How Vitamin K2-MK7 Can Permanently Reverse Arterial Calcification (Part One)

    How Vitamin K2-MK7 Can Permanently Reverse Arterial Calcification (Part One)

    Atherosclerosis and arteriosclerosis devastate our arteries with age due to calcium infiltration, contributing to degenerative diseases.

    Recent studies show that a deficiency in a relatively unknown vitamin, Vitamin K, leads to greater vascular calcification than initially thought.

    Moreover, it appears that Vitamin K also optimizes the absorption of Vitamin D, which is crucial in the fight against autoimmune diseases.

    Despite common belief that cancers are the most widespread and devastating, cardiovascular diseases actually top the list worldwide in terms of causes of death.

    Recent research has identified a simple vitamin, such as Vitamin K, as a potential and crucial anti-calcification agent for the arteries, a central factor in heart and vessel-related pathologies that particularly devastate Western populations.

    Indeed, epidemiology has demonstrated that the majority of people over the age of 60 progressively develop increasing calcium mineral deposits in their major arteries. (5)

    A researcher, William Faloon, reviewed the extensive scientific literature on the subject and found many truly interesting and surprising facts about Vitamin K in relation to artery obstruction.

    Aortic vascular calcification reduces arterial elasticity, which damages cardiovascular hemodynamics, causing morbidity (the period in one’s life when one or more pathologies occur) and mortality (6-8) in the form of:

    • Hypertension
    • Aortic stenosis, which is the narrowing of an orifice (in this case, the aorta) but also of a duct, a blood vessel, or a hollow organ, such that it obstructs or impedes the normal passage of substances that physiologically pass through them.
    • Cardiac hypertrophy
    • Myocardial infarction and ischemia of the lower limbs
    • Congestive heart failure
    • Compromised structural integrity. (9-11)

     

    The severity and extent of mineralization reflect the burden of atherosclerotic plaque (12), so much so that morbidity and cardiovascular mortality can be predicted based on it (13). Amidst this disaster, Vitamin K can help us in an unexpected and substantial way, but first, let’s understand what it is.

    The name Vitamin K refers to a group of fat-soluble substances called naphthoquinones, known since 1929 in the form of Vitamin K1, which is recognized for its regulatory effects on blood coagulation: the letter K indeed comes from the German word “Koagulation.”

    Vitamin K1 (phytomenadione or MK1) is the natural form of Vitamin K found in plants and provides the primary source of Vitamin K for humans through dietary intake. Vitamin K2 compounds (menaquinones or MK7) are produced by bacteria in the human intestine, are essential nutrients, and provide a smaller amount than the human requirement.

    Vitamin K2 is an essential nutrient that is part of the Vitamin K group, which includes Vitamins K1, K3, K4, and K5. Except for K3 and K5, only K1, K2, and K4 are significant for the human body.

    Vitamin K is thus necessary for normal blood coagulation in humans; more specifically, it is required by the liver to produce the factors necessary for optimal blood clotting. A deficiency in Vitamin K or liver dysfunction (e.g., severe liver failure) can lead to a deficiency in coagulation factors and excessive bleeding.

    Foods rich in Vitamin K include:

    • Leafy green vegetables (such as spinach, broccoli, asparagus, watercress, cabbage, cauliflower, peas)
    • Beans
    • Olives
    • Rapeseed
    • Soybeans
    • Meat
    • Cereals
    • Dairy products

    Vitamin K is decidedly a “paleo” substance in the sense that today we consume much less greenery compared to the Paleolithic era (thus creating a chronic deficiency of the substance), and up until 10,000 years ago, we did not eat certain foods that contained it, such as beans, rapeseed, soybeans, cereals, and dairy products. Therefore, eating them today, although they contain the precious Vitamin K, could cause harm because we have not evolved with them.

    Additionally, there are people at risk of baseline deficiency, such as those with chronic malnutrition, alcoholics, biliary obstruction, celiac disease, ulcerative colitis, cystic fibrosis, etc.

    Vitamin K deficiency is nonetheless rare but can lead to coagulation problems and excessive bleeding, especially if taking certain medications that can reduce Vitamin K levels by altering liver function or destroying the intestinal flora (normal gut bacteria) that produce Vitamin K, such as antibiotics, aspirin, anticonvulsant drugs, and some sulfa drugs.

    It is evident, therefore, that even though our body produces a certain amount, it is totally insufficient for our needs today.

    Particularly interesting and well-studied is the relationship between Vitamin K and a widely used anticoagulant drug: Warfarin (commercial name: Coumadin).

     

    High Blood Pressure

    When arteries are soft and elastic, they readily expand and contract with each heartbeat. When arteries harden (calcification) and lose their youthful elasticity, there is a progressive increase in blood pressure (14). This occurs because the heart is forced to beat harder to push blood through an increasingly rigid arterial system.

    Calcification of the large arteries leaving the heart (the aorta) helps explain why blood pressure increases with age. A hallmark of long-term hypertension is the enlargement of the left ventricle of the heart (15), which is the chamber of the heart that pumps blood into the aorta, from where it is distributed throughout the body.

    The increased cardiac workload caused by aortic stiffness (calcification) contributes to heart failure, which affects 5% of Italians (3,000,000 individuals) and more than 5 million Americans (15-17).

     

    Aortic Valve Stenosis

    A dilemma faced by elderly individuals is the progressive dysfunction of the valve between the heart and the aorta, which opens and closes with each heartbeat. When the aortic valve fails to close completely, blood regurgitates back into the left ventricle of the heart (18-19).

    Without surgical replacement/repair of the aortic valve, death from congestive heart failure often occurs (20).

    The elderly are called to fully recover from aortic valve replacement, even though more recent intra-arterial techniques are becoming available, whereby an artificial valve is threaded through the aorta and sewn into place (21). Those who have successfully replaced their valves with mechanical ones usually require lifelong anticoagulant therapy and medications, such as Warfarin, which, however, causes a range of side effects (22).

    It was once thought that aortic stenosis was caused by a stressful life (23), but it is now clear that it is primarily the calcification of the aortic valve leaflets that causes aortic valve malfunction, with chronic inflammation, elevated blood sugar, high homocysteine, and low magnesium levels (24-31).

    Homocysteine is an amino acid (i.e., a constituent of proteins) that, if too high in the blood, becomes an important risk factor for cardiovascular diseases (myocardial infarction, stroke), and perhaps also for Alzheimer’s disease, as several studies have confirmed.

    A high rate of homocysteine in the blood (over 12% of normal values) increases the risk of stroke or heart attack threefold. Hyperhomocysteinemia is also dangerous in menopause because it increases cardiovascular risks and also facilitates and amplifies osteoporosis.

    To lower homocysteine, folic acid supplementation, a B vitamin, is very effective.

     

    Calcification of the Coronary Arteries

    The blockage of coronary arteries that supply the heart muscle requires enormous hospital expenses each year in the form of open-heart coronary bypass surgeries and intra-arterial stent placement procedures.

    A stent is a cylindrical metal mesh structure that is introduced into lumen organs (i.e., hollow organs or viscera, such as the intestine, or blood vessels) and expanded until its diameter equals that of the lumen. This can, for example, reduce stenosis, exclude an aneurysm, or keep the viscera open.

    It is interesting to note that when an open-heart surgery is performed to replace a calcified aortic valve, the surgeon often also performs a bypass on the coronary arteries in the same patient (32). This is normal since coronary atherosclerosis and aortic valve stenosis have similar underlying causes such as elevated homocysteine, chronic inflammation, and calcification (33-36).

    Calcification plays a significant role in accelerating the formation of atherosclerotic plaque that narrows coronary arteries with aging. In patients with coronary artery disease, calcification is present in 90% of cases (37-38).

    Clinically, vascular calcification is now accepted as a valid predictor of coronary artery disease (39), yet most cardiologists use it only as a diagnostic marker (with a test called coronary calcium score) instead of directly combating the primary cause of coronary pathologies, which is the calcifications themselves… (40).

     

    What causes arterial calcification?

    Many of the known risk factors underlying atherosclerosis have been shown to promote arterial calcification. Many of these are already known (and still not entirely confirmed in some cases) such as elevated LDL cholesterol, high homocysteine, diabetes, kidney failure, chronic inflammation, and oxidative stress (33, 41-55).

    Additional contributors to calcification include low levels of magnesium (a natural calcium antagonist), hormonal imbalances, and hyperparathyroidism, which cause excess calcium in the blood (56-88).

    In fact, one of the main reasons why our vascular system calcifies with age is certainly the most underestimated (and even opposed): insufficient intake of vitamin K.

    Indeed, a low blood level of vitamin K2 stimulates a protein in the vascular wall that binds calcium in the arteries, heart valves, and other soft tissues.

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