While vitamin K2 has a substantial body of evidence demonstrating its benefits for bone and cardiovascular health, researchers continue to examine its mechanism of action and explore potential applications for the betterment of society.
Some exciting areas showing great promise are:
Vitamin K was identified some 40 years ago as essential for the synthesis of sphingolipids, which are present in high concentrations in brain cell membranes and are now known to possess important cell-signaling functions. Vitamin K-dependent proteins are now known to play key roles in the central and peripheral nervous systems. Notably, protein Gas6 has been shown to be actively involved in cell survival cell growth.
As vitamin K helps regulate brain biochemistry, scientists are examining if a vitamin K deficiency might be a contributing factor to the development of Alzheimer’s disease. A recent study found that patients with early-stage Alzheimer’s disease consumed less vitamin K than did subjects who were cognitively intact.
Further, Parkinson’s patients have several genetic defects, including PINK 1 and Parkin mutations that lead to reduced mitochondrial activity. But vitamin K2 plays a role in the energy production of defective mitochondria, and Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven, succeeded in undoing the effect of one of the genetic defects that leads to Parkinson’s using vitamin K2 – a discovery that gives hope to Parkinson’s patients.
Most patients with stage 5 chronic kidney disease (CKD) suffer from extensive vascular calcifications.4 Matrix Gla protein (MGP) is a powerful inhibitor of vascular calcification, and requires vitamin K2 to be fully activated.
Meanwhile, patients with end stage renal disease (ESRD) exhibit reduced vitamin K intake, and uremia also interferes with vitamin K recycling. Levels of uncarboxylated dephosphorylated Matrix Gla Protein (uc-dp-MGP), the inactive form of MGP, increase with each CKD stage. Further, dp-c-MGP inversely correlates with all-cause and cardiovascular mortality in end-stage kidney disease. Taken together, indirect evidence suggests that vitamin K supplementation may attenuate the progression of vascular calcification in patients with renal failure and beneficially affect mortality in these patients.
In recent years, various reports have shown that vitamin K2 has anti-oncogenic effects in various cancer cell lines, including leukemia, lung cancer, ovarian cancer, and hepatocellular cancer. Although the exact mechanisms by which vitamin K2 exert its antitumor effect are still unclear, processes, such as cell cycle arrest and apoptosis, appear to contribute to the therapeutic effects of vitamin K2.
In view of vitamin K2’s potential to reduce osteoporosis and atherosclerosis risk, and given the fact that these two pathologies are frequently associated with prostate cancer patients undergoing hormonal therapy, development of vitamin K2 as a treatment strategy for prostate cancer could have far-reaching impacts on prostate cancer patients.
Previously, Nimptsch et al. showed an inverse relationship between dietary intake of vitamin K2 and risk of prostate cancer. Interestingly, serum undercarboxylated osteocalcin (ucOC), a biomarker of vitamin K status, is inversely associated with vitamin K2 intake and the development of advanced prostate cancer. Thus, these studies suggest that the intake of vitamin K2 may be beneficial in preventing the progression of prostate cancer. Moreover, vitamin K2 is also shown to enhance the chemotherapeutic efficacy of conventional anticancer drug Sorafenib in the most common type of liver cancer, hepatocellular carcinoma.
Cardiovascular disease and osteoporosis are major age-related health concerns in Western society, and these two conditions are characterized by the presence of chronic inflammation. Epidemological studies have shown that dietary insufficiency of vitamin K, especially vitamin K2 as menaquinone-7 (MK-7), may be a leading factor in the multifactorial origins of the two conditions.
Researchers have hypothesized the molecular mechanism of MK-7 insufficiency in chronic inflammation fueled by pro-inflammatory cytokines. Tumor necrosis factor-α (TNF-α) exemplifies the pro-inflammatory cytokine, implicated in the process of vascular calcification and osteoporosis.
A recent study tested a hypothetical role of vitamin K2 in modulation of immune cells in vitro. The results show that vitamin K2 inhibits the production of pro-inflammatory mediators by human and mouse macrophages in vitro. Researchers plan to test additional biomarkers of immune and inflammatory response in the presence of vitamin K2 in vitro. This work may elucidate the anti-inflammatory mechanism of vitamin K2 and establish the potential biomarker targets in clinical testing of vitamin K2’s role in cardiovascular health.