Vitamin K2 and Vascular Disease

I have been asked to talk about the role of Vitamin K (K2 specifically) in the pathogenesis of vascular disease.  This is a controversial topic as “mainline cardiology” has not yet embraced the data and the “jury” is not yet out as to the importance of vitamin K2 in preventing and treating cardiovascular disease.  The data I will summarise is extremely interesting and I believe we will be incorporating this knowledge into prevention and management of atherosclerotic vascular disease soon.

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Introduction:

We have been conventionally taught that the role of vitamin K was solely ascribed to coagulation and coagulation was thought to be involved only in the venous system.

This view has dramatically changed with the recent (last decade) discovery of vitamin K-dependent proteins outside the coagulation cascade and the role of coagulation factors in the pathogenesis of atherosclerosis on the arterial side. Vitamin K-dependent proteins are involved in the regulation of vascular smooth muscle cell migration, apoptosis (programmed cell death), and vascular calcification.

Vascular calcification is a well recognised important independent predictor of cardiovascular disease and closely correlates cardiac morbidity and mortality. The involvement of vitamin K-dependent proteins such as matrix Gla-protein (MGP) in vascular calcification makes that calcification amendable for intervention with high intake of vitamin K2. 

Nutritional vitamin K consists of two forms:

  • vitamin K1 (a phylloquinone also known as phytonadione)
  • vitamin K2 (a menaquinone)

Vitamin K1 is found in leafy green vegetables (lettuce, spinach and broccoli)where it is tightly bound to the chloroplast membrane resulting in a poor absorption (poor bio-availability) of vitamin K1 from vegetables but it is still the dominant form making up about 90% of the vitamin K in a typical Western diet.

natto-1

Vitamin K2 is found in fermented foods such as cheese, sauerkraut and the Japanese Natto (a foul-smelling sticky web of fermented soybeans typically served with a Japanese breakfast.derived from the bacterium Bacillus subtilis). The absorption of vitamin K2 is apparently much better as compared to vitamin K1 comprising 10% of our vitamin K consumption.  Vitamin K2 importantly can be synthesised in the colon by microflora. There are apparently 4 isoforms of vitamin K2 determined by the number of prenyl side chains (MK-4; MK-7; MK-8 & MK-9). MK-4 is found in meat whereas the MK-7 to 9 tend to come from the fermented foods.

k_formulas

Importantly the bioavailability of the isoforms differ with MK-4 demonstrating very poor bioavailability at a nutritional level dose compared to excellent bioavailability with MK-7.

After being absorbed in the intestine, vitamin K, as a fat soluble vitamin is transported by lipoproteins, as it has no specific carrier protein. The different lipophilicity (fat solubility) of K1 and K2 may result in substantial differences in plasma transport, half-life and delivery to target tissues (t1/2 for K1 ~ 3 hours; 1.5 hours for MK-4 and > 70 hours for MK-7; MK-8 & MK-9).

Vitamin K-dependent proteins:

Vitamin K-dependent proteins constitute a family of 16 known proteins with diverse functions, not only involved in the haemostatic coagulation pathway. The vitamin K dependent coagulation proteins (clotting factors II, VII, IX and X) are essential for the coagulation cascade and are γ-carboxylated in the liver to be functionally active. They are well-balanced by the anticoagulant factors protein C and protein S.

All these vitamin K-dependent proteins are mainly synthesized and γ-glutamylcarboxylated in the liver, with the exception of proteins S which is synthesized in part by endothelial cells.

Over the past decade an enormous amount of evidence has suggested that coagulation factors play an important role in (chronic) inflammation. Phagocytosis of apoptotic cells by macrophages is thought to limit the inflammatory response and Protein S has been identified as a factor responsible for stimulation of this phagocytosis. Additionally protein S regulates the expression and function of scavenger receptor A (SR-A) on macrophages resulting in diminished uptake of acetylated low density lipoprotein.

Protein C deficiency is associated with severe coagulation response to endotoxin and this Protein C also plays a significant role in the inflammatory response with activate Protein C inhibiting endotoxin-induced production of important cytokines like TNF-alpha, IL-1, IL-6 and Il-8 by momocytes/macrophages.

Extrahepatic vitamin K-dependent proteins:

Within the arterial vessel wall vitamin K-dependent proteins are synthesized with functions not related to blood coagulation.

Growth arrest specific gene 6 protein (Gas-6) is a vitamin K-dependent protein produced by vascular smooth muscle cells (VSMCs). Gas-6 seems to protects VSMCs from calcification by inhibiting apoptosis as the cell death may act as a nidus for calcification.

The vitamin K-dependent matrix Gla-protein (MGP) is regarded as the strongest inhibitor of vascular calcification (VC) and produced by many cells, including VSMCs. Rescue experiments in MGP null mice demonstrated that MGP acts locally in the vascular tissue as restoration of MGP expression in arteries completely rescued the arterial mineralization phenotype, whereas hepatic MGP expression, resulting in high systemic MGP levels, did not.

Vascular calcification as a marker of atherosclerosis risk stratifies into high risk outcome:

Vascular calcification (VC) is associated with increased cardiovascular mortality and morbidity, and is recognised as a strong and independent risk factor for cardiovascular death. The amount of VC, as measured and quantified by multidetector computed tomography (CT-coronary angiography) is an important predictor of:

  • all-cause mortality
  • vascular complications
  • myocardial infarction and stroke

Patients with higher coronary artery calcification scores have approximately ten times more chance to have a cardiac event in the next 3–5 years. Patients with a calcification-progression over 15% per year had a 17.2 fold increased risk of myocardial infarction compared to patients without significant progression.

Vascular calcification is an even stronger predictor than the Framingham Risk Score (FRS) which is currently used to score 10-year risk prediction for cardiovascular events.

Clinically,VC causes stiffening of the vascular arteries via elastic fiber and VSMC calcification resulting in:

  • decreased arterial compliance with the development of chronic systemic hypertension
  • development of left ventricular hypertrophy leading to diastolic heart failure
  • decreased coronary perfusion 

In spite of this data, calcification of arteries has been generally neglected and considered to be clinically unmodifiable, often regarded as an end stage passive process not amenable to therapeutic intervention.  Recent data however suggests that punctated and spotty calcification in the atherosclerotic plaque influence stability negatively and render the plaque vulnerable to rupture thus potentiating the progression of atherosclerosis and vascular events.

As VC is a complex and actively regulated process involving cells and vitamin K dependent proteins acting as catalysts and inhibitors. Recruitment of macrophages in the atherosclerotic plaque and consequently their secretion of inflammatory cytokines may serve as a signal for intimal calcification.  When VSMCs phagocytose calcium crystals it seemingly destabilize atherosclerotic plaques by initiating inflammation and by causing SMC death. Vascular calcification

Circulating biomarkers (MGP) for detecting vascular calcification:

This is an attractive concept to screen for and perhaps regulate mechanisms of VC.  Vitamin K-dependent proteins have been associated with the earliest calcification areas in the plaque. Uncarboxylated MGP seemingly strongly correlates with both medial and intimal calcification. By measuring circulating MGP isoforms it has been shown that the majority of the healthy population have sub-optimal levels of vascular vitamin K. Preliminary data suggest that some MGP conformations are associated with aspects of cardiovascular disease for instance patients with high VC scores display high levels of inactive MGP, especially dialysis patients.

This creates possibilities for targeting VC with vitamin K therapy. Indeed high intake of vitamin K has been shown to regress preformed medial calcification in a rat model and the first data is available in dialysis patients showing that vitamin K supplementation markedly reduced the level of plasma uncarboxylated prothrombin, uncarboxylated osteocalcin and inactive MGP.

Conclusion:

Effort must be directed towards retarding or reversing the development of calcification in the vasculature, especially in those patients prone to vascular calcification (chronic kidney disease, diabetes, atherosclerotic cardiovascular disease). In these patients the treatment with vitamin K antagonists should be reconsidered perhaps with a view to used specific Thrombin inhibitors in cases where anticoagulation is required.

Therefore, it is of importance to identify patients with vascular disease and to evaluate different strategies that are more effective in the prevention of hypercoagulability as well as vascular calcification.

Here lies the real interest in high dose vitamin K2 replacement to minimise and reverse vascular calcification as part of general prevention and management of atherosclerotic vascular disease.

This is consistent with separate research also showing superior health benefits from vitamin K2, including:

  • The Rotterdam Study the first study demonstrating the beneficial effect of vitamin K2, showed that people who consume 45 μg/d of K2 daily live seven years longer than people getting 12 μg/d
  • Data from the Prospect EPIC Cohort published in
    Nutrition, Metabolism & Cardiovascular Diseases
    Gast et.al. Volume 18, Issue 7 Pages 504-510, September 2009
    suggested a high menaquinone intake reduces the incidence of coronary heart disease (CHD). 16,057 women, enrolled between 1993 and 1997 and aged 49–70 years, who were free of cardiovascular diseases at baseline. Intake of vitamin K and other nutrients was estimated with a food frequency questionnaire. After a mean follow-up of 8.1±1.6 years, with 480 incident cases of CHD. Mean vitamin K1 intake was 211.7±100.3 μg/d and vitamin K2 intake was 29.1±12.8 μg/d.After adjustment for traditional risk factors and dietary factors, the authors observed an inverse association between vitamin K2 and risk of CHD with a Hazard Ratio (HR) of 0.91 [95% CI 0.85–1.00] per 10 μg/d vitamin K2 intake. This association was mainly due to vitamin K2 subtypes MK-7, MK-8 and MK-9. Vitamin K1 intake was not significantly related to CHD

Foto_home

Um food for thought….

Blessings Cardiologydoc

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36 thoughts on “Vitamin K2 and Vascular Disease

  1. Thanks again, for your post on Vitamin K2 and Vascular Disease.
    In the future, can you make a post on Triglycerides.
    Is it true, people with triglycerides under 70 have Pattern A LDL.
    Is it also true, on a Lipid panel test, if your triglycerides are under 100, that can mark your ldl look higher then they are, if so what test do I ask for.

    My triglycerides were in the 200’s, now they are under 100, that why I am asking.
    Also I see my DR two time a year, I just like to have something to take to him about!

  2. Sure I will address Triglycerides in blog but briefly you can have very low TG with independently high LDL (ie independent risks). Low TG also does NOT guarantee type A pattern LDL but high TG is often associated with high risk pattern B LDL.

    Best test is Apo-B Apo-A1 which measures total athergenic lipoproteins verses total non atherogenic lipoproteins. The ratio Apo-B/ Apo-A1 < 0.5 defines low risk.

    Regards Cardiologydoc

  3. Thanks again Doc,
    I love your blog, it’s good to have a real doctor, to take the time, to help us understand heart health. when I see my DR, I will ask him about the “Apo-B Apo-A1” test.

    Also I ask about triglycerides under 100, because I saw somewhere , that the Friedewald equation can be off, if your TG were under 100 or over 400.

    I have been on a three year journey, to improve my health, thanks again for your help!

  4. Sam you are 100% correct that a high TG (> 400) causes inaccuracies with LDL calculation using the Friedewald equation. This is one of the reasons to fast as this excludes contamination from possilbe posprandial triglyceridaemia

    Regards Cardiologdoc

  5. My wife recently had an arterial CT scan that revealed extensive calcification. She was a smoker (I say “was” because she currently down to 1-2 cigarettes a day and, hopefully, will be be down to zero soon). She has been taking the LEF product, Super K (1,000 mg or K1; 1000 mcg of Mk4; 200 of MK7) for the past several years. However, in light of her calcium score on the CT scan, it doesn’t seem to have had any effect. I realize that Vitamin K is no “magic bullet” and that she needs to work on other things, such as diet, as well. The reason I am writing is that there is a company VRP that sells a product, “Ultra K2” (MK7 form): each gel capsule is 10 mg and the recommended dosage is 3/d. What I don’t understand is that, as far as I can tell, the average dose capsule of K2 is measured in micrograms, not milligrams. I have called the company for information on how they came up with such a megadose. They promised to get back to me. In any case, I have never read anything in the literature on Vitamin K2 about possible overdose. Is it possible that such a high dose is both safe and effective in helping to reverse arterial calcification?

    • Hi Irwin

      Thanks for taking the time to comment. Arterial calcification takes decades and is a marker of your Wife’s lifelong risk factor burden for atherosclerosis. Even passive smoking is associated with progression of atherosclrotic vascualr disease (and therfore progression of vascular calcification). You are absolutely correct that the pathophysiology of arterial disease (calcification) is multifactorial (9 factors) of which abnormal ApoB/ApoA1 is the top abnormality (lipoprotein disorder) with smoking second.

      To prevent vascular disease the dose of K2 as MK 7 is about 45 micro grams per day (mcg/d) but to provent progression in people who have calcification doses up to 450 mcg/d have been used. I’m not aware of information of studies showing REVERSAL of calcification with K2.

      In other words your wife should aggressively address all 9 risk factors (see my blog) to optimal levels and to perhaps take ~200-450 mcg/d of K2 as MK7.

      Regards Cardiologydoc

      • Some sources are recommending that the K2 dose should be based on Vitamin D intake. I have seen one recommendation that for every 1000UI of Vitamin D you should be taking 180 to 200 mcg of K2 (presumably MK7?). This would work out to about 900 to 1000mcg for a person taking 5000IU of vitamin D which about the right amount for many people although to get the correct vitamin D dose you should have you serum levels checked.

        I suspect that the actual optimum dose for K2 should actually be based on vitamin d serum levels rather than vitamin d dose.

        Presumably tying K2 dosage to vitamin D intake is because as Vitamin D levels increase we produce more MGP and as a result we need more K2 to activate all (or most of) the MGP at these higher levels.

      • Hi Hal

        Thanks for the coment. I agree but generally we nees 1000 to 2000 units Vitamin D per day for healthy living.

        Regards Cardiologydoc

  6. 5years ago I had a calcium score of 17. It is now 104 I am 51yo female w BMi of 22.2, trig 44, Hal 86, LDL 107, blood pressure 120/78, take 3 grams omega 3, vit d3 5000, 500 mg magnesium, multi. Just diagnosed w low thyroid t3. Walk 2 to3 miles 3-5 times per week. Any thoughts on the significant calcium score. Family history of heart disease w obesity and diabetes.

  7. For many years, I smoked heavily, was overweight, nearly totally sedentary. and ate anything. My cholesterol was 230 when I was 35. I had chronic sinusitis and used antibiotics as often as not.

    Over the last several years, I’ve stopped smoking, became vegan, my cholesterol is now 150 or less, my weight is almost normal, my blood pressure is 100/70 and I *feel* great. I’m 48 now and often feel better than I did in my 20s. I treadmill and walk and do weights and feel like my stamina and heart/lungs are better than ever …

    But then …

    I very recently discovered I have aortic regurgitation and calcification of my aortic valve. It’s mild but it was alarming to find out I have, basically, at least some heart disease. I’m so happy with how good I feel now and I really hate having something physically wrong with me. I had no recognizable symptoms and it was found by accident. A friend is a mobile ultrasound tech and needed a guinea pig on which to test out a new machine, and he found it.

    I’ll be taking Vitamin K as well as magnesium and also upping my intake of kale, broccoli, spinach, etc.

    Is there anything else I can do to ensure this condition remains stable? Is there any indication from anywhere that valve and arterial calcification can be reversed?

    • Hi Sel

      Great to hear about your health transformation. Aortic valve calcification and vascular atherosclerosis
      share epidemiological risk factors and pretty much reflects your risk profile prior to your transformation. With the association of conventional risk facts driving a chronic inflammatory process, to prevent progression of the vascular calcification you need to optimise your risk profile as you are doing (LDL < 70; Apo-B/ ApoA1 < 0.4; Apo-B < 80; BP ~ 120/80 or less; BMI < 25; glucose < 100 and us-CRP < 1.0; non-smoking and optimal nutrition and exercise).

      Although there are studies in animal models for reversing vascular calcification with Vitamin K2 there are no definitive studies in humans but with the observational data that high intake of Vitamin K2 is associated with less vascular calcification I would agree you should supplement with K2. Be sure your Vitamin D3 is optimal (don't over supplement)and don't supplement with over the counter (OTC) Ca++ supplements.

      If you are successsful with the above the mild aortic regurgitation and mild AV calcification may not porgress or may progress very slowly.

      Cardiologydoc

  8. This is a great blog and very informative. Vitamin K2 and Mg are supposed to redirect calcium out of the vascular and soft tissues to the bones or urine. There is also the Linus Pauling therapy of Vit C and amino acids that are supposed to prevent AND reverse CHD. There are also studies of complete vegan diets stopping and reversing CHD- this may be the right nutrients fixing the body up especially the stomach flora which then produces vitamin K2.

    • Hi Brian

      Thanks for your interest. One of the best reports I have seen covering the very controversial topic of calcium supplementation is: “Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis” by Bolland MJ et al. BMJ 2010;341:c3691

      The group investigated whether calcium supplements lead to increase the risk of cardiovascular events (trial level meta-analyses between November 2007 – March 2010). Eligible studies were randomised, placebo controlled trials of calcium supplements (≥500 mg/day), with 100 or more participants of mean age more than 40 years and study duration more than one year. 15 trials were eligible for inclusion,11 with trial level data (11 921 participants, mean duration 4.0 years).

      In this pooled analysis of around 12 000 participants from 11 randomised controlled trials, calcium supplements were associated with about a 30% increase in the incidence of myocardial infarction and smaller, nonsignificant, increases in the risk of stroke and mortality. The findings were consistent across trials, with an increased relative risk of myocardial infarction with calcium observed in six of the seven trials in which at least one event occurred, although no individual trial reported a statistically significant effect. The risk of myocardial infarction with calcium tended to be greater in those with dietary calcium intake above the median but was independent of age, sex, and type of supplement.

      This study is consistent with trials of patients with renal failure, in which calcium supplements were associated with an increase in mortality and another study reported a 24% increase in coronary heart disease in Finnish postmenopausal women using calcium supplements (with or without vitamin D) compared with non-users.

      This data is in contrast to the large “Women’s Health Initiative” reporting that calcium and vitamin D had no effect on the risk of coronary heart disease or stroke. The Women’s Health Initiative however used low dose vitamin D supplements, and vitamin D deficiency has been associated with increased risk of cardiovascular disease and vitamin D supplementation with decreased mortality. Also, the participants differed from those in this meta-analysis: on average they were younger (mean age 62 v 75 years), heavier (mean weight 76 v 68 kg); had higher calcium intakes (mean 1150 v 830 mg/day), and a higher proportion were using hormone replacement therapy.

      The precise mechanism for the increase in vascular morbidity and mortality is not known although vascular calcification is a cardiovascular risk. Vitamin K2 may be the missing link, directing calcium into the bone rather than the artery but we have NO definitive data.

      DO I take calcium supplements – NO
      DO I keep my Vitamin D3 > 30 ng/mL – YES
      DO I eat whole food, rich in calcium and Vitamin K2 – YES

      Blessings Cardiologydoc

  9. High levels of triglycerides are sometimes associated with high Lp(a) in LDL and this is a very atherogenic combination also very resistant to treatment. Not all LDL are equal. Treating with high doses statins may help but not much the type with high Lp(a) which is very genetic in origin. It’d be interesting to see if Vitamin K2 may help in this cases of dyslipidemias bearing high Lp(a).

    • Hi Jose

      You are right. Lipoprotein “a” is an “LDL-like” lipoprotein and is atherogenic. High TG are associated with small dense LDL (as in diabetes and “metabolic syndrome”) and also associated with high non-HDL (LDL + VLDL + IDL) and account for the increased athergenic lipoproteins associated with high TG. We don’t have an effective treatment strategy for Lp “a” (although Nicotinic acid works well) and there is no data using Vitamin K2.

      In the stting of high TG with high atherogenic LDL and non-HDL we try to improve the metabolic chaos (diet and exercise) and treat aggressivly with high potency high dose Statin therapy.

      Regards Cardiologydoc

    • Hi Abhishek

      I’m so sorry to hear you have obstructive coronary disease. The pathological process is almost certainly atherosclerosis with obstructive plaque narrowing your arteries. This not “calcium blockage” as the calcium is just part of the degenerative plaque and sadly no large evidence based studies have ever shown reversal of arterial calcification and reversal of the arterial obstruction just with Vitamin K2 supplements. We would still advise revascularisation via angioplasty/ stents or formal coronary artery bypass surgery should it be necessary.

      Kind regards
      Cardiologydoc

      • Well, doc, by now you should know that pomegranate juice reverses atherosclerosis by 30 to 40+ % in one year, if one ounce to 8 ounces are ingested each day for a year.
        This IS from PubMed , double-blind, randomized, with placebo arm, studies (with a capital “S”)
        Type in ” carotid artery stenosis pomegranate juice 3 year study” or “aortic stenosis pomegranate” find the studies at PubMed at NIH.gov and the Mayo Clinic.

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  11. The Rotterdam Study and the Prospect Epic Cohort study were both self reported diet studies. There are firms today who are using these studies as ” gold standards” in the marketing of K2 tablets. To my knowledge there are no studies showing that intake of such tablets can prevent or minimize the risk of arterial calcification and hence a.g a myocardial infarction.A correlation between dietary intake of K2 and arterial calcification can not be used as an argument that K2 tablets may have the same effect. This have to be tested in a randomized,double blind study using these tablets where the incidens of cardiovascular disease should be the end-points. I wonder if such a study will ever be performed.

  12. I’m a 68 year old female recently diagnosed with MILDLY aortic thickening and calcified aortic. Also, distolic dysfunction ( Ejection fraction o 50-55%) of left ventricle and mild leaflet thickening of the mitral valve. AM I INTO HEAVEY VASCULAR DISEASE?

    never smoked, no history of heart problems, ideal weight, no diabetes, avid exerciser, feeling great, lots of energy, no symptoms.

    I’ve had a high LDL since menopause, but my ratio has always been in the good zone. Where has this monster come from? In process of getting on vegan diet with K 2/D3 supplication. BUT WHAT DOSAGE WOULD YOU RECOMMEND OF THE k2 AND D3 AND WHERE WOULD YOU RECOMMEND PURCHASING IT TO ASSURE IT IS A QUALITY PRODUCT.

    • Hi Marlaine

      Aortic valve “sclerosis” & mitral annular calcification is a form of vascular atherosclerosis. Diastolic dysfunction represents a relaxation abnormality of the left ventricle often age-related. In the setting of menopause and high LDL this would confer increased event rate moving forward but as yet you do not have “advanced” vascular disease. You need to correct for any Vitamin D3 deficiency usually 2000 u per day with K2 45 micro g/ day. Your LDL should be kept < 70-100 or ~ 1.8 mmol/l.

      Regards
      Cardiologydoc

  13. I have high Vit d 3 levels of 120 ng. and was quite suprised..i have been supplementing with btw 1000-2000iu a day . i understand it is unusual for high vit d 3 levels like mine, however i have a body that seems to overabsorb everything from iron to copper to vitamin d to cholesterol! believe it may in part be due to the MTHFR 677ct variant, I also have very high genetic lpa of 135nmol.(my ldl is 12, trigs 52, hdl 93) i know that lpa can increase blood clotting issues and how does that play part in supplementing with MK 7 which is beneficial in other ways is 45 mcg a day safe for someone with lpa?
    I currently take 3000mg IR niacin first thing in am and some methyl bs and magensium as well as boulouke which is a lumbrokinese enzyme that reduces fibrin (is mk 7 and boulouke (or asprin) antagonistic?

    • Hi Amy

      Your are obviously well informed about matters of CVD. Your high Vitamin D3 is not necessarily surprising as 400 u/d in some folk is enough and depending on sun exposure and other dietary sources of Vitamin D3 taking 2000 u per day is clearly too much for you. Your very high Lipoprotein “a” is clearly a risk for athero thrombosis and vascular calcification. One model studied is degenerative calcific aortic valve stenosis which is more common with very high Lp “a”. Sadly we have NO definitive studies to show supplementation with Vitamin K2 at 45 mcg/d will slow calcific AS. I personally correct Vitamin D3 and supplement with K2 in all patients with calcific vascular disease including the early stages of degenerative aortic valve sclerosis/ stenosis. I can’t answer the mk 7/ boulouke antagonism but there is no reason for antagonism with Aspirin.

      Finally is your LDL really 12?

      Regards
      Cardiologydoc

      • opps no LDL is 123! so not so great. I am very fit and actually could use a few more lbs (so any sort of “restricted fat/carbs diet” isnt possible that a lot of people use to lower their CVD risk) I exercise 7 days week and eat VERY clean and healthy. just crappy genes i guess in choleserol area. (ap0e 3.4 as well) My mk7 concern is if it is contradicted in someone with high lpa as it increases blood clotting and lpa “people” are more prone to hypercoagulation. will increase the prone ness towards hyper clotting? anoth niacin question, i take IR niacin all in one dose first thing in am and tolerate is very well (3000mg) instead of 1500 mg niaspan (usually taken at bedtime) is the niacin better taken in say two doses of 1500 spread out or is it just as effective taken in the one dose in the morning.? I plan to take MK 7 with dinner, my heaviest meal
        thank you so much for your feedback

  14. Hi Cardio Doc again

    i have read mixed information on which form of vit 2 is better ..i understand bone health mk4, heart health mk 4 but have read some studies where drs prefer mk4 for both bone and calcification reduction. would it make sense to take a supplement with both forms?

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