Vitamin K2

Vitamin K is essential in the blood coagulation process via the modification of protein molecules. Vitamin K2 is expected to have various health benefits [1], preventing or alleviating cardiovascular disease, bone fracture, diabetes mellitus, cancer, liver disease, chronic kidney disease, immune disorder, neurological disease, and obesity.

There are two main types of Vitamin K. These are Vitamin K1 and Vitamin K2. Many studies have reported more health benefits with Vitamin K2 than with K1. It contributes to skin health and bone metabolism and prevents heart-related diseases. And promotes proper brain function. Additionally, Vitamin K2 is essential in the body’s use of calcium to help build bones and inhibit blood vessel calcification. Vitamin K2 is found in animal foods and preserved foods like sauerkraut and fermented beans. It does not exist in junk food or restrictive Western diets. Vitamin K2 may also be found in cereals, fatty meat, eggs, and fish. Some bacteria in the large intestine are also known to synthesise vitamin K2.

Recommended daily intake

Since Vitamin K2 is still ongoing, there is no formal recommendation for Vitamin K2 intake. In 2005 the Rotterdam study (4807 men and women) showed that the average intake of Vitamin K2 was 28.5 micrograms per day, and it seems that those who consume more might be healthier. The same study showed that those consuming >32.7 micrograms per day had lower cardiovascular disease risk factors than those consuming <21.6 micrograms per day.

Clinical trials tested the health benefits of Vitamin K2 when taking doses ranging from 50 to 300 micrograms per day. ImmuneX365 provides you with 200 micrograms per day, which helps you avoid becoming Vitamin K2 deficient.

Symptoms of Vitamin K2 deficiency

How Vitamin K2 and Vitamin D3 work together

One of the main functions of Vitamin D is to help your body absorb calcium and metabolise it from foods that you eat. Vitamin K2 works synergetically with Vitamin D because it helps direct the calcium around the body to where it needs to be (your bones). Vitamin D activates proteins so that you can break down and absorb the calcium mineral, while vitamin K2 directs it to your bones where it is most beneficial.

"Dr. Rhonda Patrick, PhD, is an American biochemist who has done extensive research on aging, cancer, and nutrition. Her groundbreaking work includes studies of how vitamin and mineral inadequacies impact metabolism, inflammation, DNA, and aging, and whether supplementation can reverse the damage.

K2 MK-7, the superior form of K2, activates the osteocalcin proteins that incorporate calcium to bones. Meanwhile, vitamin D3 aids calcium absorption into the blood and has been linked to a reduced risk of breast cancer.

As mentioned above, vitamin K2 plays a central role in the metabolism of calcium — the main mineral found in your bones and teeth. Vitamin K2 activates the calcium-binding actions of two proteins — matrix GLA protein and osteocalcin, which help to build and maintain bones

We ALWAYS recommend taking vitamin D with vitamin K2 if you are supplementing. Vitamin D is a fat soluble vitamin Vitamin D increases calcium levels in the body. Vitamin K helps the body use calcium by shuttling it to your bones."

Osteoporosis

Osteoporosis, a disorder characterized by porous and fragile bones, is a serious public health problem that affects more than 10 million U.S. adults, 80% of whom are women. Consuming adequate amounts of calcium and vitamin D, especially throughout childhood, adolescence, and early adulthood, is important to maximize bone mass and reduce the risk of osteoporosis. The effect of vitamin K intakes and status on bone health and osteoporosis has been a focus of scientific research.

Vitamin K is a cofactor for the gamma-carboxylation of many proteins, including osteocalcin, one of the main proteins in bone. Some research indicates that high serum levels of undercarboxylated osteocalcin are associated with lower bone mineral density. Some, but not all, studies also link higher vitamin K intakes with higher bone mineral density and/or lower hip fracture incidence.

Although vitamin K is involved in the carboxylation of osteocalcin, it is unclear whether supplementation with any form of vitamin K reduces the risk of osteoporosis. In 2006, Cockayne and colleagues conducted a systematic review and meta-analysis of randomized controlled trials that examined the effects of vitamin K supplementation on bone mineral density and bone fracture. Most of the trials were conducted in Japan and involved postmenopausal women; trial duration ranged from 6 to 36 months. Thirteen trials were included in the systematic review, and 12 showed that supplementation with either phytonadione or MK-4 improved bone mineral density. Seven of the 13 trials also had fracture data that were combined in a meta-analysis. All of these trials used MK-4 at either 15 mg/day (1 trial) or 45 mg/day (6 trials). MK-4 supplementation significantly reduced rates of hip fractures, vertebral fractures, and all nonvertebral fractures.

A subsequent clinical trial found that MK-7, the type provided by ImmuneX365, supplementation (180 mcg/day for 3 years) improved bone strength and decreased the loss in vertebral height in the lower thoracic region of the vertebrae in postmenopausal women. Other randomized clinical trials since the 2006 review by Cockayne et al. have found that vitamin K supplementation has no effect on bone mineral density in elderly men or women . In one of these studies, 381 postmenopausal women received either 1 mg phylloquinone, 45 mg MK-4, or placebo daily for 12 months. All participants also received daily supplements containing 630 mg calcium and 400 IU vitamin D3. At the end of the study, participants receiving either phylloquinone or MK-4 had significantly lower levels of undercarboxylated osteocalcin compared to those receiving placebo.

However, there were no significant differences in bone mineral density of the lumbar spine or proximal femur among any of the treatment groups. The authors noted the importance of considering the effect of vitamin D on bone health when comparing the results of vitamin K supplementation studies, especially if both vitamin K and vitamin D (and/or calcium) are administered to the treatment group but not the placebo group. The administration of Vitamin D and/or calcium along with Vitamin K could partly explain why some studies have found that vitamin K supplementation improves bone health while others have not.

In Japan and other parts of Asia, a pharmacological dose of MK-4 (45 mg) is used as a treatment for osteoporosis. The European Food Safety Authority has approved a health claim for vitamin K, noting that “a cause and effect relationship has been established between the dietary intake of vitamin K and the maintenance of normal bone”. The FDA has not authorized a health claim for vitamin K in the United States.

Coronary heart disease
Vascular calcification is one of the risk factors for coronary heart disease because it reduces aortic and arterial elasticity. Matrix Gla-protein (MGP) is a vitamin K-dependent protein that may play a role in the prevention of vascular calcification. Although the full biological function of MGP is unclear, a hypothesis based on animal data suggests that inadequate vitamin K status leads to undercarboxylated MGP, which could increase vascular calcification and the risk of coronary heart disease. These findings might be particularly relevant for patients with chronic kidney disease because their rates of vascular calcification are much higher than those of the general population.

In an observational study conducted in the Netherlands in 564 postmenopausal women, dietary menaquinone (but not phylloquinone) intake was inversely associated with coronary calcification. Menaquinone intake was also inversely associated with severe aortic calcification in a prospective, population-based cohort study involving 4,807 men and women aged 55 years and older from the Netherlands. Participants in this study who had dietary menaquinone intakes in the mid tertile (21.6–32.7 mcg/day) and upper tertile (>32.7 mcg/day) also had a 27% and 57% lower risk of coronary heart disease mortality, respectively, than those in the lower tertile of intake (<21.6 mcg/day). Phylloquinone intake had no effect on any outcome.

Despite these data, few trials have investigated the effects of vitamin K supplementation on arterial calcification or coronary heart disease risk. One randomized, double-blind clinical trial examined the effect of phylloquinone supplementation in 388 healthy men and postmenopausal women aged 60–80 years. Participants received either a multivitamin (containing B-vitamins, vitamin C, and vitamin E) plus 500 IU vitamin D3, 600 mg calcium, and 500 mcg phylloquinone daily (treatment) or a multivitamin plus calcium and vitamin D3 only (control) for 3 years. There was no significant difference in coronary artery calcification between the treatment and control groups. However, among the 295 participants who adhered to the supplementation protocol, those in the treatment group had significantly less coronary artery calcification progression than those in the control group. Furthermore, among those with coronary artery calcification at baseline, phylloquinone treatment reduced calcification progression by 6% compared to the control group. Based on these findings, the authors did not make any clinical recommendations, and they called for larger studies in other populations.

At this time, the role of the different forms of vitamin K on arterial calcification and the risk of coronary heart disease is unclear, but it continues to be an active area of research in the general population and in patients with chronic kidney disease.

Health Risks from Excessive Vitamin K
The FNB did not establish ULs for vitamin K because of its low potential for toxicity. In its report, the FNB stated that “no adverse effects associated with vitamin K consumption from food or supplements have been reported in humans or animals.”

Interactions with Medications