Low Vitamin K1 and K2 Levels Linked to Worse COVID-19 Outcomes

A new study entitled Reduced Vitamin K Status as A Potentially Modifiable Prognostic Risk Factor in COVID-19 indicates that low vitamin K levels may be connected to increased poor outcomes from COVID-19. Additionally, using drugs that impair vitamin K availability such as warfarin (Coumadin) may be increase risks.

The study explains coagulation disorders are common in COVID-19 and that vitamin K dependent biochemical processes are related to maintaining proper coagulation.

As there is little data on the use of common vitamin K antagonist (VKA) anti-coagulation medications such as warfarin and COVID-19, the authors point to how COVID-19 patients often develop lung damage resembling that in Idiopathic Pulmonary Fibrosis (IPF). They then refer to two studies on IPF patients that show very different outcomes likely due to their effects on vitamin K levels.

One study used short-term prednisolone (an anti-inflammatory drug) on patients, with some also receiving an anticoagulation drug (low molecular weight heparin). This approach achieved a much higher survival rate.

A second study used the long-term anticoagulant medication warfarin and had a much worse outcome, so much so that it was prematurely terminated due to harming patients.

One difference between these approaches is their effect on vitamin K activity in the body. Heparin does not interact with vitamin K, whereas warfarin does.

Warfarin is a commonly known “Vitamin K Antagonist” drug that functions by reducing vitamin K levels by impairing vitamin K recycling. Vitamin K is needed for making many coagulation factors and other necessary compounds, especially those used to grow and maintain bone. Warfarin disrupts production of these coagulation factors by lowering active vitamin K levels, but at the expense of causing many other health problems.

The study discusses other possible vitamin K related mechanisms to explain COVID-19 symptoms and outcomes. COVID-19 patients appear to have damaged elastic fibers in the lungs. It appears that vitamin K is involved both in processes for forming elastin for these elastic fibers and for mineral transport, especially of calcium, that keeps these fibers from being damaged by mineralization. A relevant quote from the study:

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Vitamin K deficiency induced by administration of VKAs caused both elastic fiber degradation and calcification in an animal model [43]. Remarkably, upregulation
of MMP synthesis preceded overt mineralization [43]. In the present study, an inverse correlation was found between vitamin K status and pDES in COVID-19 patients, suggesting a pathomechanistic link between vitamin K deficiency and accelerated elastolysis. This relationship has previously also been demonstrated in patients with COPD [15] and may be an indication for a link between vitamin K deficiency, insufficient MGP carboxylation and aberrant tissue remodeling in patients with COVID-19.

There are studies that connect low vitamin K levels with increased elastin degradation in diseases such as COPD (Chronic Obstructive Pulmonary Disease). Additionally, COPD is a known risk factor for worsened COVID-19.

The study used testing data from COVID-19 patients based upon a marker that is a reliable indirect indicator of vitamin K status. The data collected show that patients with worse outcomes have lower vitamin K levels.

Vitamin K is used in the body for many processes, not just coagulation and elastic fiber maintenance. For example, it is a key factor in processes involved in calcium transport such as in bone formation and maintenance.

Type 2 diabetes, cardiovascular disease, and hypertension (high blood pressure) are major risk factors for COVID-19. Prior scientific research has found low vitamin K tied to higher risks for developing all three of those conditions.

Osteoporosis, bone fracture, and dental caries (cavities) risks are also higher due to low vitamin K2 levels because K2 is necessary for osteocalcin to transport calcium into bones and teeth. Although this may not be directly related to COVID-19, certainly these are significant health problems on their own which could be helped by increased vitamin K levels.

Proposed Follow-up Studies

The authors hypothesize that vitamin K combined with low molecular weight heparin could both prevent elastic fiber degradation in the lungs while preventing dangerous coagulation without impacting vitamin K dependent processes as VKA drugs do. An intervention study should be undertaken.

Also, they note that it is unknown whether vitamin K deficiency predisposes people to develop severe COVID-19 and suggest further study of this.

How to Raise Vitamin K Levels

Your diet has a huge impact on your vitamin K levels, and those levels are important to your health even if you never develop COVID-19.

Increasing intake of foods high in vitamin K1 (e.g. spinach, leafy greens, broccoli) and K2 (e.g. eggs from pastured chickens, certain cheeses from pastured milks, natto [a fermented soybean dish common in Japan]) can raise these vitamin levels.

Supplements could also be used to help raise vitamin K levels.

Please also read Dr. Mercola’s full article Spinach, Eggs and Gouda Cheese to Combat COVID? for additional details. Here are a few key quotes from it:

One study looking into vitamin K bioavailability even found that circulating concentrations of vitamin K2 were about 10 times higher after the consumption of natto than they were of vitamin K1 after eating spinach.

“I have worked with a Japanese scientist in London,” Janssen told The Guardian, “and she said it was remarkable that in the regions in Japan where they eat a lot of natto, there is not a single person to die of Covid-19; so that is something to dive into, I would say.”

Keep in mind that vitamin K2 also works in tandem with vitamin D and magnesium. So, it’s important to remember that vitamin K2 needs to be considered in combination with calcium, vitamin D and magnesium, as these four all have a synergistic relationship that impacts your health.

Vitamin K Antagonist Medications

Heparin is a common anti-coagulation medication administered via injection or IV. It is often used in hospital settings, but there are versions such as low-molecular weight heparins that are prescribed for patients to self-administer. These drugs do not affect vitamin K levels.

If you are taking oral anti-clotting medications, at present the most common of them is warfarin (often referred to via brand name Coumadin). Warfarin is vitamin K antagonist drug. It and other vitamin K antagonist drugs block vitamin K activity by blocking recycling of inactive to active vitamin K. They thereby cause a functional vitamin K deficiency as they are commonly used.

This makes it much more difficult to reach healthy levels of biochemical activities that need vitamins K1 or K2.

For those taking warfarin, if you simply start increasing intake of vitamin K foods or supplements, it will cause your INR test levels to fall or PT (Prothrombin Time) to increase. This means your clotting risk is going up, which will result in your medical care provider likely advising you to reduce vitamin K intake or take even more warfarin. Therefore if you are taking these drugs and want to do anything about raising your vitamin K levels, you should find a competent medical care provider who understands the drugs and the high importance of vitamin K to figure out what to best do for you.

Please see these articles for more details about the harm caused by warfarin and low vitamin K:

There are many approaches to reduce excessive blood clotting risk that can work with or without warfarin. The article Supplements That Can Aid Warfarin Users By Reducing Abnormal Clotting and Bleeding Risks discusses several possibilities to consider.

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