Vitamin K is an essential vitamin found in plants or produced from intestinal bacteria. It plays an essential role in bone health and regulates blood clotting.

Vitamin K2 prevents heart diseases by the prevention of calcification of the arteries [Beulens et al., High dietary menaquinone intake is associated with reduced coronary calcification., Atherosclerosis. 2009]

MK-4 activates gene expression for bone making genes in osteoblasts [Ichikawa et al., Vitamin K2 induces phosphorylation of protein kinase A and expression of novel target genes in osteoblastic cells (Journal of Molecular Endocrinology (2007)]

MK-7 stimulates blood clotting [Schurgers et al., Vitamin K–containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7, Blood. 2007]

MK-4 supplementation doubles testosterone production in rats [Ito et al., Menaquinone-4 enhances testosterone production in rats and testis-derived tumor cells, Lipids Health Dis. 2011]

“MK-4 also inhibits the growth of various cancers of the liver, gut, and bone” [Shearer and Newman, Metabolism and cell biology of vitamin K, Thromb Haemost. 2008]

“Scientists observed that Ubiad1 was often silenced in tumors of the bladder, prostate, and kidney. Conversely, experimental overexpression of Ubiad1 inhibited the growth of prostate cancer cells. Since the enzyme that Ubiad1 codes for converts other K vitamins to MK-4, these results underscore that the anticancer properties of vitamin K belong specifically to MK-4.”

The gene that is now known to code for the enzyme that converts other K vitamins to MK-4, Ubiad1, was known years earlier as a tumor-suppressor gene [Shearer and Newman Recent trends in the metabolism and cell biology of vitamin K with special reference to vitamin K cycling and MK-4 biosynthesis, J Lipid Research, 2014]

Vitamin K1 can be converted to MK-4 but the rate of conversion varies greatly. Some animals can perform the conversion better than others. "Among rats, Wistar rats (Thijssen, 1994) seem to make the conversion better than Lewis rats (Ronden, 1998)"

If the conversion would be sufficient in humans, it shouldn't matter which vitamin K form we consume but studies show otherwise. Consumption of vitamin K2 but not K1 was associated with a lower risk for heart diseases [Geleijnse et al., Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study, J Nutr. 2004],

Risk for heart diseases was reduced by 10% for every 10µg/d vitamin K2 intake [Gast et al., A high menaquinone intake reduces the incidence of coronary heart disease, Nutrition, Metabolism & Cardiovascular Diseases (2009)]

Vitamin K2 intake is inversely correlated with an increased risk for prostate and lung cancer [https://www.ncbi.nlm.nih.gov/pubmed/18400723] [https://www.ncbi.nlm.nih.gov/pubmed/20335553]


Ubiad1 expression depends on zinc (Funahashi, 2015) and its enzymatic activity depends on magnesium (Hirota, 2015), suggesting that deficiencies of either of these minerals could also compromise the conversion. “

Dose

General USDA recommendation is 90µg total vitamin K. No differentiation between vitamin K1 and Vitamin K2

Chris Masterjohn recommends 100-200µg of vitamin K2 (https://chrismasterjohnphd.com/2016/12/09/the-ultimate-vitamin-k2-resource/)

Minimum effective dose for maximal desired effect

vitamin K deficiency in blood vessels, and improved the carboxylation status of osteocalcin. 360µg/d was the most efficient but big parts of the benefits were already obtained with 180µg/d. [Dalmeijer et al., The effect ofmenaquinone-7 supplementation on circulating species of matrix Gla protein, Atherosclerosis, 2012]

Doses that were 90 μg/d or greater of MK-7 caused statistically significant decreases in undercarboxylated osteocalcin, but only the 180 μg and 360 μg doses increased the levels of carboxylated osteocalcin or improved the ratio. [Knapen et al., Association of vitamin K status with adiponectin and body composition in healthy subjects: uncarboxylated osteocalcin is not associated with fat mass and body weight, British Journal of Nutrition, 2012]

“In further support of this conclusion, Ikeda (2006) found that postmenopasual women who reported consuming enough natto to provide 200 μg/d K2 or more (mostly as mostly MK-7) suffered less bone loss over the course of three years than women who consumed less. [Ikeda et al., Intake of fermented soybeans, natto, is associated with reduced bone loss in postmenopausal women: Japanese Population-Based Osteoporosis (JPOS) Study., J Nutr, 2006] “


Food sources

Natto 100g contain 950µg vitamin K2 -> fermented food in general?

Cheese

Egg yolk and dark meat of chicken -> four whole eggs provides over 20 μg and 100 grams of dark chicken meat provides 60 μg

“Our own gut microbiota also synthesize K2: Bacterioides synthesize MK-10 and MK-11, Enterobacteria synthesize MK-8, Veillonella synthesize MK-7, and Eubacterium lentum synthesizes MK-6 (Shearer, 2014). However, this probably makes little if any contribution to our own vitamin K status for two reasons: first, most of this occurs in the large intestine, which is well past the sites of vitamin K absorption in the small intestine, and all the K2 is stuck in bacterial membranes that would have to be digested to release it.”

MK-4 (animal foods), MK-7 (natto) or MK-8 and MK-9 (cheese)