Vitamin K2, a group of compounds called menaquinones, is a fat-soluble nutrient that has attracted considerable attention for its potential role in cardiovascular health. The focus of this interest is its influence on arterial calcification, a process where calcium deposits accumulate in the walls of blood vessels. This calcification is a significant component of atherosclerosis, often referred to as “hardening of the arteries,” which contributes to arterial stiffness and increases the risk of adverse cardiovascular outcomes. Scientific discussion centers on whether increasing K2 intake can slow, halt, or even reverse this calcium buildup in the soft tissues of the circulatory system.
K2’s Role in Directing Calcium
The physiological function of Vitamin K2 in vascular health involves activating specific proteins that manage calcium distribution throughout the body. K2 acts as a necessary cofactor for an enzyme that modifies these proteins through carboxylation, enabling them to bind to calcium ions.
One of the most significant Vitamin K-dependent proteins in the vasculature is Matrix Gla Protein (MGP). Produced by smooth muscle cells within the artery walls, MGP is a potent natural inhibitor of soft tissue calcification. When sufficient K2 is available, MGP is fully activated (carboxylated), allowing it to chelate calcium and prevent its deposition into arterial tissue.
Without adequate K2, MGP remains inactive (uncarboxylated) and cannot properly bind calcium. This allows calcium to deposit freely in the arterial walls, leading to plaque formation. By activating MGP, K2 helps direct calcium away from the arteries and toward the bones and teeth, where it is structurally beneficial.
Understanding K2 Types and Absorption
Vitamin K2 is not a single compound but a family of related molecules known as menaquinones (MK-n). The two forms most relevant to supplementation and research are menaquinone-4 (MK-4) and menaquinone-7 (MK-7). These variations differ significantly in their sources, structure, and behavior once consumed.
MK-4 is a short-chain menaquinone found in animal products like eggs and meat. Supplemental MK-4 is often synthetic and has a very short half-life in the bloodstream, typically only a few hours. Maintaining consistent levels requires multiple doses throughout the day.
In contrast, MK-7 is a long-chain menaquinone primarily sourced from fermented foods, such as natto. Its elongated structure allows it to be packaged into cholesterol particles, resulting in a much longer half-life, extending to several days. This means MK-7 can be administered once daily while maintaining stable levels to activate Vitamin K-dependent proteins. MK-7’s superior bioavailability and prolonged activity have made it the more common form studied for cardiovascular health benefits.
Scientific Findings on Plaque Progression
Research into K2’s effect on vascular health points toward a protective role against the development and progression of arterial calcification. Early observational studies, such as the landmark Rotterdam Study, demonstrated a strong correlation between high dietary intake of menaquinone and a reduced incidence of arterial calcification and coronary heart disease mortality. This study of over 4,800 participants found that those with the highest K2 intake had a 50% lower risk of arterial calcification compared to those with the lowest intake.
Intervention trials have focused on K2 supplementation’s ability to influence the progression of existing calcification, often measured by coronary artery calcification (CAC) scores. Human trials suggest that K2, particularly the MK-7 form, can significantly slow the progression of arterial stiffness and calcification in both healthy and at-risk populations. For example, a three-year study using MK-7 demonstrated that it inhibited the age-related stiffening of arteries, maintaining arterial flexibility compared to the placebo group.
The question of whether K2 can remove established, calcified plaque is addressed with caution. While the mechanisms inhibit new calcium deposition and slow progression, robust human data showing true reversal or regression of already calcified, hardened plaque is currently limited. The evidence suggests that K2 functions primarily as a preventative and progression-slowing agent, rather than an agent that actively dissolves large, existing calcium deposits.
Recommended Intake and Practical Dosage
Since there is no official dietary reference intake for Vitamin K2, practical dosage recommendations are derived from clinical trials and population studies. For general cardiovascular maintenance, the MK-7 form is recommended due to its long half-life and high bioavailability. Typical supplemental ranges for MK-7 fall between 100 and 300 micrograms (\(\mu\)g) per day, which is effective in activating key Vitamin K-dependent proteins.
The required dosage for the MK-4 form is significantly higher, measured in milligrams (mg) rather than micrograms. In research settings, doses are often set at 45 mg per day, typically split into three smaller doses throughout the day to sustain effective blood levels due to its short half-life.
Any change in K2 intake, especially supplementation, can interfere with certain medications, such as the blood thinner Warfarin. Warfarin works by antagonizing Vitamin K action, and increasing K2 intake can reduce the medication’s effectiveness, potentially leading to dangerous changes in blood clotting time. Individuals taking Warfarin or similar vitamin K antagonists must consult with a healthcare provider for monitoring before starting K2 supplementation.