The Surprising Longevity Benefits of Vitamin KSeptember 2014
By Judy Ramirez
Dr. Bruce Ames is one of the world’s leading authorities on aging and nutrition. Four years ago, Dr. Ames published research indicating that optimum intake of vitamin K plays an important role in longevity.1
A new 2014 study on vitamin K confirms that ample vitamin K intake can indeed help you live longer.2 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.
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.2
Vitamin K is capable of opposing many of the leading causes of death in modern-day Americans—including atherosclerosis,3 osteoporosis,4 diabetes,5,6 and cancer2,7—because it has the unique ability to activate proteins involved in these conditions.
In this article, we will review a host of new studies that detail the impact of vitamin K supplementation on preventing these and other major age-related diseases.
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.8 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.9,10
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.11
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.12-16 According to 2014 research, 16 different vitamin K-dependent Gla-proteins have been identified.17 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.18
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.13,14,19 Fortunately, studies show that vitamin K supplementation can significantly increase the amount of activated Gla-proteins in tissues—without over-activating the clotting proteins.18
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.20 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.19,21 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.3,14,15,19,22-24 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.14,16 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.23
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.16 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.25,26
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.27 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.28 (Some of these effects may be related to increased levels of another vitamin K-dependent Gla-protein that suppresses inflammation and promotes glucose tolerance.) 29
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.30
Vitamin K1 (phylloquinone) is the main dietary form of the vitamin, but vitamin K2 (menaquinone) has a stronger relationship to arterial calcification.15
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.3 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.30
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.22 And 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.14
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.31 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.32
Intriguingly, it is now apparent that women with atherosclerosis are more likely to have lower bone mass than women without atherosclerosis. They’re also 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).20
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.33 With inadequate vitamin K, bones can’t hold on to vital calcium, which leads to osteoporosis.34 To make matters worse, the calcium has to go somewhere, so it enters the bloodstream, where it contributes to stiffening arteries.33
Fortunately, supplementation with vitamin K is an effective means of protecting your bones from osteoporosis.
A study of healthy postmenopausal women between 50 and 60 years old demonstrated that three years of supplementation with 1 mg/day of vitamin K1, plus 8 micrograms (320 IU)/day of vitamin D together with minerals, reduced the loss of bone in the hip and spine compared both to placebo recipients and to those supplemented with vitamin D and minerals alone.35
In another study, postmenopausal women with pre-existing osteoporosis took 1,500 mg of calcium carbonate and 45 mg of vitamin K2 or placebo each day for 48 weeks. Compared to baseline values, the women experienced an increase in spinal bone mineral density and a 55.9% reduction in inactive osteocalcin levels, while a 9.3% reduction occurred in the group taking only the calcium supplement.36 The same dose of K2 was later shown to maintain hip bone strength and improve the overall geometry of the femoral neck over a three-year period, while placebo recipients lost hip bone strength during that time.37
Even lower doses of 180 micrograms/day of vitamin K2 (especially in the form of longer-lasting MK-7, which is derived from natto or fermented soybeans), when given for three years, increased the amount of activated osteocalcin and produced significant improvements in bone mineral content and density in the lower spine and femoral neck, while also increasing bone strength and preventing loss of height in spinal vertebrae.38
Vitamin K2 has recently been recognized by the European Food Safety Authority as having an important role in maintaining normal bone health.38 When added to alendronate, a common anti-osteoporosis drug, vitamin K2 significantly increased bone mineral density in the femoral neck compared with alendronate alone.39
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.40 Conversely, people with the highest vitamin K1 intakes have reductions in inflammatory markers related to diabetes.28
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.41 And 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.6
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.5
In addition to reducing the risk of diabetes, vitamin K has been shown to reduce the effects of diabetes as well.
Supplementation studies in animals show that diabetic rats, like diabetic humans, develop bone mineral loss. However, when diabetic rats were supplemented with vitamin K2, not only was osteopenia prevented, hyperglycemia was prevented as well.42
Human supplementation studies demonstrate that both K1 and K2 are effective in combating the effects of diabetes. In older, non diabetic men, three years of supplementation with 500 micrograms/day of vitamin K1 produced a significant reduction in insulin resistance compared with controls.43 And in a study of healthy young men, just four weeks of supplementation with 30 mg of K2 three times daily improved insulin sensitivity.44 This may have occurred as a result of an increase in the vitamin K-dependent Gla-protein osteocalcin, which has been shown in animal studies to increase insulin secretion and sensitivity.45