Bone and cardiac health: Are vitamins K1 and K2 the missing links to the epidemic of osteoporosis and arterial calcification?

Major questions, that need to be addressed about osteoporotic bone and arterial calcification, have fallen through the cracks. Why have vitamin K1 (phylloquinone) and vitamin K2 (menaquinone) not been part of the discussion regarding preventive measures for osteoporosis and arterial calcification? After all, it is now known that vitamin K2 is a calcium carrier that moves calcium from the blood into bone matrix, thereby strengthening bone and preventing calcification of the arterial lining, a dreaded complication of aging . . . hardening of the arteries. Has Western medical practice become so fixated on pharmaceutical fixes that obvious nutritional remedies are missed or underplayed?

Vitamin K1 is found in green leafy vegetables. Vitamin K2 is found in egg yolks, organ meats, fermented soy and cheese, thus making it less available to those following heart healthy dietary recommendations to avoid eggs, dairy, fish and animal flesh. Rarely do we find any other than the Japanese dipping into fermented soy (Natto), the plant source of vitamin K2. And while some vitamin K2 is made in the healthy gut, if the small intestine is compromised then even that source is questionable.

Hence vegans have a problem getting sufficient vitamin K2 but they are not alone; patients placed on Coumadin therapy that effectively destroys Vitamin K share a common medical side effect, arterial calcification.[1] This discussion is one that needs to take front and center and not be relegated to the back bench.

The silence from health care professionals about this topic is a most curious phenomenon because, during the 1980s, 1990s and into the 21st Century, Western trained physicians pushed high doses of calcium (1200–1400 mg per day) on patients, without considering the role of at least two vitamins (K1 and K2).

The calcium recommendations came from Standards of Care advocated by what is considered to be Best Practice Medical Care and followed by most, if not all health care practitioners. This recommendation has now been brought into question by the high rate of arterial calcification present in the American population among those following a Western diet and particularly among those receiving Coumadin therapy. Coumadin effectively removes vitamin K from the body; thereby preventing blood from clotting. While this is an effective therapy to prevent emboli (clot formation), it carries a high risk for arterial calcification and osteoporotic fractures. [2] [3]

Make no mistake there are valid medical reasons for some people to prevent emboli that can lead to strokes, but is Coumadin (warfarin) the best solution to fix this problem or is this therapy one that needs a new perspective? Are there better ways to prevent rapid blood clotting than by destroying the body’s store of vitamin K?

What does Vitamin K2 do for us? Recent research shows that Vitamin K2 is a calcium carrier that moves calcium from the arterial system to bone. If calcium does not move into bone, it tends to attach to the arterial vessel walls and causes arterial calcification, also known as “hardening of the arteries.”

One of the hallmarks of aging involves calcification of soft tissue throughout the body including heart valves, glands and blood vessels. But does this phenomenon necessarily need to be part of normal aging? According to several research reports the answer is a resounding no! As we age, we lose our ability to regulate calcium balance and then suffer the lethal consequences of systemic calcification. A low cost nutrient (Vitamin K2) can restore calcium homeostasis. [4]

The scientific literature is complex and often confusing because most of the earlier research was done on vitamin K1 (phylloquinone) that has to do with blood clotting. More recently the role of vitamin K2 (menaquinone) in calcium metabolism has been discovered and its role in both bone and cardiovascular health has emerged.

For example, in Japan, vitamin K2 has been successfully used to treat osteoporosis while the primary treatment in the U.S. is bisphosphonate therapy. These are two very divergent approaches to a problem that has reached epidemic proportions in the U.S., Canada and U.K.

Bisphosphonate therapy is pharmaceutical driven and carries a myriad of serious side effects while nutritional and vitamin supplement therapy is relatively inexpensive and appears to deal with underlying causation. Bisphosphonate drugs (Fosamax, Actonel, Boniva, and Reclast) are drugs that work by preventing osteoclasts from being removed from bone. All bone has two types of cells osteoclasts (that break down old bone cells) and osteoblasts (that reform and remodel bone). Bone homeostasis is maintained by a balance between bone resorption and formation.[5] If the pharmaceutical remedy prevents the breakdown of old bone cells then bone tissue will be brittle and prone to fracture. It is hypothesized that long term use of the bisphosphonate drugs may lead to spontaneous fractures of the femur (thigh bone), one of the strongest bones in the body.[6] In 2010, the FDA mandated that bisphosphonate drugs must now bear a warning label about the increased risk for two types of atypical femur fracture. [7]

Dr. Susan Brown, a nutrition specialist, has published a key article on bone nutrition. [8] It may be helpful for patients to come into their physician’s offices armed with key research findings as you have that conversation about treatments available to combat and prevent osteoporosis and arterial calcification. For example Brown reports:

• It is a well known fact that Vitamin K antagonists such as warfarin (Coumadin) double arterial calcification in humans.
• The decade-long, 4,800 person Rotterdam study documented that people who consumed the most vitamin K2 have a 50 percent reduced risk of arterial calcification. They also have a 50 percent reduced risk for cardiovascular events during this 10-year period.
• In 2009, a 16,000-person study by Gast and colleagues showed that the high intake of vitamin K2, but not K1 protected from cardiovascular disease.[9]
• A recent animal study by Schurgers and colleagues (2007) showed regression of warfarin-induced arterial calcification when given adequate amounts of vitamin K2.[10]

Brown also reports that Vitamin K2 can be produced in the body by certain intestinal bacteria; however, the long-term use of antibiotics compromises this process as well as anti-coagulant therapy.

So what are our options?

Can we safely introduce the topic of nutritional solutions for some very serious medical problems? Will our concerns be batted away like pesky mosquitoes? Will vitamin K2 in the form of MK-7 (natto based supplement) be discussed?

Will we be told that Vitamin K won’t solve our problems? Will bisphosphonate therapies continue to be recommended regardless of serious side effects?

In today’s medical and financial environment is a conversation even possible?

References

[1] Faloon. W. Protection against arterial calcification, bone loss, cancer and ageing. Life Extension Magazine (January 2009).

[2] Schurgers, LJ, Aebert H, Vermeer C. et al. (2004). Oral anticoagulant treatment: Friend or foe in cardiovascular disease? Blood: 104(10): 3231–2.

[3] Gage, BF, et al. (2006). Risk of osteoporotic fracture in elderly patients taking warfarin: Results from the national registry of Atrial Fibrillation 2. Arch Internal Med. January 23: 166(2): 241–6.

[4] Faloon. W. Protection against arterial calcification, bone loss, cancer and ageing. Life Extension Magazine (January 2009).

[5] DeHart, SS (2008; 2010). Strontium and Osteoporosis: A treatment not offered to American Women.

[6] Ott, SM (2005). Long term safety of bisphosphonates. Journal of Clinical Endocrinology and Metabolism, 90(3): 1897–1899.

[7] Lowes, R. (October 13, 2010). FDA adds femur fracture warning to bisphosphonate labels.

[8] Brown, SE. Vitamin K: the overlooked bone builder and heart protector. Nutrition and Bone Health.

[9] Gast GCM, et al., (January 2009). A high menaquinone reduces the incidence of coronary heart disease in women. Nutrition, Metabolism and Cardiovascular Diseases.

[10] Schurgers LJ, et al. Regression of warfarin-induced medial Elastocalcinosis by high intake of vitamin K in rats, Blood, 2007. 109(7): 2823–2831.

Sara S. DeHart, MSN, Ph.D. is Associate Professor Emeritus University of MN, School of Nursing. She also served as a Visiting Scholar University of Washington. She currently resides in the Northwest and writes about various issues including public health and public policy. See “Substituting Deception for Sound Public Health Policy” in Jerry “Politex” Barrett’s “Big Bush Lies,” (2004) Riverwood Books (117–128). She may be contacted at dehart.ss@frontier.com.