top of page
Search

VITAMIN K AND LONGEVITY

New research confirms that vitamin K can slash the risk of arterial calcification, coronary heart disease, cancer, type II diabetes, and metabolic syndrome. Most compelling is a study showing that those with the highest intakes of vitamin K are less likely to die from any cause.



A new 2014 study on vitamin K confirms that ample vitamin K intake can indeed help you live longer. In a group of more than 7,000 people at high risk for cardiovascular disease, people with the highest intake of vitamin K were 36%less likely to die from any cause at all, compared with those having the lowest intake.

  • Once thought to be exclusively concerned with blood coagulation, vitamin K is now known to affect at least 16 Gla-proteins in the body.

  • These include proteins involved in protecting arteries from calcification, those protecting bones from losing calcium, and ones that help prevent against diabetes and cancer.

  • A new study demonstrated that people with higher vitamin K intakes are less likely to die from all causes

  • A multitude of studies now point to the fact that adequate vitamin K intake can offer prevention against atherosclerosis, osteoporosis, diabetes, and cancer.

This protection even extended to those with initially low vitamin K intake who boosted their consumption during the course of the study—demonstrating that it’s never too late to start gaining the benefits of vitamin K supplementation. Increasing intake conferred protection against cardiovascular death as well.


Vitamin K is capable of opposing many of the leading causes of death in modern-day Americans—including atherosclerosis, osteoporosis, diabetes, and cancer — because it has the unique ability to activate proteins involved in these conditions.


The Many Benefits Of Vitamin K Vitamin K was first discovered in 1935, when it was found to be an essential nutrient to prevent abnormal bleeding in chickens. For decades thereafter, vitamin K was identified as the “coagulation vitamin” (in fact, the initial “K” comes from the German spelling, koagulation). During that time, it was established that vitamin K worked by activating certain proteins made in the liver that are required for normal blood clotting. Without sufficient vitamin K, blood would not clot, and severe bleeding would ensue.

Vitamin K activates those blood-clotting proteins by making a small but vital chemical change in the proteins’ structure, specifically on the protein building block called glutamic acid.

By the turn of the 21st century, scientists had learned that vitamin K produces similar changes to glutamic acid molecules to activate a handful of other vital proteins in the body, with the collective name of Gla-proteins. According to recent research, 16 different vitamin K-dependent Gla-proteins have been identified. This means that they depend on vitamin K to activate them in order to carry out their intended role. With the discovery of the Gla-proteins, scientists learned that vitamin K is vital for much more than the healthy clotting of blood. For example, the Gla-protein in bone, called osteocalcin, is responsible for making sure calcium is deposited in bones, while the Gla-protein in arterial walls, called matrix Gla protein, prevents calcium from being deposited in arteries.

Insufficient blood clotting was thought to be the main sign of vitamin K deficiency. However, scientists have since learned that you can have enough vitamin K to promote healthy blood clotting, yet still not have enough vitamin K for it to activate the Gla-proteins necessary to help prevent cardiovascular disease, osteoporosis, diabetes, and cancer, all conditions in which vitamin K-dependent proteins are known to be factors. Vitamin K And Atherosclerosis As we age, calcium that belongs in our bones begins to make its appearance in other unwanted areas, including inside the linings of major arteries. Over time, normal smooth muscle cells in artery walls transform into bone-like cells through the deposition of calcium, essentially turning sections of artery into bony tissue that is not resilient and flexible, and does not have the ability to effectively regulate blood flow. This process lends literal reality to the term “hardening of the arteries,” which we now know as late-stage atherosclerosis.

Nature has provided a powerful inhibitor of arterial calcification in the form of matrix Gla protein, one of the 16 Gla-proteins activated by vitamin K. This specific Gla-protein is produced in arterial walls, but is only activated when sufficient vitamin K is present. In the absence of sufficient vitamin K, arterial calcification is able to continue unopposed, leading to advanced atherosclerosis and its deadly consequences, heart attacks and strokes. Indeed, in older men and women who had the highest levels of inactive matrix Gla protein (indicating low vitamin K levels), there was a nearly 3-fold increased risk of cardiovascular disease compared to those with the lowest levels.

Researchers have known for nearly 20 years that insufficient vitamin K intake in the diet is related to atherosclerosis in the aorta, the body’s largest blood vessel. Since that time, a host of basic science and laboratory studies have indicated that higher vitamin K intake is essential for preventing atherosclerosis in major vessels of all kinds. Animal studies even show that vitamin K can “rescue” calcified arteries that occur as a result of the overuse of drugs that inhibit vitamin K, such as certain blood thinners.

Another way matrix Gla proteins help protect against atherosclerosis is by inhibiting the production of inflammatory signaling molecules (cytokines), which contribute to plaque formation and calcification. People with the highest dietary intake of vitamin K have significantly lower levels of those inflammatory markers, and also of substances involved in appetite generation and insulin resistance, both of which are important in preventing atherosclerosis.

Human Studies On Vitamin K Human studies on dietary vitamin K intake have been somewhat inconsistent, probably because of confusion about which form of the vitamin is most important.

Vitamin K1 (phylloquinone) is the main dietary form of the vitamin, but vitamin K2 (menaquinone) has a stronger relationship to arterial calcification.

In one study, people with the highest intake of vitamin K2 were 57% less likely to die of coronary heart disease compared with those with the lowest intake. In another study, women with the highest intake of vitamin K2 were found to be at a 20% lower risk for coronary artery calcification compared with women with the lowest intake levels, while the same study found that vitamin K1 had no significant impact.

Vitamin K supplementation studies suggest that both forms of the vitamin contribute to protection from arterial calcification in atherosclerosis, with a slight edge for vitamin K2. For example, when healthy men and postmenopausal women supplemented with 500 micrograms of vitamin K1 per day, they experienced a modest 6% reduction in the progression of arterial calcification, but only in subjects with the most advanced disease at baseline. A study using vitamin K1 in combination with vitamin D and minerals demonstrated that the combined supplement could slow the loss of arterial suppleness and promote elasticity.

Similarly, supplementation with both 180 and 360 micrograms of vitamin K2 significantly reduced the amounts of inactivated matrix Gla protein, thereby lowering the risk of atherosclerosis with calcification; placebo recipients in that study showed no effect. In another study, a group of kidney disease patients on hemodialysis (who have a very high risk for advanced atherosclerosis with calcification) took either 135 or 360 micrograms of vitamin K2. Supplementation dramatically decreased the amount of inactivated matrix Gla protein by 77% at the lower dose, and 93% at the higher dose.

Intriguingly, it is now apparent that women with atherosclerosis are more likely to have lower circulating vitamin K levels, highlighting the age-related trade-off between calcium in bones (which is desirable) and calcium in arterial walls (which is undesirable).

Vitamin K And Osteoporosis Sufficient vitamin K is also required in order to activate the Gla-protein osteocalcin, which binds tightly to bone minerals to create strong bones. With inadequate vitamin K, bones can’t hold on to vital calcium, which leads to osteoporosis. To make matters worse, the calcium has to go somewhere, so it enters the bloodstream, where it contributes to stiffening arteries.

Vitamin K And Diabetes Type II diabetics have an increased risk of bone fracture. This is likely due in part to the incomplete activation of the Gla-protein osteocalcin (caused by lack of vitamin K), and the decrease of calcium being deposited in bone that occurs as a result. Conversely, people with the highest vitamin K1 intakes have reductions in inflammatory markers related to diabetes.

Vitamin K has also been found to have a direct impact on the diabetic state itself. In a group of healthy volunteers between 26 and 81 years old, higher dietary vitamin K1 intake was associated with greater insulin sensitivity and lower post-meal glucose levels. In a study of older adults at high risk for cardiovascular disease, the risk of developing type II diabetes was reduced by 17% per 100 micrograms of K1 intake per day.

Another study demonstrated that both vitamins K1 and K2 reduced the risk of developing diabetes. However, the stronger and more significant association occurred with K2, which reduced the risk of type II diabetes by 7% for each 10-microgram increase in intake. In addition to reducing the risk of diabetes, vitamin K has been shown to reduce the effects of diabetes as well.

TYPES OF VITAMIN K It is clear that vitamin K affects specific and vital proteins throughout the body, well beyond the blood-clotting functions originally described for the vitamin. Less clear, at least for now, are differences in impact on the human body of several different types of vitamin K.

Phylloquinone, or K1, is the predominant source of vitamin K in the diet, and it becomes converted to menaquinone, or K2 , in humans. Vitamin K2 itself has several different subtypes, based on molecular structure variations. The subtype MK-4, or menaquinone-4, predominates in animal tissues; it is the natural product of K1 modification in the gastrointestinal tract.

It is likely that both K1 and K2 are necessary for overall normal vitamin K function, and it appears that supplementation with both is useful, especially for the mounting number of biological tissues other than blood clotting that rely upon adequate vitamin K. The subtype of K2 called MK-7, menaquinone-7 has recently been shown to be more bioavailable than MK-4.58

Vitamin K And Cancer Studies of vitamin K intake reveal potent preventive properties against several types of cancer, including prostate, colon, and liver cancers.

When prostate cancer cells in culture are treated with vitamin K2, both those sensitive to male hormones (androgens) and those resistant to male hormones are unable to reproduce, and eventually die. Vitamin K2 has been associated with a 63% lower risk of advanced prostate cancer in men with the highest intake of the nutrient. Similarly, a higher ratio of vitamin K-activated osteocalcin versus inactive osteocalcin correlates closely with reduced prostate cancer risk, demonstrating the molecular connection.

In human colon cancer cells, vitamin K2 has been shown to induce cancer cell death by several different mechanisms and to suppress the growth of colon tumors implanted into mice.

Supplementation studies also reveal vitamin K’s powerful effect on the most common kind of liver cancer, called hepatocellular carcinoma. This cancer is almost always associated with alcoholism or hepatitis B or C infection. Although surgical or radiation treatment can destroy the primary tumor, recurrence is common and typically determines the long-term prognosis. Several human studies show that vitamin K2 supplementation can dramatically reduce the recurrence rate in hepatocellular carcinoma and may impact the survival rate as well.

As with most nutrients, vitamin K is not the single answer to cancer prevention, but it shows tremendous promise, which highlights the importance of maintaining adequate levels through boosting your intake. A large European study showed that cancer death was 28% less likely overall in those with the highest versus lowest intakes of vitamin K2.


THE DANGERS OF BLOOD THINNERS

People at risk for dangerous blood clots include those with various heart rhythm abnormalities (e.g., atrial fibrillation), as well as those with artificial heart valves, stents, and other hardware, and those at risk for certain kinds of strokes. For these people, blood-thinning drugs known as anticoagulants offer significant protection.

But many traditional blood thinners, such as Coumadin® (warfarin), act specifically by inhibiting the action of vitamin K to produce clotting proteins. The emerging science of vitamin K is revealing a disturbing fact: While inhibiting vitamin K action on blood clotting proteins, these drugs also inhibit other vitamin K-dependent proteins, including the matrix Gla protein that naturally prevents arterial calcification.

Studies in both animals and humans now show that the use of anticoagulant drugs such as Coumadin (warfarin), while effective at clot prevention, do indeed accelerate arterial calcification, placing patients at increased risk for cardiovascular disasters. The good news is that by supplementing with low-dose vitamin K, you may help rescue arteries from calcification induced by warfarin.

However, if you are taking a blood-thinning drug, DO NOT stop using it and DO NOT begin any vitamin K supplementation on your own. Instead, speak with your doctor about starting a vitamin K supplement at a proper dose. With careful monitoring of coagulation tests, you are likely to find a balance between the benefits and the risks of anticoagulant use.

Newer blood-thinning drugs such as Pradaxa® (dabigatran) and Eliquis® (apixaban) are not affected by vitamin K intake, meaning you can take full-dose vitamin K and not compromise the desired anticoagulant effects.


Final Thoughts

A recent large study confirms that people with the highest vitamin K intakes are significantly less likely to die from any cause, compared with those having the lowest intakes.


Because of its unique ability to activate proteins involved in atherosclerosis, osteoporosis, diabetes, and cancer, vitamin K is capable of opposing many of the leading causes of death in modern-day Americans. A host of new studies details the impact of vitamin K supplementation on preventing these, and possibly other, major age-related diseases.

Once considered just a blood coagulation vitamin, vitamin K2 has now achieved the status of a multi-function vitamin. If you are interested in a longer and healthier life, consider supplementing with this often- overlooked nutrient.


If you are taking a blood-thinning drug, check first with your doctor to coordinate doses and follow-up testing.



References

  1. Ames BN. Prevention of mutation, cancer, and other age-associated diseases by optimizing micronutrient intake. J Nucleic Acids. 2010 Sep 22;2010.

  2. Juanola-Falgarona M, Salas-Salvado J, Martinez-Gonzalez MA, et al. Dietary Intake of Vitamin K Is Inversely Associated with Mortality Risk. J Nutr. 2014 May;144(5):743-50.

  3. Geleijnse JM, Vermeer C, Grobbee DE, et al. Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study. J Nutr. 2004 Nov;134(11):3100-5.

  4. Cockayne S, Adamson J, Lanham-New S, Shearer MJ, Gilbody S, Torgerson DJ. Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials. Arch Intern Med. 2006;166(12):1256-61.

  5. Beulens JW, van der AD, Grobbee DE, Sluijs I, Spijkerman AM, van der Schouw YT. Dietary phylloquinone and menaquinones intakes and risk of type 2 diabetes. Diabetes Care. 2010 Aug;33(8):1699-705.

  6. Ibarrola-Jurado N, Salas-Salvado J, Martinez-Gonzalez MA, Bullo M. Dietary phylloquinone intake and risk of type 2 diabetes in elderly subjects at high risk of cardiovascular disease. Am J Clin Nutr. 2012 Nov;96(5):1113-8.

  7. Nimptsch K, Rohrmann S, Linseisen J. Dietary intake of vitamin K and risk of prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg). Am J Clin Nutr. 2008 Apr;87(4):985-92.

  8. Carpenter, KJ. A short history of nutritional science: part 3 (1912–1944). J Nutr. 2003;133(10):3023-32.

  9. Mammen EF. Coagulation abnormalities in liver disease. Hematol Oncol Clin North Am. 1992 Dec;6(6):1247-57.

  10. Mammen EF. Coagulation defects in liver disease. Med Clin North Am. 1994 May;78(3):545-54.

  11. Stanley TB, Wu SM, Houben RJ, Mutucumarana VP, Stafford DW. Role of the propeptide and gamma-glutamic acid domain of factor IX for in vitro carboxylation by the vitamin K-dependent carboxylase. Biochemistry. 1998 Sep 22;37(38):13262-8.

  12. Willems BA, Vermeer C, Reutelingsperger CP, Schurgers LJ. The realm of vitamin K dependent proteins: Shifting from coagulation toward calcification. Mol Nutr Food Res. 2014 Feb 17.

  13. Kaneki M. Genomic approaches to bone and joint diseases. New insights into molecular mechanisms underlying protective effects of vitamin K on bone health. Clin Calcium. 2008 Feb;18(2):224-32.

  14. Braam LA, Hoeks AP, Brouns F, Hamulyak K, Gerichhausen MJ, Vermeer C. Beneficial effects of vitamins D and K on the elastic properties of the vessel wall in postmenopausal women: a follow-up study. Thromb Haemost. 2004 Feb;91(2):373-80.

  15. Shea MK, Holden RM. Vitamin K status and vascular calcification: evidence from observational and clinical studies. Adv Nutr. 2012 Mar;3(2):158-65.

  16. Jie KS, Bots ML, Vermeer C, Witteman JC, Grobbee DE. Vitamin K intake and osteocalcin levels in women with and without aortic atherosclerosis: a population-based study. Atherosclerosis. 1995 Jul;116(1):117-23.

  17. Okano T. Gla-containing proteins. Clin Calcium. 2014 Feb; 24(2):241-8.

  18. Theuwissen E, Cranenburg EC, Knapen MH, et al. Low-dose menaquinone-7 supplementation improved extra-hepatic vitamin K status, but had no effect on thrombin generation in healthy subjects. Br J Nutr. 2012 Nov 14;108(9):1652-7.

  19. Wallin R, Schurgers L, Wajih N. Effects of the blood coagulation vitamin K as an inhibitor of arterial calcification. Thromb Res. 2008;122(3):411-7.

  20. Jie KG, Bots ML, Vermeer C, Witteman JC, Grobbee DE. Vitamin K status and bone mass in women with and without aortic atherosclerosis: a population-based study. Calcif Tissue Int. 1996 Nov;59(5):352-6.

  21. Weaver J. Insights into how calcium forms plaques in arteries pave the way for new treatments for heart disease. PLoS Biol. 2013; 11(4): e1001533.

  22. Shea MK, O’Donnell CJ, Hoffmann U, et al. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr. 2009 Jun;89(6):1799-807.

  23. van den Heuvel EG, van Schoor NM, Lips P, et al. Circulating uncarboxylated matrix Gla protein, a marker of vitamin K status, as a risk factor of cardiovascular disease. Maturitas. 2014 Feb;77(2):137-41.

  24. Vermeer C, Theuwissen E. Vitamin K, osteoporosis and degenerative diseases of ageing. Menopause Int. 2011 Mar;17(1):19-23.

  25. Erkkila AT, Booth SL. Vitamin K intake and atherosclerosis. Curr Opin Lipidol. 2008 Feb;19(1):39-42.

  26. Chatrou ML, Winckers K, Hackeng TM, Reutelingsperger CP, Schurgers LJ. Vascular calcification: the price to pay for anticoagulation therapy with vitamin K-antagonists. Blood Rev. 2012 Jul;26(4):155-66.

  27. Clauser S, Meilhac O, Bieche I, et al. Increased secretion of Gas6 by smooth muscle cells in human atherosclerotic carotid plaques. Thromb Haemost. 2012 Jan;107(1):140-9.

  28. Juanola-Falgarona M, Salas-Salvado J, Estruch R, et al. Association between dietary phylloquinone intake and peripheral metabolic risk markers related to insulin resistance and diabetes in elderly subjects at high cardiovascular risk. Cardiovasc Diabetol. 2013;12:7.

  29. Kuo FC, Hung YJ, Shieh YS, Hsieh CH, Hsiao FC, Lee CH. The levels of plasma growth arrest-specific protein 6 is associated with insulin sensitivity and inflammation in women. Diabetes Res Clin Pract. 2014 Feb;103(2):304-9.

  30. Beulens JW, Bots ML, Atsma F, et al. High dietary menaquinone intake is associated with reduced coronary calcification. Atherosclerosis. 2009 Apr;203(2):489-93.

  31. Dalmeijer GW, van der Schouw YT, Magdeleyns E, Ahmed N, Vermeer C, Beulens JW. The effect of menaquinone-7 supplementation on circulating species of matrix Gla protein. Atherosclerosis. 2012 Dec;225(2):397-402.

  32. Westenfeld R, Krueger T, Schlieper G, et al. Effect of vitamin K2 supplementation on functional vitamin K deficiency in hemodialysis patients: a randomized trial. Am J Kidney Dis. 2012 Feb;59(2):186-95.

  33. Bentkowski W, Kuzniewski M, Fedak D, et al. Undercarboxylated osteocalcin (Glu-OC) bone metabolism and vascular calcification in hemodialyzed patients. Przegl Lek. 2013;70(9):703-6.

  34. Zittermann A. Effects of vitamin K on calcium and bone metabolism. Curr Opin Clin Nutr Metab Care. 2001 Nov;4(6):483-7.

  35. Braam LA, Knapen MH, Geusens P, et al. Vitamin K1 supplementation retards bone loss in postmenopausal women between 50 and 60 years of age. Calcif Tissue Int. 2003 Jul;73(1):21-6.

  36. Purwosunu Y, Muharram, Rachman IA, Reksoprodjo S, Sekizawa A. Vitamin K2 treatment for postmenopausal osteoporosis in Indonesia. J Obstet Gynaecol Res. 2006 Apr;32(2):230-4.

  37. Knapen MH, Schurgers LJ, Vermeer C. Vitamin K2 supplementation improves hip bone geometry and bone strength indices in postmenopausal women. Osteoporos Int. 2007 Jul;18(7):963-72.

  38. Knapen MH, Drummen NE, Smit E, Vermeer C, Theuwissen E. Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women. Osteoporos Int. 2013 Sep;24(9):2499-507.

  39. Hirao M, Hashimoto J, Ando W, Ono T, Yoshikawa H. Response of serum carboxylated and undercarboxylated osteocalcin to alendronate monotherapy and combined therapy with vitamin K2 in postmenopausal women. J Bone Miner Metab. 2008;26(3):260-4.

  40. Iwamoto J, Sato Y, Takeda T, Matsumoto H. Bone quality and vitamin K2 in type 2 diabetes: review of preclinical and clinical studies. Nutr Rev. 2011 Mar;69(3):162-7.

  41. Yoshida M, Booth SL, Meigs JB, Saltzman E, Jacques PF. Phylloquinone intake, insulin sensitivity, and glycemic status in men and women. Am J Clin Nutr. 2008 Jul;88(1):210-5.

  42. Iwamoto J, Seki A, Sato Y, Matsumoto H, Takeda T, Yeh JK. Vitamin K(2) prevents hyperglycemia and cancellous osteopenia in rats with streptozotocin-induced type 1 diabetes. Calcif Tissue Int. 2011 Feb;88(2):162-8.

  43. Yoshida M, Jacques PF, Meigs JB, et al. Effect of vitamin K supplementation on insulin resistance in older men and women. Diabetes Care. 2008 Nov;31(11):2092-6.

  44. Choi HJ, Yu J, Choi H, et al. Vitamin K2 supplementation improves insulin sensitivity via osteocalcin metabolism: a placebo-controlled trial. Diabetes Care. 2011 Sep;34(9):e147.

  45. Patti A, Gennari L, Merlotti D, Dotta F, Nuti R. Endocrine actions of osteocalcin. Int J Endocrinol. 2013; vol. 2013, Article ID 846480.

  46. Lamson DW, Plaza SM. The anticancer effects of vitamin K. Altern Med Review. 2003;8(3).

  47. Samykutty A, Shetty AV, Dakshinamoorthy G, et al. Vitamin k2, a naturally occurring menaquinone, exerts therapeutic effects on both hormone-dependent and hormone-independent prostate cancer cells. Evid Based Complement Alternat Med. 2013;2013:287358.

  48. Nimptsch K, Rohrmann S, Nieters A, Linseisen J. Serum undercarboxylated osteocalcin as biomarker of vitamin K intake and risk of prostate cancer: a nested case-control study in the Heidelberg cohort of the European prospective investigation into cancer and nutrition. Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):49-56.

  49. Ogawa M, Nakai S, Deguchi A, et al. Vitamins K2, K3 and K5 exert antitumor effects on established colorectal cancer in mice by inducing apoptotic death of tumor cells. Int J Oncol. 2007 Aug;31(2):323-31.

  50. Kawakita H, Tsuchida A, Miyazawa K, et al. Growth inhibitory effects of vitamin K2 on colon cancer cell lines via different types of cell death including autophagy and apoptosis. Int J Mol Med. 2009 Jun;23(6):709-16.

  51. Donato F, Tagger A, Chiesa R, et al. Hepatitis B and C virus infection, alcohol drinking, and hepatocellular carcinoma: a case-control study in Italy. Brescia HCC Study. Hepatology. 1997 Sep;26(3):579-84.

  52. Kakizaki S, Sohara N, Sato K, et al. Preventive effects of vitamin K on recurrent disease in patients with hepatocellular carcinoma arising from hepatitis C viral infection. J Gastroenterol Hepatol. 2007 Apr;22(4):518-22.

  53. Mizuta T, Ozaki I, Eguchi Y, et al. The effect of menatetrenone, a vitamin K2 analog, on disease recurrence and survival in patients with hepatocellular carcinoma after curative treatment: a pilot study. Cancer. 2006 Feb 15;106(4):867-72.

  54. Nimptsch K, Rohrmann S, Kaaks R, Linseisen J. Dietary vitamin K intake in relation to cancer incidence and mortality: results from the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg). Am J Clin Nutr. 2010 May;91(5):1348-58.

  55. Vermeer C. Vitamin K: the effect on health beyond coagulation - an overview. Food Nutr Res. 2012 Apr 2;56.

  56. Okano T, Shimomura Y, Yamane M, et al. Conversion of phylloquinone (Vitamin K1) into menaquinone-4 (Vitamin K2) in mice: two possible routes for menaquinone-4 accumulation in cerebra of mice. J Biol Chem. 2008 Apr 25;283(17):11270-9.

  57. Al Rajabi A, Booth SL, Peterson JW, Choi SW, Suttie JW, Shea MK, et al. Deuterium-labeled phylloquinone has tissue-specific conversion to menaquinone-4 among Fischer 344 male rats. J Nutr. 2012 May;142(5):841-5.

  58. Sato T, Schurgers LJ, Uenishi K. Comparison of menaquinone-4 and menaquinone-7 bioavailability in healthy women. Nutr J. 2012 Nov 12;11:93.

  59. Choi HW, Navia JA, Kassab GS. Stroke propensity is increased under atrial fibrillation hemodynamics: a simulation study. PLoS One. 2013 Sep 5;8(9):e73485.

  60. Dasi LP, Simon HA, Sucosky P, Yoganathan AP.Fluid mechanics of artificial heart valves. Clin Exp Pharmacol Physiol. 2009 Feb;36(2):225-37.

  61. Price PA, Faus SA, Williamson MK. Warfarin causes rapid calcification of the elastic lamellae in rat arteries and heart valves. Arterioscler Thromb Vasc Biol. 1998 Sep;18(9):1400-7.

  62. McCabe KM, Booth SL, Fu X, et al. Dietary vitamin K and therapeutic warfarin alter the susceptibility to vascular calcification in experimental chronic kidney disease. Kidney Int. 2013 May;83(5):835-44.

  63. Schurgers LJ, Spronk HM, Soute BA, Schiffers PM, DeMey JG, Vermeer C. Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats. Blood. 2007 Apr 1;109(7):2823-31.

  64. Ford SK, Misita CP, Shilliday BB, Malone RM, Moore CG, Moll S. Prospective study of supplemental vitamin K therapy in patients on oral anticoagulants with unstable international normalized ratios. J Thromb Thrombolysis. 2007 Aug;24(1):23-7.

  65. Sconce E, Avery P, Wynne H, Kamali F. Vitamin K supplementation can improve stability of anticoagulation for patients with unexplained variability in response to warfarin. Blood. 2007 Mar 15;109(6):2419-23.

  66. Erkkila AT, Booth SL, Hu FB, et al. Phylloquinone intake as a marker for coronary heart disease risk but not stroke in women. Eur J Clin Nutr. 2005 Feb;59(2):196-204.

  67. Gast GC, de Roos NM, Sluijs I, et al. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovasc Dis. 2009 Sep;19(7):504-10.

  68. Pan Y, Jackson RT. Dietary phylloquinone intakes and metabolic syndrome in US young adults. J Am Coll Nutr. 2009 Aug;28(4):369-79.

1 comment

Recent Posts

See All
bottom of page