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Protection Against Arterial Calcification, Bone Loss, Cancer, and Aging!

January 2009

By William Faloon

Cancer Patients Prone to Vitamin K Deficiency

Cancer Patients Prone to Vitamin K Deficiency

Many patients with advanced cancer are malnourished from the disease or from the use of chemotherapy, which may cause nausea and poor appetite. Ten percent of these patients experience hemorrhagic (bleeding) side effects.45

Since vitamin K deficiency causes bleeding, doctors conducted a study to establish vitamin K status in advanced cancer patients receiving palliative care.

The findings were published in April 2008 and showed that 22% of these cancer patients were deficient in vitamin K1, which is considered below the lower limit of the reference range (below 0.33 nmol/L of blood).45

A startling 78% of these cancer patients showed evidence of a functional vitamin K deficiency, as indicated by elevated levels of an under-carboxylated protein that vitamin K normally carboxylates.

The doctors concluded that patients with advanced cancer are prone to vitamin K deficiency and that blood tests should be done to monitor vitamin K status before an increased risk of bleeding develops.45

Advantage of Vitamin K2 Over K1

In nature, vitamin K is found in two forms: vitamin K1, which occurs in leafy green vegetables; and vitamin K2, which exists in organ meats, egg yolks, dairy products, and particularly in fermented products such as cheese and curd. While some ingested K1 is converted to K2 in the body, significant benefits occur when vitamin K2 itself is supplemented.46

Advantage of Vitamin K2 Over K1
Arterial calcification in warfarin-treated rats. Images A-F show arterial calcification in rats treated with warfarin and vitamin K1. Images G-J show uncalcified arteries from rats treated with warfarin and vitamin K2 (MK-4).32

The absorption of K2 into the bloodstream is relatively efficient, whereas relatively little K1 is absorbed from plant foods.47 The kinds of foods rich in K2 in the Western world (organ meats, eggs, and dairy) should not be eaten in excess. Japanese who eat large quantities of a fermented soybean food called natto have lower rates of heart disease and osteoporosis.36,48 Natto is naturally rich in vitamin K2, but most people in Western worlds find it unpalatable.

In a fascinating study, rats given vitamin K1 plus warfarin were not protected against arterial calcification. The scientists fed rats a diet containing warfarin plus vitamin K1, vitamin K2 (MK-4), or both vitamin K1 and K2 (MK-4). None (0%) of the rats that received vitamin K2 developed arterial calcification, while 100% of the rats that received vitamin K1 without vitamin K2 displayed calcification in the aorta and carotid arteries!49 A more recent study showed that higher-dose vitamin K decreased arterial calcium content by 50% in rats.49 What makes this finding so remarkable is that most people over age 30–40 already have some degree of arterial calcification and up until now have had no means to reverse it.

One of the most convincing studies showing the cardioprotective benefits of K2 can be seen in a large-scale, well-controlled trial called the Rotterdam Heart Study—a Dutch trial that tracked 4,800 participants for seven years.46

The Rotterdam Heart Study revealed that participants who ingested the greatest quantities of vitamin K2 in their diet experienced a 57% reduction in death from heart disease compared with people who ingested the least. The same relationship did not hold for vitamin K1.46

Higher intakes of vitamin K2 in this study corresponded to less calcium deposition in the aorta (an indirect measure of atherosclerosis), whereas participants who ingested less K2 were more likely to show moderate or severe calcification.46

The size and quality of the Rotterdam Heart Study gave credibility to the powerful association between vitamin K2 dietary intake and heart disease and suggests that vitamin K2 may confer cardiovascular benefits by inhibiting arterial calcification.46

Scientists are now intensely interested in finding ways to halt the accumulation of coronary calcium, since they know that it comprises a significant portion of atherosclerotic plaque. They may have to look no further than a new form of vitamin K that remains biologically active in the body for more than 24 hours!

Far Greater Absorption of Vitamin K2 Into Cells

The Long-Acting Form of Vitamin K2
Figure 1
Efficacy of the MK-7 Form on a Marker of Bone Health
Figure 2
Far Greater Absorption of Vitamin K2 Into Cells
Figure 3

A study compared the absorption and arterial wall uptake of vitamin K1 and K2. This study is important because of the large body of epidemiological data showing significant reductions in heart attack risk in those ingesting high amounts of vitamin K2.

The results of this study showed that vascular cells preferentially take up vitamin K2 compared with vitamin K1. The poor absorption of K1 into vascular cells helps explain why K1 has not conferred significant protection against heart disease.32

The scientists who conducted this study next evaluated the effect of the K2 absorbed into vascular smooth muscle cells. Their findings documented that K2 enables the formation of smooth vascular muscle without nodules, such nodules that can protrude through into the endothelium and contribute to arterial blockage and atherosclerosis.50

The Long-Acting Form of Vitamin K2

There are two forms of vitamin K2 that have demonstrated remarkable benefits in published scientific studies.

The MK-4 form of vitamin K2 is the most rapidly absorbed and has proven clinical benefits. Yet MK-4 remains active in human blood for only a few hours after ingestion. The MK-4 form shows activity as an anti-atherosclerotic, has anti-tumor effects in some cancer cells, and helps to aid in bone formation activity.51-56

The MK-7 form of vitamin K2, on the other hand, remains bioavailable in the human body many days after ingestion and is the form found naturally in natto (fermented soybeans).57

In a human clinical trial, comparisons of bioavailability after ingestion of vitamins K1 and K2 (MK-7 form) were performed. The results showed that over a 24-hour period, MK-7 was present in the blood 2.5-fold better than K1. Over a 96-hour period, MK-7 was six-fold better than K1.57 (Shown to the right on Figure 1.)

A dose-response study was done where healthy volunteers received increasing doses of K1 and K2 (MK-7). The results showed no effect of K1 observed 24 hours after a 200 microgram dose, whereas 100 micrograms of K2 provided optimal vitamin K blood levels over a 24-hour period.57 (Shown to the right on Figure 2.)

A third clinical study compared K1 with K2 (MK-7 form) at the same dose over a six-week period. Compared with K1, the level of MK-7 form of vitamin K2 was seven- to eight-fold higher in the blood and there was no cumulative effect of K1! This suggests that MK-7 is more efficacious than K1.57 (Shown to the right on Figure 3.)

Efficacy of the MK-7 Form on a Marker of Bone Health

A sensitive indicator of vitamin K status in the body is the amount of activated osteocalcin in the blood.58 Osteocalcin is produced mainly by osteoblasts (bone-forming cells) and when activated by vitamin K, has properties that allow calcium and other minerals to be laid down into the bone, promoting bone density. When compared with K1, the MK-7 form of vitamin K2 was found to be three times more effective in promoting activated osteocalcin, indicating greater benefits for the bone.57

High bone turnover is associated with bone loss. One aim of osteoporosis prevention is to decrease bone turnover. A higher amount of inactivated (under-carboxylated) osteocalcin is correlated with reduced bone mass. When administered to a group of study subjects, MK-7 was shown to decrease bone turnover and increase bone density.59 A variety of studies done in humans and animals provides much support for the use of MK-7 in the prevention of osteoporosis.59-62

It should be noted that these markers not only provide a partial indication of overall bone health but hint of a strong protective effect of the MK-7 form of vitamin K2.