGP in maintaining vascular health. (6)
1. Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study
2. A high menaquinone intake reduces … [Nutr Metab Cardiovasc Dis. 2009] – PubMed – NCBI
3. Vitamin K status and vascular calcification: eviden… [Adv Nutr. 2012] – PubMed – NCBI
4. Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence
5. Regression of warfarin-induced medial elastocalcinosis… [Blood. 2007] – PubMed – NCBI
6. Two sides of MGP null arterial disease: chondrogenic lesions dependent on transglutaminase 2 and elastin fragmentation associated with induction of adipsin.