A study from Sweden’s Karolinska Institute observed 20,721 healthy Swedish men, ages 45 to 79, for 11 years and found the following ways in which lifestyle changes can reduce risk of heart disease:
36 percent risk reduction attributed to not smoking.
18 percent reduction for eating a diet rich in fruits, vegetables, legumes, nuts, reduced-fat dairy products, whole grains and fish.
12 percent reduction for maintaining a waistline of 37 inches or less (for men). (For women, this waistline circumference would be about 35 inches or less, said Dr. Sweitzer.)
11 percent reduction for drinking fewer than two alcoholic drinks per day. (Probably one drink per day for women.)
3 percent reduction for moderate daily and weekly exercise routines.
A large risk factor is high blood pressure. More than 50 million people in the U.S. have hypertension, or high blood pressure, making it the most common heart disease risk factor.
2. Natural Products that have individuals who have reversed their heart disease:
Vitamin K4 and K7: Recently found to have powerful effects on preventing heart disease: See comprehensive addendum
Aspirin is a proven way to help some people prevent a second heart attack or stroke. When aspirin is used this way it is called aspirin secondary prevention. It appears that aspirin also may help prevent a first heart attack or stroke in some people.Who may benefit?
Aspirin primary prevention is not right for everyone. Aspirin primary prevention may be beneficial for adults who:
- Are 50 to 69 years old, with the greatest benefit for adults aged 50 to 59;
- Have a 10 percent or higher risk of cardiovascular disease in the next 10 years; and
- Are able and willing to take low-dose aspirin, about 81 mg per day, for at least 10 years.
Currently, there is not enough evidence to:
- Support the use of aspirin primary prevention in patients who are younger than 50 years or older than 70 years.
- Know whether aspirin primary prevention benefits or risks differ between men and women or between different races or ethnicities.
Talk to your doctor to find out whether aspirin is right for you to help prevent heart attack, stroke, or other conditions. Do not start aspirin without first talking with your doctor about your risks and benefits. There are conditions, such as atrial fibrillation and deep vein thrombosis, where aspirin alone would not be enough protection. If you have either of these conditions, be sure to talk with your doctor about what prevention method is best for you.
Why does aspirin prevent heart attack and stroke?
Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that is commonly used to relieve pain. But, aspirin also may prevent the formation of blood clots. Aspirin does this by inhibitingfrom promoting clotting in blood vessels where cholesterol and may be partially blocking blood flow. This clotting can lead to heart attack and stroke. By inhibiting clotting, aspirin helps reduce damage to the heart and brain and helps prevent heart attack and stroke.
What are the risks?
Bleeding is the most common side effect of aspirin. The risk of bleeding is higher in men versus women, and the risk increases in patients who:
- Are older
- Are using aspirin at a higher dose or for longer periods of time
- Are using aspirin at the same time as other medicines that increase the risk of bleeding
- Have uncontrolled high blood pressure
- Have or previously had ulcers in their gastrointestinal tract
- Have other medical conditions such as kidney failure, liver disease, and certain bleeding or blood disorders
Talk to your doctor to find out whether aspirin is right for you. Don’t start taking aspirin without first talking to your doctor.
THE GREAT STATINS DEBATE: ARE THEY GOOD OR BAD?
Statins have been used since the 1980s to treat people with high levels of ‘bad’ LDL cholesterol in the blood, which prevents the build-up of fatty deposits and reduces the risk of a heart attack or stroke.
Most people with cardiovascular disease, or who has already suffered a heart attack, are given the pills to stop them suffering a repeat attack.
They are the most commonly prescribed medication on the NHS, with around six million patients taking them.
But the drugs, which cost the NHS less than £2 a month, have been the subject of controversy since NHS watchdog NICE advised that millions more should take them – even if they do not have any symptoms of heart disease.
Statins are given to most patients with cardiovascular disease to stop them suffering from a repeat attack
That guidance, published in 2014, suggested that anyone with a 10 per cent chance of developing cardiovascular disease over the next decade should be offered the pills – making virtually everyone over the age of 40 eligible for the drugs.
Many experts warned that the guidance represented risked ‘medicalising’ Britain – with millions of healthy people taking pills.
The waters of the debate have been muddied by an ongoing row about the extent of side effects.
A major review in The Lancet, published earlier this month, concluded statins are safe and their benefits far outweigh any harm.
It was the biggest ever review into their use, but last Friday rival journal The BMJ cast doubt on the assertions by claiming ‘adverse’ side effects are far more common than the study implied.
Dame Sally Davies, chief medical officer for England, has now been asked to step in and conduct a truly independent inquiry to end the ‘increasingly bitter and unproductive dispute’ over the pills. She is yet to respond.
The science of statins: They work to optimize your different forms of cholesterol, as well as to decrease inflammation. Statins cut the risk of repeat heart attacks by around 15 per cent.
However, as discussed below, 1/2 of heart attacks and heart disease are in people with normal cholesterol.
The danger of Statins is pictured below–they block an enzyme that produces cholesterol AND Coenzyme Q10 — a vital molecule for your cell’s energy production: Make sure to supplement with CoQ10 if you are on a Statin.
See Background of how drug companies were aware of this danger but did not go forward with the production of a Statin/CoQ10 medication at end of page.
C. Bempedoic acid: A convenient, complementary, cost-effective, oral, once-daily small molecule for lowering elevated LDL-Cholesterol. Bempedoic acid’s mechanism of action is actually similar to statins in that it inhibits cholesterol synthesis and upregulates LDL receptors on liver cells. However, bempedoic acid is inactive until it hits the liver. Unlike statins, bempedoic acid does not inhibit the cholesterol biosynthesis pathway in skeletal muscle, nor promote the associated cytotoxicity believed to lead to muscle-related side effects.
D.Potential Future Combination: Even better than Bempedoic Acid alone, Esperion has successfully demonstrated in clinical trials a combination therapy that could be more powerful than statins: They hope to be able to bring to market a fixed dose combination pill of bempedoic acid and ezetimibe as an effective orally administered solution that has shown powerful LDL-Cholesterol lowering effects.
E. The PCSK9 inhibitors (PSK9i) are a class of injectable drugs that have been shown to dramatically lower LDL cholesterol levels, by up to 60% when combined with a statin.
These drugs are monoclonal antibodies. They target and inactivate a specific protein in the liver. Knocking out this protein, called proprotein convertase subtilisin kexin 9, dramatically reduces the amount of harmful LDL cholesterol circulating in the bloodstream.
Who Needs a PCSK9 Inhibitor?
About 1 in 5 patients on statins cannot lower their cholesterol adequately at all; some due to serious genetic defects. In addition, some patients stop their statin treatment due to side effects. PCSK9 inhibitors may be used alone or in combination with statins like Lipitor or Crestor to further lower the hardest-to-treat elevated cholesterol levels for patients who cannot tolerate any statin drug due to side effects.
Clinical Studies for PCSK9 Inhibitors
Several PCSK9 studies were published in the New England Journal of Medicine (NEJM) show that two agents, evolocumab (Repatha) or alirocumab (Praluent), when combined with statins, lower cholesterol better than the statin alone.
After one year, those patients who were taking both the PCSK9 inhibitor and the statin together had LDL levels that were at least 60 percent lower than the group taking only statins. LDL levels dropped dramatically. Larger studies are ongoing to evaluate PCSK9 inhibitors on the ability to lower outcomes like heart attack or stroke, but early results suggest cardiovascular events could be lowered by half.
F. Binders: Welchol binds cholesterol in the gut as another way to reduce cholesterol. This is because many substances, including cholesterol, are re-absorbed lower in the gut. In short, there is a re-circulation process, and Welchol can be helpful not only in ridding the body of cholesterol, but also other toxins such as mycotoxins.
F. The Cutting Edge : In the future , it appears the first line of treatment will be medications that dramatically decrease inflammation, as a new study has just suggested:
Cholesterol-busting statins are given to millions of adults deemed to be at risk of heart disease. But half of heart attacks occur in people who do not have high cholesterol at all. Now scientists have found that reducing inflammation in the body can protect against a host of conditions – including heart disease. The drug canakinumab, given by injection every three months – cut repeat heart attacks by one quarter.
Statins cut the risk by around 15 per cent. Experts said the findings have “far-reaching” implications for prevention of heart attacks. Professor Paul Ridker of Harvard Medical School, presenting his findings at the European Society of Cardiology congress in Barcelona yesterday, said it opens up a “third front” in the war on heart disease. The landmark study tracked 10,000 heart attack victims who were given canakinumab, a drug which targets inflammation. Typically, around a quarter of survivors will go on to have another event within five years, despite taking statins. The four-year study found those given the new treatment saw a 24 per cent reduction in heart attacks and 17 per cent fall in angina.Speaking at the world’s biggest gathering of heart experts, Harvard scientists said the approach promises to “usher in a new era” of treatment.
G. Mechanisms for many natural substances. One of the most common is to change the specific types of cholesterol in your bloodstream to increase the healthy ones and decrease the unhealthy ones. They seek to:
Lower your “Lp(a)” – a degenerative form of the LDL. Many researchers have demonstrated that this is the most dangerous component of heart disease.
Reduce “oxidized LDL (oxLDL)” – See STOP INFLAMMATION to lower oxLDL
Lower small dense LDL particles that oxidize more easily and penetrate the artery wall–Beginning the process of producing “foam cells” that will clog your arteries
Increase large fluffy LDL particles that are less likely to penetrate the vessel wall. Fish oil can help, too.
Lower “Apo Lipoprotein B” – A measure of the time cholesterol stays in your bloodstream
Increase HDL cholesterol – the “good” cholesterol: It removes the cholesterol build up at your heart cells and disposes of it. The many good effects of a higher HDL level:
Keep your HDL above 60:
Just a 1 mg/DL increase in HDL decreases Heart Disease by 2 – 3%
Increase HDL Cholesterol with Exercise, some Statins, Niacin, Gugguls, Tocotrienols, Ginseng, Pantothenic Acid, and Magnesium as enzyme catalyst. Policosanol has weak support in the literature. KEY: For some, you can reduce “flush” of niacin with ASA and pectin.
Increase HDL 2B > 35% of HDL total
Increase HDL C to increase Apo A1, Apo A2: Tocopherols and other antioxidants can help.
Another Strategy: Put more LDL cholesterol in the body’s TRASH DISPOSAL:
a. Statins, Red Yeast Rice, Cranberries and others decrease LDL synthesis and increase LDL receptors on the liver (cholesterol uptake and excretion into GI tract by the liver)
b. Binders (Welchol, Cholesteramine, etc) of bile acids block cholesterol from “recycling” back into your body and arteries
Another Strategy is to Stop the Silent, Ongoing Inflammation in Your Body
Inflammation is beginning to be seen as potentially the most important cause of heart disease. It is the inflammation that causes “oxidation” of LDL particles that penetrate your artery.
As illustrated below, total blood cholesterol is not a good indicator of heart disease. That is why many health professionals target the different types of cholesterol–as outlined above.
Inflammation triggers are most often at where the outer world contacts the inner body: the digestive system and the lungs. After eating a meal look for signs of inflammation that may include fatigue, abdominal discomfort or bloating, small rashes, and increased blood pressure or heart rate. Inflammation can be triggered in the lungs by breathing excessive toxins: diesel or other combustable fumes (put your car’s ventilation system on recirculate,) molds, seasonal allergies, formaldehyde, small particles in the air that can have heavy metals attached, chlorine and other vapors that are emitted from an unfiltered shower head.
Inflammation can lead to “oxidation” of your LDL cholesterol particles which are widely seen as the first step to hear disease.
Find out if you have hypertension and reduce it to a normal range. Hypertension likely increases the tears and leaks in the vessel wall and has been shown to promote heart disease.
Maintain optimal ratio of Omega-3 to Omega-6 fatty acids: OmegaCheck and other labs will check this extremely important factor in heart disease.
Supplement enzymes that reduce inflammation and “chew up” the “clogging” in the artery. Dr. William Wong has noted that between the age of 27 to 35, your enzyme levels plummet, with an inadequate ability to calm disease and “chew” up the unwanted clogging in the body’s tissues.
Reduce Homocysteine: Important risk factor –Homocysteine forms from incomplete metabolism of an amino acid that may be irritating to blood vessels.
Reduce “Sticky” platelets and blood components:
Block pathways that cause blood elements–Especially platelets–from “clumping”: Garlic, fish oil, ginkgo and multiple medications.
Reduce “sticky” blood: Reduce fibrinogen (The vessel tries to repair these tears and leaks with higher fibrinogen, but unfortunately repeated episodes of high fibrinogen contributes to clogging of the arteries) and PAI-1 levels:
Lower fibrin deposits on artery walls: See serrapeptase results from Dr. Nieper’s clinical experience or consider Nattokinase or Lumbrokinase as an alternative. Consult with your doctor to make sure you are not at risk for hemorrhagic problems.
Support “Opening” of the Arteries: Exercise, supplemention with the amino acid L-Arginine, and other natural products can increase the opening (vasodilation) of your arteries by stimulating the cells eNOS, prostacyclin and others
Reduce “closing” (vasoconstriction) of the arteries: Reduce excessive inflammation of RAS, ET and others
Now you can see that heart disease involves a lot more than just total Cholesterol. Cells need a certain amount of cholesterol as a lubricant for healthy cell membranes, the production of steroids and other important functions.
In fact, some studies have suggested that very low cholesterol levels in men can increase risk of death.
For the best care, you need the resources and expertise of physicians who fully understand the more complex story of lipids and who have access to more advanced testing methods.
We strive to uncover your risk factors by consulting with the experts and with the best and most accurate labs in the country – One of which is “NMR LipoProfile.”
Background on Statins and Coenzyme Q10
The structure of coenzyme Q10 (CoQIO or ubiquinone) was determined by the Merck scientist Karl Folkers after its discovery in 1957 (seehttp://www.nutrition.org/cgi/content/full/131/9/2227 ). There have been at least 35 clinical studies showing CoQIO’s massive benefits for heart patients, especially patients suffering heart failure (see http://www.coqlOsupplement.com ). And in Japan, until last year CoQIO was a heart medication only available by prescription.
The drug giant Merck learned during its research into lowering cholesterol that statin drugs block the body’s production of its own CoQIO. This blockage of CoQIO synthesis is a serious action of statins that causes fatigue, muscle pain and skeletal myopathy (a grave deterioration of muscle). Drug advertisements in Canada must carry the CoQIO statin-depletion warning, but the US FDA does not require these important warnings, keeping US medical doctors in the dark and putting their patients at risk (see http://www.naturesperfectstatin.com/warn.htm ).
Merck has more than one 1990 patent for adding CoQIO to statins as a means of circumventing the issue of blocking CoQIO biosynthesis (US patent No. 4,933,165). Their having these patents since 1990 is proof that members of the Merck Corporation have been aware that statins cause muscle deterioration. (The Merck patents were never implemented, probably because the world supply of CoQIO is far too limited to supply all statin drug users.
Vitamin K2 is a potent anti-calcification nutrient via GLA protein carboxylation. Let’s look at this process of calcification and the potency of these various forms of vitamin K2. Then talk about the MK-4 vs Mk-7. Which is best for you? And why?
Vitamin K2 forms
There are currently three forms of vitamin K available. Vitamin K1 (phylloquinone) has been extensively studied. It is not the most potent form. Vitamin K2 is currently available in two forms. MK-4 also known as menaquinone-4 or menatetranone. MK-7 (menaquinone-7) is currently advocated as the most potent form of vitamin K2. You can see in fig 1 that the MK-4 and MK-7 have long “tails” with multiple (poly unsaturated) double bonds. This increases lipid solubility. These are fat soluble as opposed to water vitamins.
So what is the connection between Vitamin K2 and tissue calcification? Why do we petrify as we grow older? Why do we grow stiffer? This is a combination of calcification and glycation. Glycation is secondary to excess carbohydrates, rising hemoglobin A1c (>5.6%), and impaired fasting blood sugars (>100 mg).
Calcification is an impaired healing process. Arterial injuries initiate a process of calcium deposition as a repair mechanism. Calcification is the end result of chronic inflammatory processes. This is a key concept.
How can we prevent or reverse this ossification process?
For many years I have struggled to understand the process of “reverse calcification.” As we grow older there is a tendency to lose bone calcium matrix causing osteopenia or osteoporosis. And contrariwise, an increase in arterial and cardiac (heart) valvular calcification. When we were younger, calcium deposition was a bone building process. As we age it becomes a cardiovascular risk.
Coumadin as an Experimental Model
As it turns out, we have an excellent model from widespread use of Coumadin (Wafarin) anticoagulation. From empirical observation over 20 years and through extensive medical literature research, it is now proven that Coumadin accelerates osteoporosis and arterial calcification – coronary artery disease. How is that possible? Because Coumadin’s main action is antagonizing vitamin K2 action. That is the goal. Depleted Vitamin K thins the blood. It inhibits thrombosis and emboli (blood clots). Fig 2 shows the essential vitamin K-dependent steps that are blocked. [refer back my earlier discussion of coagulation and the prevention of heart attacks and strokes]
Now the good news is high doses of vitamin K2 does not cause the opposite. It does not cause abnormal clotting or thickening. The Japanese have carried out experiments using high doses of vitamin K2 for up to two years without any untoward effects. Even the World Health Organization has not determined an upper limit of vitamin K intake. It is only the insufficiency or blockage of vitamin K2 that thins the blood.
Carboxylation of GLA Proteins
Now the rest of the vitamin K2 calcium connection is the effect on GLA proteins. These are proteins that are absolutely essential for calcium regulation. And this is where so much of the vitamin K research has been focused. The activation of these GLA proteins are all Vitamin K dependent. See figure 3 the Vitamin K cycle. Once again, notice where warfarin blocks the final production of the active form of vitamin K (KH2) that is essential for carboxylation.
So what are these GLA proteins? This is a contraction or acronym for gamma-carboxyglumatic acid proteins. Each one of these is essential for calcium regulation. The most important of these include:
- Osteocalcin (BGP — bone GLA proteins)
- MGP (matrix GLA proteins)
- GRP (GLA rich proteins)
- and more
Experimentally, these proteins have been classified as either under-carboxylated (ucMGP or ucOC) or sufficiently carboxylated (cMGP or cOC). Under-carboxylated forms of these GLA proteins promotes vascular and valvular calcification. There is a rare syndrome – the Keutel Syndrome — characterized by abnormal calcifications and defective MGP. Now refer to figure 4.
The picture is now complete. You want healthy inflow of calcium for strong bones. We want to reverse or prevent calcium outflow and accumulation in arteries and heart valves. Vitamin K2 as MK-4 or MK-7 are potent activators of matrix GLA proteins (MGP) and Osteocalcin.
We have long struggled with this paradox. Progressive arterial calcification leading to coronary artery disease or peripheral vascular disease. Very little attention has been focused on valvular calcification which is even more serious. Eventually leading to open heart surgery with aortic or mitral valve replacements.
My friends in the alternative community at ACAM (American Academy for Advancement in Medicine) have long advocated the use of chelation therapy. Chelation therapy uses EDTA and other micronutrients infused intravenously to reverse calcification. Various alternatives to intravenous EDTA include oral and even rectal suppositories with some degree of success.
To further strengthen this connection let’s consider one final pathologic model. Chronic renal disease. Refer to figure 4.
Repeating, Osteocalcin is essential for bone building and health. It is a strong biomarker for vitamin K levels and activity. Osteocalcin must be carboxylated to exhibit full activity. Under carboxylated Osteocalcin is not fully active. It is totally Vitamin K2 dependent. So measuring ucOsteocalcin (under carboxylated) is a stronger biomarker for Vitamin K2 activity. Until recently this test was not available. This is slowly changing. Genova Diagnostics is one source.
MK-4 vs MK-7 Research
A large body of research on the phylloquinone or vitamin K1 form has been conducted. It has been concluded that this is an insufficient approach to the carboxylation of the GLA proteins. So that more recent experimentation with MK-4 has demonstrated sufficient potency to activate the carboxylated GLA proteins.
Then the MK-7 form was investigated. MK-7 is naturally found in the natto bean which is the source of Nattokinase. So much of the controversy currently is focused on MK-4 versus MK-7. Both of these are lipids soluble as previously mentioned..
Extensive literature research will reveal various shortcomings. Most experiments fail to use good basic pharmacological principles of the dose response curves. That is, what is response at various doses.
I frequently use the example of Lipitor. If we conduct an experiment with 1 mg of Lipitor for 1 to 5 years as an example, we will conclude that Lipitor is ineffective at lowering LDL. On the other hand, if we use a dose of 100 mg Lipitor for even one year we will find a very high rate of significant side effects intolerances and eventual discontinuation of the drug. So based on the initial dose we will find an appropriate response.
I have often questioned how researchers even pick the initial dose of any agent they are studying. What is this decision-making process?
So there have never been direct comparisons between high doses of MK-4 and MK-7. The Japanese of studied vitamin K2 (MK-4) in doses up to 30 to 40 mg (30,00 – 45,000 µg). These are “attack” doses. MK-7 has been tested in doses initially from 45 µg and much more recently as high as 400 µg. But there are no studies that compare head-to-head high doses of MK-4 with high dose of MK-7.
So Which Form of Vitamin K2 is Best for Me?
All we know is that researchers have concluded that even the “high” doses of MK-7 do not fully carboxylate the GLA proteins. So what is the appropriate dose of MK-7? Some researchers speculate it may be as high as 1000 µg.
I contend that both are lipid soluble. There are various factors including lipid solubility, volume of distribution (Vd), half-lives and ultimately carboxylation of GLA proteins. That is the goal. It is not serum levels. It is not half-lives. It is what is the optimal dose that fully carboxylates these GLA proteins? Especially MGP – matrix GLA protein and osteocalcin. There is a realization that this is the realistic approach.
So you will read that MK-7 is more potent than MK-4. This is primarily based on persistent blood levels of the MK-7 version. There is a difference between lipid solubility, tissue activity and blood levels. Even I measure serum levels of all hormones knowing that there are other part compartments such as saliva, urine.
Now I am beginning to see a combination of MK-4 and MK-7 to “hedge your bets.” We do not know the ideal dose. We do know that there is no upper dose of vitamin K that is toxic. This is why am now recommending at least 30 mg (30,000 µg) of vitamin K2 in the MK-4 version in at-risk patients. While 15 mg is my standard daily dose of Vitamin K2 MK-4. The MK-7 dosing is still in evolution. There is a sense that 400 µg is far more potent than the 45-90 µg that you have currently been taking in various combinations.
The reverse calcification paradox is solved. The experimental evidence is so compelling. Vitamin K2 is essential for healthy arteries and heart valves. This extends to healthy veins as well. The only controversy or decision is the form?
MK-4, MK-7 or a combination of both? Some of this will be practically solved by prices. What is more “affordable” to you? In the end it is all so much more efficient and less expensive than even a single day in a hospital or an extended ER visit.
I continue to recommend 15-30 mg of the MK-4 but remain open to a combination. I always had difficulty rationally understanding how 45 mcg of MK-7 was more potent than 15,000 – 30,000 mcg of MK-4. That would be at least 666 times. Nearly 3 orders of magnitude? I have seen no evidence in the literature to prove this assertion.
The real issue is monitoring. We have been testing Vitamin K with SpectraCell analysis for the last 20 years. Testing functional sufficiency levels. ucMGP and ucOS, as they are more available, will be the real test of Vitamin K efficacy. Will we see evidence of calcification reversal and increased bone density with higher doses? Imaging studies can confirm effectiveness of our therapies. Carotid ultrasound, CIMT (carotid intimal media thickness), ultrafast CT HeartScans and DEXA scans.
Take your vitamin D3 and Vitamin K2 together. My unfailing recommendation to you for the last 15-20 years.
I want to personally thank Lara Pizzorno for help with background literature research. Her writings on Vitamin K are highly recommended.
References and Bibliography
 Rogier Caluwe, Lotte Pyfferoen, Koen Boeck, An S. De Vriese: Effects of vitamin K supplementation vitamin K antagonists on progression of vascular calcification: ongoing randomized controlled trials. Clinical Kidney Journal, 2016, volume 9, no 2, 273-279
 Elke Theuwisse, Egbert Smit, and Cees Vermeer: The role of vitamin K in soft tissue calcification. Adv. Nut 3: 166-173, 2012
 Masataka Shiraki andNaoko Tsugawa, Toshio Okano: Recent advances in vitamin K -dependent GLA containing proteins and vitamin K nutrition. Korean Society of Osteoporosis 2015
 Takafumi Okura, Mie Kurata, Daijiro Enomoto, Masanori Jotoku, Tomoaki Nagao, Veena Raiska Desilva, Jun Irita, Len Ichi Miyoshi, Jitsuo Higaki: Under carboxylation of osteocalcin is a biomarker of carotid calcification in patients with essential hypertension. Kidney Blood Pressure Res 2010, 33:66-71.
 Rick H van Gorp and Leon J. Schurgers: New insights into the pros and cons of the clinical use of vitamin K antagonists (VKA’s) versus direct oral anticoagulants (DOACs). Nutrients 2015, 7, 9538-9557; DOI: 10.3390/nu7115479. citation link
 Toshiro Sato, Leon J. Schurgers and Kazuhiro Uenishi: Comparison of menaquinone-4 and menaquinone-7 bioavailability in healthy women. Sato et al nutrition Journal 2012, 11. citation link
 Ellen G.H.M.van den Heuvel, Natasha M. van Schoor, Paul Lips, Elke J.P. Magdeleyns, Dorly J.H. Deeg, Cees Vermeer, Martin den Heijer: Circulating un carboxylated matrix GLA protein, a marker of vitamin K status, is a risk factor of cardiovascular disease. Maturitas 77 (2014) 137-140 1 citation link