re: Calcium Scores (Heart)

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In summary, our data from this largest clinical study involving 1,062 participants suggest that NK at the daily dose of 10,800 FU, which is higher than the recommended dose of 2,000 FU, is significantly effective in the management of atherosclerosis progression and hyperlipidemia. No adverse effects associated with the use of NK is observed. The study advances our understanding of the action of NK and the importance of the dosage of NK. We also demonstrate that other factors, including lifestyle and co-use of vitamin K2 and aspirin, could contribute positively to the clinical outcome. Our findings provide evidence that promising and positive clinical outcome in the management of atherosclerosis progression and hyperlipidemia can be achieved safely by using NK at a dose of 10,800 FU per day.

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Using randomised picking method, all patients were randomly assigned to one of two groups, nattokinase (NK) and statin (ST) group. NK Group-patients were given NK at a daily dose of 6000 FU and ST Group-patients were treated with statin (simvastatin 20 mg) daily. The treatment course was 26 weeks. Common carotid artery intima media thickness (CCA-IMT), carotid plaque size and blood lipid profile of the patients were measured before and after treatment.

A total of 82 patients were enrolled in the study and 76 patients completed the study. Following the treatments for 26 weeks, there was a significant reduction in CCA-IMT and carotid plaque size in both groups compared with the baseline before treatment. The carotid plaque size and CCA-IMT reduced from 0.25±0.12cm2 to 0.16±0.10cm2 and from 1.13±0.12mm to 1.01±0.11mm, repectively. The reduction in the NK group was significantly profound, a 36.6% reduction in plaque size in NK group versus 11.5% change in ST group. Both treatments reduced total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG).

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Our findings from this pioneer clinical study suggests that daily NK supplementation is an effective way to manage the progression of atherosclerosis and potentially may be a better alternative to statins which are commonly used to reduce atherosclerosis and further to prevent cardiovascular attack and stroke in patients. The mechanism underlying the reduction of carotid atherosclerosis by NK may be independent from its lipid-lowering effect, which is different from that of statins.

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nattokinase supplementation resulted in a reduction in SBP and DBP. These findings suggest that increased intake of nattokinase may play an important role in preventing and treating hypertension.

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The highest quartile of natto intake compared with the lowest intake was significantly associated with a decreased risk of mortality from total CVD after control for covariates: the HR was 0.75 (95% CI: 0.64, 0.88, P-trend = 0.0004). There were no significant associations between the risk of mortality from total CVD and intakes of total soy protein, total soy isoflavone, and soy protein or soy isoflavone from soy foods other than natto. The highest quartiles of total soy protein and natto intakes were significantly associated with a decreased risk of mortality from total stroke (HR = 0.75, 95% CI: 0.57, 0.99, P-trend = 0.03 and HR = 0.68, 95% CI: 0.52, 0.88, P-trend = 0.0004, respectively). The highest quartile of natto intake was also significantly associated with a decreased risk of mortality from ischemic stroke (HR = 0.67, 95% CI:0.47, 0.95, P-trend = 0.03).

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Nattokinase seems to reduce blood clotting by breaking down fibrin (a molecule that entangles platelets and creates blood clots) by degrading plasminogen activator inhibitor-1 (PAI-1, a protein that makes clotting more efficient). PAI-1 disables plasminogen activators (PAs), including tissue-type plasminogen activator (tPA), a serine protease which is administered therapeutically to break up blood clots in conditions such as ischemic stroke and heart attack.[4][14] Studies in humans have shown that ingesting a single dose of nattokinase increases blood levels of tPA for about 3 hours,[15] while regular administration (taking 1,300 mg of nattokinase 3 times daily for 8 days) seems to gradually increase tPA in the blood over time.[7] Small studies conducted in generally healthy people, as well as people on dialysis and with cardiovascular disease, showed that taking 800 mg (4,000 fibrinolytic units) of enteric-coated nattokinase 30 minutes after dinner every day for 2 months reduced serum fibrinogen by 7–10%, factor VII by 7–14%, and factor VIII by 17–19% compared to baseline. The reduction in fibrinogen in people with cardiovascular disease and the reduction in factor VII in people on dialysis did not reach statistical significance, possibly due to insufficient power in the study.[16]

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This study further supports that nattokinase can be used as an effective adjunctive therapy for hypertension, but relatively low-dose supplementation of nattokinase may have no significant lipid-lowering effect. More work will need to be done to determine whether the positive efficacy of nattokinase on cardiovascular risk factors is dose-dependent.

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Ten patients were supplemented with PJ for 1 year and five of them continued for up to 3 years. Blood samples were collected before treatment and during PJ consumption. In the control group that did not consume PJ, common carotid intima-media thickness (IMT) increased by 9% during 1 year, whereas, PJ consumption resulted in a significant IMT reduction, by up to 30%, after 1 year. The patients’ serum paraoxonase 1 (PON 1) activity was increased by 83%, whereas serum LDL basal oxidative state and LDL susceptibility to copper ion-induced oxidation were both significantly reduced, by 90% and 59%, respectively, after 12 months of PJ consumption, compared to values obtained before PJ consumption. Furthermore, serum levels of antibodies against oxidized LDL were decreased by 19%, and in parallel serum total antioxidant status (TAS) was increased by 130% after 1 year of PJ consumption. Systolic blood pressure was reduced after 1 year of PJ consumption by 21% and was not further reduced along 3 years of PJ consumption. For all studied parameters, the maximal effects were observed after 1 year of PJ consumption. Further consumption of PJ, for up to 3 years, had no additional beneficial effects on IMT and serum PON1 activity, whereas serum lipid peroxidation was further reduced by up to 16% after 3 years of PJ consumption.
The results of the present study thus suggest that PJ consumption by patients with CAS decreases carotid IMT and systolic blood pressure and these effects could be related to the potent antioxidant characteristics of PJ polyphenols.

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Consumption of pomegranate juice which is rich in tannins, possess anti-atherosclerotic properties which could be related to its potent anti-oxidative characteristics. As some antioxidants were recently shown to reduce blood pressure, we studied the effect of pomegranate juice consumption (50 ml, 1.5mmol of total polyphenols per day, for 2 weeks) by hypertensive patients on their blood pressure and on serum angiotensin converting enzyme (ACE) activity. A 36% decrement in serum ACE activity and a 5% reduction in systolic blood pressure were noted. Similar dose-dependent inhibitory effect (31%) of pomegranate juice on serum ACE activity was observed also in vitro. As reduction in serum ACE activity, even with no decrement in blood pressure, was previously shown to attenuate atherosclerosis, pomegranate juice can offer a wide protection against cardiovascular diseases which could be related to its inhibitory effect on oxidative stress and on serum ACE activity.

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The experimental and control groups showed similar levels of stress-induced ischemia (SDS) at baseline (p >0.05). After 3 months, the extent of stress-induced ischemia decreased in the pomegranate group (SDS -0.8 +/- 2.7) but increased in the control group (SDS 1.2 +/- 3.1, p <0.05). This benefit was observed without changes in cardiac medications, blood sugar, hemoglobin A1c, weight, or blood pressure in either group. In conclusion, daily consumption of pomegranate juice may improve stress-induced myocardial ischemia in patients who have CHD.

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Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation

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Or should I do 2x a day?

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Nattokinase- LINK quote:In summary, our data from this largest clinical study involving 1,062 participants suggest that NK at the daily dose of 10,800 FU, which is higher than the recommended dose of 2,000 FU, is significantly effective in the management of atherosclerosis progression and hyperlipidemia. No adverse effects associated with the use of NK is observed. The study advances our understanding of the action of NK and the importance of the dosage of NK. We also demonstrate that other factors, including lifestyle and co-use of vitamin K2 and aspirin, could contribute positively to the clinical outcome. Our findings provide evidence that promising and positive clinical outcome in the management of atherosclerosis progression and hyperlipidemia can be achieved safely by using NK at a dose of 10,800 FU per day.

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