In the previous section, we explored the fundamental biology behind vitamin K2 and vitamin K2-dependent proteins in the body. When we take a step back, it’s obvious that vitamin K2 is involved in a staggering number of functions and conditions. We’ve only just begun to understand the different ways vitamin K2 can help us. Here is a brief summary of functions and conditions that vitamin K2 is involved in.
Vitamin K2 improves mineralization and metabolism in bones. It activates matrix Gla protein, which is responsible for delivering dietary calcium to the bone and integrating it into the bone matrix. It also activates osteocalcin which helps to form collagen fibril bands in the bone. These bands help to absorb tension and stress on the bone, improving fracture resistance.
Vitamin K2 activates matrix Gla protein (MGP) in the blood which inhibits calcification of arteries and other soft tissues. Vascular calcification reduces the elasticity of blood vessels, resulting in arterial stiffness. It can also lead to calcium plaque buildup further obstructing blood flow. Coronary artery calcification is an independent predictor of cardiovascular disease.
Like the calcium deposits that can build up and clog your sink, calcium salt deposits can build up inside arterial walls, obstructing blood flow. Vitamin K2-activated MGP helps prevent calcium from precipitating into calcium salts in your blood.
Vitamin K2 deficiency can explain why high intakes of dietary calcium can still lead to poor bone mineral density, as well as cause arterial calcification. Without vitamin K2 to activate the calcium-transporting matrix Gla protein, dietary calcium cannot properly mineralize the bone and instead builds up in the soft tissues of the blood vessels.
Studies on the effect of vitamin K2 MK-7 on cardiovascular health show a significant reduction in arterial stiffness and slower progression of calcification. As mentioned above in the Knapen et al. study, supplementation with 180 mcg of MK-7 over a 3 year period, revealed a significantly improved stiffness index and MGP activation among healthy postmenopausal women.
It explains why osteoporosis sufferers are also more likely to exhibit atherosclerotic calcification while those with atherosclerosis (arterial deposits/plaque) are more likely to have weaker, brittle bones.
Evidence linking K2 to cardiovascular health is only growing. One study in 2016 looked at the effect various factors played in cardiovascular disease across 168 countries. They found that vitamin K2 deficiency was linked to early cardiovascular disease mortality – even to the same degree that tobacco use is.
Like our bones, our teeth need vitamin K2 to support mineralization and prevent tooth decay. Odontoblasts, which line the dentin layer just underneath the enamel of teeth, produce osteocalcin. This osteocalcin needs to be activated by vitamin K2 before it can incorporate calcium into the dentin matrix.
Incidentally, some of the highest amounts of vitamin K2 in the body are found in our saliva. It has been observed that K2 has antimicrobial effects and reduces the number of cavity-causing bacteria, which helps to prevent tooth decay.
Childhood and adolescence are both periods of intense skeletal growth. Bone development begins as early as six weeks after conception and continues well into adulthood. Peak bone mass (bone mineral density) is achieved sometime around the age of 20, before beginning a natural and steady decline. Vitamin K2, and MK-7, in particular, are important for incorporating calcium properly into quickly developing bone structure.
Vitamin K2 activated matrix Gla protein is also needed to protect the cartilage in the growth plates of the bones from prematurely calcifying. This cartilage is essential for the bones to grow longer. If this cartilage calcifies too soon, child growth may be stunted.
Studies have shown that supplementing with vitamin K during childhood years can have a significant impact on bone mineral density and decreased bone turnover. In one particular 2009 study, pre-pubertal children supplemented with 45 mcg of K2 MK-7 K2 over 8 weeks, were found to have increased concentrations of both circulating MK-7 and carboxylated osteocalcin.
Research indicates that during pregnancy, vitamin K2 is particularly important for both the mother and the fetus.
Pregnant women can become calcium deficient because of substantial skeletal remodeling to prepare for birth and the baby’s high demand for skeletal formation. In extreme cases, this can result in pregnancy-associated osteoporosis, a condition characterized by severe pain from vertebral fractures. K2 supplementation has been shown to relieve this pain and improve bone health in expectant mothers.
Vitamin K2 is also needed by the infant to support skeletal development both during gestation and after birth. A K2 deficiency during gestation can be detrimental for future bone health.
Maternal supplementation of vitamin K2 can make all the difference. A Japanese study showed that women given 20 mg of vitamin K2 seven days prior to birth had more K2 in their blood than women who were not supplementing. More interestingly, K2 levels were also found to be elevated in umbilical cord blood, indicating that the transfer to the developing baby had occurred. None of the children born to these K2-treated women showed signs of vitamin K deficiency at birth, compared to 90% of the babies whose mothers were not given vitamin K2.
After birth, infants are also at risk of vitamin K2 deficiency as the levels of vitamin K in breast milk are typically very low. Lactating mothers can increase the levels of vitamin K2 in their breast milk with supplementation. The transfer seems to be successful as the breastfed children in these studies also had elevated vitamin K levels in their blood. It is, however, recommended that additional K2 supplementation in infants be considered as transfer adequacy of K2 from breastmilk is still unclear.
Vitamin K2 helps to activate and build up stores of a protein called osteocalcin in the bone. This supply of osteocalcin is regularly released into the bloodstream and used by the body to increase insulin production in the pancreas, as well as, to improve insulin sensitivity and glucose metabolism.
Studies show that osteocalcin-lacking mice suffer from poor glucose tolerance, insulin levels and insulin sensitivity. Pre-diabetics and untreated diabetics have decreased levels of serum osteocalcin.
K2 has been shown to fight inflammation by inhibiting pro-inflammatory markers produced by white blood cells called monocytes. Researchers looking at the effect of K2 on rheumatoid arthritis (an autoimmune inflammatory condition that affects the entire body but particularly the joints) found that supplementation with K2 lowered levels of inflammatory markers.
Vitamin K2’s effects on our glucose metabolism and cardiovascular system may help with athletic performance. An 8-week, double-blind, placebo trial with 26 male and female athletes showed 12% increase in maximal cardiac output after daily supplementation with MK-7 vitamin K2.
Osteocalcin released from the bone is thought to upregulate the synthesis of enzymes needed for the biosynthesis of testosterone, increasing male fertility. Osteocalcin deficient male mice exhibited poor fertility, lower testosterone levels and lighter weighing reproductive organs than their wild counterparts.
K2 is key in controlling vascular calcification, which is a common condition and risk factor for people who suffer from chronic kidney disease (CKD). Indirect evidence suggests that vitamin K2 supplementation may reverse vascular calcifications in CKD patients. A four-week supplementation trial with MK-7 vitamin K2 showed decreased inactive forms of matrix Gla protein, possibly reversing calcification.
Another randomized controlled trial found that vitamin K supplementation, in conjunction with vitamin D supplementation, reduced the progression of atherosclerosis in patients with CKD significantly more than vitamin D supplementation alone.
Vitamin K2 paired with calcification inhibiting matrix Gla protein may help prevent strokes and other blood obstructions to the brain. One study suggests that osteocalcin crosses the blood-brain barrier to act in the brainstem, midbrain and hippocampus, influencing the synthesis of monoamine neurotransmitters. Other studies show that vitamin K2 dependent proteins might act as antioxidants to prevent oxidative stress, which can cause nerve cell and brain damage.
Benign Prostate Hyperplasia (BPH) – the enlargement of the prostate gland – is pervasive among older men in modern society, but its root cause is still unknown. However, recent research discovered that BPH does not occur without a varicocele – a twisted and swollen varicose vein found in the scrotum. The swelling causes blood from the testes to backflow into the prostate gland. The high testosterone levels in this blood may lead to enlargement of the prostate.
How does vitamin K2 factor in? Varicose veins have been characterized by high levels of undercarboxylated-MGP, which suggests that a vitamin K2 deficiency might be a factor in varicose veins and varicocele. Supplementing with K2 may prove beneficial for BPH prevention in aging men.
Some of the latest research suggests that vitamin K2 plays a role in protecting skin elasticity. In the same way that K2 prevents calcification in other soft tissues, it prevents the calcification of our skin’s elastin, the protein that gives skin its elasticity and smooths out lines and wrinkles.
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