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Vitamin K2 in the Prevention of Cardiovascular Diseases and Diabetes

"It is easier to change a person's religion than to change their diet." – Margaret Meade

"He is the best physician that knows the worthlessness of most medicines." – Benjamin Franklin

All of us in health care have seen the seemingly inexorable and relentless increase in chronic diseases during the last 50 or so years. The tour de force, the masterpiece of medicine, the cure, rarely occurs these days, apart from some infections, and even these are diminishing owing to decades of overprescribing of antibiotics for everything, including the slightest sniffle, not to mention all the antibiotics used in our foodstuff. In medicine, everything else is controlled: blood sugar, blood pressure, cholesterol levels, etc. The almighty prescription pad is whipped out and another pill prescribed for each symptom. Theories and causes abound for what has caused these chronic diseases. Presented here is an evidence-based explanation for the plausible etiology of 2 of these chronic and increasingly inexorable disorders: cardiovascular diseases (CVDs) and diabetes, and the use of vitamin K2 to prevent them.

CVD remains the number one cause of death worldwide. In the United States, more than 600 000 people die annually from CVD, and globally, approximately 30% of all deaths are due to CVD.  In high-income countries, 38% of all deaths are due to CVD, whereas the rate is 28% in low-income countries. In the general population, those aged 60 years or older account for 80% of deaths from CVD in high-income countries.1

Diabetes (DM) is now a pandemic and is a leading cause of death in the United States. In its 2016 Global Report on Diabetes, the World Health Organization in Geneva, Switzerland, related that the number of people with diabetes has almost quadrupled from 1980 to 2014, from 108 million to 422 million. The most common form, affecting 90% to 95% of the population, is type 2 diabetes, involving 30 million people in the United States. The disease is a major cause of heart attacks, stroke, blindness, kidney failure, and peripheral vascular disease complications leading to lower limb amputation.

In the United States, to assist patients in lowering their risks of DM, the American Heart Association recommends replacing fats with carbohydrates. However, an Israeli study that looked at 3 types of diet to improve markers for diabetes, the low-fat diet, the Mediterranean diet, and the

low-carbohydrate diet, and found that the last one proved to be the best. This begs the question: Is increased intake of carbohydrates a major cause of DM? There is another important point to consider: The increase in DM increased steeply after 1980 with the introduction of high-fructose corn syrup as pointed out by Gross et al. Their data imply that DM is associated with an increase in carbohydrate intake, especially of fructose, which is several-fold more reactive than glucose with hemoglobin. In a study that compared glucose-sweetened beverages and fructose-sweetened beverages for 10 weeks, there were increased lipid levels and visceral adiposity and decreased insulin sensitivity in participants who were overweight and obese in the fructose sweetened group.2-7

It has been widely recognized that there is a positive association between CVD and type 2 DM and vice versa; they are both a major risk factor for each other. Several medical organizations recommend that statins drugs be taken by both groups of patients, including the American College of Cardiology and the American Heart Association in its 2013 guidelines, and the American Diabetes Association in theirs in 2015. This is puzzling, as the mechanisms by which DM causes CVD and how elevated levels of low-density lipoprotein cholesterol cause DM are uncertain and yet to be determined. Statins are not the answer.8,9


Statins are known to inhibit 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase to lower blood cholesterol levels. An essential component of the mitochondrial electron transport chain is coenzyme Q10, which statins inhibit as well as the formation of adenosine triphosphate (ATP), the energy source for cellular activities. The depletion of ATP is the major cause of progression of atherosclerosis in ischemic conditions. In DM, there exists inefficient use of glucose as an energy source. Instead, ketone bodies are synthesized from fatty acids in the mitochondria and are transported into tissues for use as an energy source. However, statins inhibit ketone body synthesis. Furthermore, mitochondrial membranes are abundant in cholesterol. Use of statins will change mitochondrial integrity, hastening atherosclerosis and worsening diabetic conditions.10-12

The effects of taking statins on coronary artery disease have been carefully examined in the International Multicenter CONFIRM registry. In this 2012 study, coronary computed tomography angiography compared 2 groups of patients, one group taking statins and the other group not taking statins. Statin use was associated with increased numbers of calcified plaques, thus indicating that statins accelerate the progression of atherosclerosis due to inhibition of gamma carboxylation of osteocalcin (Ocn).13

Another important area that is associated with statin use are intracerebral hemorrhage (ICH).14 Low levels of cholesterol increase arterial muscle necrosis and the formation of microaneurysms.15-18

In addition, the Heart Protection Study found that the use of simvastatin, 40 mg, increased the risk of ICH. The Stroke Prevention by Aggressive Reduction in Cholesterol Levels study came to the same conclusion with atorvastatin, 80 mg, mainly in patients with hypertension and older males with a history of hemorrhagic stroke. In addition, the Cochrane Review of 2009 noted a significant increase in the risk of ICH with statins.19-21


Vitamin K1 (named after the German word Koagulation for "coagulation") is a cofactor enzyme involved in activating coagulation proteins. It is found in vegetables and in vegetable oils; therefore, it is not a common deficiency. Vitamin K1 is converted to vitamin K2 via geranylgeranyl pyrophosphate in the brain, bone, testis, pancreas, kidneys, and other organs. The microbiome also supplies vitamin K2. Statins cause a deficiency in vitamin K2 by inhibiting geranylgeranyl pyrophosphate, which leads to artery and tissue calcification—in other words, atherosclerosis. Ocn is a hormone produced in osteoblasts and is gamma-carboxylated by a vitamin K2-dependent enzyme. This then forms carboxylated Ocn (c-Ocn), which is stored in the matrix of bone. c-Ocn is secreted into the bloodstream and affects the metabolism in the pancreas, intestines, testes, and adipose tissue. Therefore, statin-induced deficiency of vitamin K2 affects insulin secretion, incretin secretion, testosterone production, homeostasis, and adiponectin secretion.22,23

Studies have shown that taking vitamin K2 is inversely associated with severe aortic calcification and with coronary heart disease mortality, including the Rotterdam study whose participants were aged 55 years or older and nonstatin users.23 A Dutch study showed that low intake of vitamin K2 but not vitamin K1 is associated with metabolic syndrome.24

The Rotterdam study demonstrated that among people aged 55 years or older with no history of either myocardial infarction or statin use, vitamin K2 was inversely associated with coronary heart disease mortality and all-cause mortality. Severe aortic calcification was also inversely associated with vitamin K2 intake. This effect of increasing vitamin K2 intake should be taken seriously with such an effect on aortic calcification and coronary heart disease mortality in comparison to reducing other known risk factors.25


One can no longer ignore the medical and scientific facts, published again and again, that statins are not the answer to CVS and DM and should be taken off the pedestal. Whether it be due to the immense profitability, or whether it be due to the enormous propaganda machine, statins have easily convinced many in health care that they are the answer to CVS and DM. However, one can no longer ignore the medical and scientific facts, published in numerous studies again and again, that statins are not the answer to CVS and DM, and they should be taken of the pedestal.  The phoenix that arises from these ashes is vitamin K2, which should replace statins, with the exception of a few narrow conditions where statins provide benefit to the user. (Altern Ther Health Med. 2017;23(2):8-10.)



Andrew W. Campbell, MD
Editor in Chief



1. Cundiff D, Agutter P. Cardiovascular disease death before age 65 in 168 countries correlated statistically with biometrics, socioeconomic status, tobacco, gender, exercise, macronutrients, and vitamin K. Cureus. 2016;8(8):e748.

2. Shai I, Schwarzfuchs D, Henkin Y, et al. Dietary Intervention Randomized Controlled Trial (DIRECT) group: Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008;359:229-241.

3. Look AHEAD Research Group, Wing R, Bolin P, et al. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med. 2013;369:145-154.

4. Goran M, Ulijaszek S, Ventura EE. High fructose corn syrup and diabetes prevalence: A global perspective. Glob Public Health. 2013;8(1):55-64.

5. Gross L, Li L, Ford ES, Liu S. Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: An ecologic assessment. Am J Clin Nutr. 2004;79(5):774-779.

6. Bunn HF, Higgins PJ. Reaction of monosaccharides with proteins: Possible evolutionary significance. Science. 1981;213:222-224.

7. Stanhope K, Schwarz J. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009;119:1322-1334.

8. Strandberg TE, Salomaa V. Factors related to the development of diabetes during a 20-year follow-up: A prospective study in a homogeneous group of middle-aged men. Nutr Metab Cardiovasc Dis. 2000;10:239-246.

9. De Lorgeril M. Cholestérol, Mensonges et Propagande. Paris, France: Thierry Souccar; 2008.

10. Okuyama H, Langsjoen P, Hamazki T. Statins stimulate atherosclerosis and heart failure: Pharmacological mechanisms. Expert Rev Clin Pharmacol. 2015;8(2):189-199.

11. Sato T, Oouchi M, Nagakubo H, et al. Effect of pravastatin on plasma ketone bodies in diabetics with hypercholesterolemia. Tohoku J Exp Med. 1998;185(1):25-29.

12. Larsen S, Stride N, Hey-Mogensen M, et al. Simvastatin effects on skeletal muscle: Relation to decreased mitochondrial function and glucose intolerance. J Am Coll Cardiol. 2013;61:44-53.

13. Nakazato R, Gransar H, Berman DS, et al. Statins use and coronary artery plaque composition: Results from the international multicenter CONFIRM registry. Atherosclerosis. 2012;225:148-153.

14. Pandit A, Kumar P, Kumar A, et al. High-dose statin therapy and risk of intracerebral hemorrhage: A meta-analysis. Acta Neurol Scand. 2016;134(1):22-28.

15. Noda H, Iso H, Irie F, et al. Low-density lipoprotein cholesterol concentrations and death due to intra- parenchymal hemorrhage: The Ibaraki Prefectural Health Study. Circulation. 2009;119:2136-2145.

16. Wang X, Dong Y, Qi X, Huang C, Hou L. Cholesterol levels and risk of hemorrhagic stroke: a systematic review and meta-analysis. Stroke J Cereb Circ. 2013;44(7):1833-1839.

17. Tirschwell D, Smith NL, Heckbert SR, Lemaitre RN, Longstreth WT Jr, Psaty BM. Association of cholesterol with stroke risk varies in stroke subtypes and patient subgroups. Neurology. 2004;63(10):1868-1875.

18. Konishi M, Iso H. Associations of serum total cholesterol, different types of stroke, and stenosis distribution of cerebral arteries: The Akita pathology study. Stroke J Cereb Circ. 1993;24:954-964.

19. Goldstein L, Amarenco P, LaMonte M, et al. Relative effects of statin therapy on stroke and cardiovascular events in men and women: Secondary analysis of the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) Study. Stroke J Cereb Circ. 2008;39:2444-2448.

20. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: A randomized placebo-controlled trial. Lancet Lond Engl. 2002;360:7-22.

21. Manktelow B, Potter J. Interventions in the management of serum lipids for preventing stroke recurrence. Cochrane Database Syst Rev. July 2009;3:CD002091.

22. Shirakawa H, Katsurai T. Conversion of menaquinone-4 in animal organs and its function. Oleoscience. 2014;14:547-561.

23. Oury F, Sumara G, Sumara O, et al. Endocrine regulation of male fertility by the skeleton. Cell. 2011;144(5):796-809.

24. 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;134:3100-3105.

25. Dam V, Dalmeijer G, Vermeer C, et al. Association between vitamin K and the metabolic syndrome: A 10-year follow-up study in adults. J Clin Endocrinol Metab. 2015;100(6):2472-2479.

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