what do you eat it with?
I agree with Brad Stanfield. Randomized controlled trials reported no benefits of Nattokinase supplementation. Only retrospective studies reported benefits which means there’s bias in these studies.
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That’s a pretty damning video on Nattokinase, thank you @KarlT .
Again, I am breaking my own rule about trusting published research based on data from China (probably because I’d greatly prefer not to start a statin I’ll need to take for the rest of my life to control negative impact of my high LDL, and don’t want to write a check for $30k to take a PCSK9 inhibitor that isn’t covered by my insurance), but the Chinese study did use a much higher (10,000 units) dose versus the doubles-blinded clinical trial (2,000 units) so perhaps there is still hope?…
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Coach,
You ever run across or consider Cavadex for plaque related issues? I’m considering it.
Basically beta cyclodextrin
Thx
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I ferment my own Nattō and use chickpeas.
Until a randomized study is done with the higher dose mentioned, I wouldn’t consider Stanfield’s suggestion that inherent bias exists and therefore nattokinase is not effective the gospel truth. He simply does not know if it can be effective at a higher dose.
He didn’t bother mentioning his own biases during the last half of the video, especially promoting semaglutide and its role (if there is one) in the removal of aterial plaque.
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Following up with a research article on cyclodextrins use for removing plaque, which is not the patented molecule/delivery of Cavadex.
https://www.sciencedirect.com/science/article/abs/pii/S0163725820301509
Cyclodextrins can interact with and dissolve both extracellular and intracellular cholesterol crystals (Zimmer et al., 2016). Moreover, an efficient efflux of free cholesterol from the cytoplasmic compartments in macrophage foam cells is required for unloading the cytoplasmic cholesterol ester stores, and to prevent toxic cytoplasmic concentrations of free cholesterol from evolving, which, otherwise would lead to cholesterol crystallization in the macrophages (Kellner-Weibel et al., 1999). As the efficiency of physiological HDL particles to induce cholesterol removal from macrophage foam cells appears to be insufficient for the promotion of regression of atherosclerotic lesions, at least in humans, cyclodextrins could be used as supportive pharmaceuticals to boost the removal of cholesterol from such lesions.
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That’s a big misunderstanding. You just need to take a statin for as long as you want to stop apoB from building up in your blood vessels. If in 30 years you suddenly decide to stop taking a statin for whatever reason, you will still have avoided 30 years worth of damage.
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The burden of proof is not on Dr. Stanfield since he has solid proof that 2000 IU worth of nattokinase does nothing while the Chinese studies using 10,000 IU are not trustworthy.
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Interesting. I used to take Longevinex Plus which is a resveratrol and the “plus” is quercetin and cyclodextrin. I took it daily for about 13 years!! I have terrible lipids but no plaque on scans. So …. Maybe?
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Thanks for the lead. Sounds great. Amazon has it in bulk powder too. I just had PRP and need to stay away from fibrolytics like nattokinase or serratopeptidase.
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I’m going down the cyclodextrin hole: a clinical trial of 75 showing 6g of oral α-cyclodextrin per day is well tolerated, and lipids decreased 10% as well as insulin resistance.
Methods
We screened for healthy subjects, males and females, between ages 18 to 75. Out of total 103 subjects interviewed, 75 subjects completed the study. Qualified individuals in each gender group were randomized into two groups in terms of which treatment arm they received first (placebo vs. α-CD, receiving 6 grams P.O. a day, for 12–14 weeks with a 7 day wash out between arms). The primary outcome variable, plasma total cholesterol, as well as other tests related to lipids and lipoprotein and glucose metabolism, were measured at baseline and at the end of each arm of the study.
Results
α-CD was well tolerated; no serious adverse events related to α-CD were observed. Approximately 8 % of the subjects on α-CD complained of minor gastrointestinal symptoms versus 3 % on placebo (p = 0.2). Small-LDL particle number decreased 10 % (p < 0.045) for subjects on α-CD versus placebo. Fasting plasma glucose (1.6 %, p < 0.05) and Insulin resistance index (11 %, p < 0.04) were also decreased when on α-CD versus placebo.
Conclusion
α-CD treatment appears to be safe and well tolerated in healthy individuals and showed a modest reduction in small LDL particles, and an improvement in glucose related parameters.
Trial registration
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Cyclodextrin family safety data from Europe:
total daily oral dose of α-CD may reach 6000 mg/day, for β-CD 500 mg/day and for γ-CD 10 000 mg/day, and for HP-β-CD as oral pharmaceutical 8000 mg/day
Here’s the 2016 Zimmer article that is referenced above showing 2-hydroxypropyl-β-cyclodextrin is effective against atherosclerosis (plaque regression) in mice:
Since cholesterol accumulation and deposition of cholesterol crystals (CCs) triggers a complex inflammatory response, we tested the efficacy of the cyclic oligosaccharide 2-hydroxypropyl-β-cyclodextrin (CD), a compound that increases cholesterol solubility, in preventing and reversing atherosclerosis. Here we show that CD treatment of murine atherosclerosis reduced atherosclerotic plaque size and CC load, and promoted plaque regression even with a continued cholesterol-rich diet. Mechanistically, CD increased oxysterol production in both macrophages and human atherosclerotic plaques, and promoted liver X receptor (LXR)-mediated transcriptional reprogramming to improve cholesterol efflux and exert anti-inflammatory effects*. In vivo* , this CD-mediated LXR agonism was required for the anti-atherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Since CD treatment in humans is safe and CD beneficially affects key mechanisms of atherogenesis, it may therefore be used clinically to prevent or treat human atherosclerosis.
And here’s an in vitro study from the Netherlands 2022 that says 2-Hydroxypropyl-beta-cyclodextrin doesn’t work to reduce plaques but does lower lipids:
Abstract
2-Hydroxypropyl-beta-cyclodextrin (2HPβCD) is able to bind and solubilize unesterified cholesterol and may therefore be able to reverse the deposition of cholesterol in macrophages within the aortic vessel wall, a hallmark of atherosclerotic cardiovascular disease. However, conflicting results regarding the potential of 2HPβCD to induce regression of established atherosclerotic lesions have been described. In the current study, we therefore also investigated the ability of 2HPβCD to stimulate cholesterol removal from macrophage foam cells in vitro and induce the regression of established atherosclerotic lesions in apolipoprotein E knockout (APOE KO) mice. In vitro studies using murine thioglycollate-elicited peritoneal macrophages verified that 2HPβCD is able to induce cholesterol efflux from macrophages in an ATP-binding cassette transporter-independent manner. Switching Western-type-diet-fed APOE KO mice with established atherosclerotic lesions back to a chow diet was associated with a reduction in the hypercholesterolemia extent and an increase in the absolute lesion size and plaque collagen-to-macrophage ratio. Importantly, parallel subcutaneous administration of 2HPβCD was not able to prevent the diet-switch-associated lesion growth or induce atherosclerosis regression. Although in our hands, 2HPβCD does effectively stimulate cellular cholesterol efflux from macrophages, we do not consider it worthwhile to further pursue 2HPβCD as therapeutic moiety in the atherosclerosis regression context.
I didn’t know you were supposed to stay away from fibrolytics after PRP. Did this come from your doctor?
No. Just read it interferes with fiber laying of the platelet fibrigen on the stressed tissue. So, I’m going to for the cyclodextrin! I usually hit Naprosin hard every November but that’ll have to wait and I’ll give the PD a chance.
My doctor said excellent results with bergamot and put me on it for three months (am starting month three) he said no statins. I use Herbs of Gold before meals twice a day- no side effects. I only weigh 53 kg but developed high LDL after Pfizer vx in 2021 and now covid recently. My GP only wants me on bergamot. I just read Peter Attias Longevity book and really enjoyed it- well written and learned a lot re cholesterol.
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I hope it works well for you; for me for me it didn’t. My doctor “prescribed” it for me as well. I took 1,000mg per day of citrus bergamot for nine months and my LDL went from 172 to 164. Id say that was statistically insignificant for my n=1: that’s not a big enough change beyond what I did or did not eat the day before.
You are on month three: have you seen a meaningful change in LDL?
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Coach,
The cavadex folks claim the only effective delivery methods are IV and enema type.
I emailed them and asked if they tried subcutaneous but haven’t heard back.
I know one of the studies used subQ on mice.
If I hear from them I’ll post here.
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