591 replies to this topic

[QuestforLife]

You may want to reread that study more carefully. It doesn't mention reduction of coronary calcium score, or even reduction of mortality. The case with statins is pretty seddled, in average it reduces 5 year mortality in 1 out of 84 how take statins for 5 years (in those with previous cardiovascular events, for primary prevention that number becomes sheer astronomical.)

The study wasn't designed to look at mortality, although we know Statins do well there. What was interesting is that there were large improvements in many measurements of arterial health including pulse wave velocity, flow mediated dilation and c-reactive protein. All correlated, I might add, to an increase in telomerase. Further papers from the same author also show the low, intermittent dose to be superior - mitigating concerns over Statins side effects.

Further investigation (done by me, here: https://www.longecit...es/#entry864097), show the telomerase effect is likely due to de differentiation of cells into endothelial progenitors via ROCK kinase inhibition.

Just something else to consider.

[Daniel Cooper]

For all the statin studies I read, the NNT to avoid a cardiac event over a 5 year horizon tends to vary from 60 to 120.  That simply doesn't wow me as a great drug to prevent, much less reverse, cardiovascular disease.

 

Meanwhile, ETDA which is held at arm's length by the medical community seems to have a NNT for the same 5 year horizon of less than 10, at least in diabetic patients with existing cardiovascular disease.

 

Statins make a lot of money for pharmaceutical companies but they are an exceedingly mediocre treatment (at best) for CVD.

 

Honestly, I wish these drugs *did* work.  I'd be more than happy to take them if they were very effective.

 

 

 

 

 

Edited by Daniel Cooper, 04 February 2019 - 06:53 PM.

[mikey]

The evidence for EDTA's effectiveness for heart disease is actually quite extensive.

http://beta.asoundst...apy_History.pdf
 

 

The American Heart Association (AHA) has the credibility of having produced a large influence on hundreds of millions of people in the world by recommending against butter and for margarine (trans fats) in the 1960s. Thus, The AHA's credibility is close to zero and no reference to their statements carries significant credibility, as they CAUSED hundreds of millions of people to experience lethal CVD by eating trans fats rather than healthy fats.

Although EDTA certainly has credible advocates, when I asked the MD that was fully without guile and resolved the loss of meniscus in my knee cartilage with Prolozone therapy (from great pain to no pain in two months) if he would perform EDTA IV chelation for my CVD he told me "It doesn't work."

He could have made money giving me IV EDTA but his interest was my well-being, not money. I remain skeptical that EDTA is effective for CVD.

Edited by mikey, 04 February 2019 - 08:10 PM.

[Daniel Cooper]

Although EDTA certainly has credible advocates, when I asked the MD that was fully without guile and resolved the loss of meniscus in my knee cartilage with Prolozone therapy (from great pain to no pain in two months) if he would perform EDTA IV chelation for my CVD he told me "It doesn't work."

 

 

You're talking about the opinion of one doctor versus a couple of decent studies that show some reasonable effectiveness.

 

You may like your doctor but I'll take the studies any time.

[Kimer Med]

You might want to reconsider never taking a statin​ as this in combination with a sartan is precisely what has been shown - in low, intermittent doses - to reverse atherosclerosis.

 

https://www.research...middle-aged_men

 

The main problem I have with statins is that they are a mitochondrial toxin. Although the effect can be partially offset with CoQ10, it can't be completely offset. The other problem I have is that they aren't very effective at treating CVD. My view (based on considerable reading and research) is that the idea of high cholesterol causing CVD is largely a hoax perpetrated on the medical community by drug companies.

 

Regarding the study you mentioned, they were looking at low/subclinical doses. That's a different regime, so I can see how it might be of interest. However, on principled grounds, it would take a lot more than a few studies to convince me that they were safe and effective at low doses. Even then, there would have to be a clear disease state for me to take the risk, as opposed to preventative only (such as to lower cholesterol, which is what 99+% of statin prescriptions are written for).

[Kimer Med]

Although EDTA certainly has credible advocates, when I asked the MD that was fully without guile and resolved the loss of meniscus in my knee cartilage with Prolozone therapy (from great pain to no pain in two months) if he would perform EDTA IV chelation for my CVD he told me "It doesn't work."

He could have made money giving me IV EDTA but his interest was my well-being, not money. I remain skeptical that EDTA is effective for CVD.

 

Things may have changed since I was last involved with this stuff, but it used to be that IV EDTA therapy was considered quackery (meaning: it threatened the drug industry), and there was considerable pressure against it by medical boards.

 

Dr Cathcart, who I mentioned above, told me he was only able to continue doing Vit C and EDTA because he had a significant independent income as a result of inventing the artificial hip joint. Without that, he said, the local medical authorities would have run him out of business. (They can pressure docs not just on the basis of threatening their license, but also by effectively killing new patient referrals, among other things).

 

After hearing that, I've never taken advice from docs seriously who say that some treatment or another "isn't effective" -- particularly when most of them have never tried it themselves. There's just way too much political back-pressure for them to be objective. This is very true today when it comes to alternative cancer therapies.

 

As @Daniel said, look at the studies, and make up your own mind.

 

After listening to Dr Levy's work on Calcium, I'm actually convinced that periodic EDTA to lower body calcium levels could end up being a very effective anti-aging therapy.

[Daniel Cooper]

After listening to Dr Levy's work on Calcium, I'm actually convinced that periodic EDTA to lower body calcium levels could end up being a very effective anti-aging therapy.

 

Late this year or early next year I intend to do an IV EDTA course and will do oral (maybe liposomal) EDTA pre and post.

 

 

Edited by Daniel Cooper, 05 February 2019 - 02:44 AM.

[mikey]

Late this year or early next year I intend to do and IV EDTA course and will do oral (maybe liposomal) EDTA pre and post.

[mikey]

The Dr that told me EDTA “doesn’t work” was located in LA Koreatown, which the CMA leaves alone as if it’s another country. So he did Prolozone, which the uptown MDs told me would them to lose their license. He always told me exactly what he knew, with no pressure to do otherwise. Therefore, I remain skeptical of EDTA since his credibility was perfect to me. We also talked “shop” since he regarded me as an equal. I also have known Stephen Levine, whose company NutriCology sells oral EDTA for, about 30 years. His credibility is also unimpeachable so this is a quandary to me. I will remain skeptical until perhaps I have the opportunity to speak with Stephen Levine, who is retired from public life. My Prolozone doctor has also retired, and although I have his personal cell phone I won’t bother him since he’s already made his opinion known to me. Perhaps after some have tried and can report their experience it will remain an unknown for me. Please have at it, guys and report your experience, hopefully with scans to support what you have to report. Kind regards.

[mikey]

Late this year or early next year I intend to do an IV EDTA course and will do oral (maybe liposomal) EDTA pre and post.

Here’s hoping you can document beneficial effects.

[QuestforLife]

The main problem I have with statins is that they are a mitochondrial toxin. Although the effect can be partially offset with CoQ10, it can't be completely offset. The other problem I have is that they aren't very effective at treating CVD. My view (based on considerable reading and research) is that the idea of high cholesterol causing CVD is largely a hoax perpetrated on the medical community by drug companies.

Regarding the study you mentioned, they were looking at low/subclinical doses. That's a different regime, so I can see how it might be of interest. However, on principled grounds, it would take a lot more than a few studies to convince me that they were safe and effective at low doses. Even then, there would have to be a clear disease state for me to take the risk, as opposed to preventative only (such as to lower cholesterol, which is what 99+% of statin prescriptions are written for).

You're quite right that chloresterol is not the cause of CVD. But ironically Statins don't work by reducing chloresterol! The fact they do reduce chloresterol (their original intended effect) is not what this helping against CVD, it is a pleitrophic effect - somehow blocking chloresterol synthesis (which also blocks Q10 production) is also inhibiting Rho-kinase, which creates endothelial progenitor cells.

Everyone loves to hate Statins, but they may be one of the best treatments we have against CVD and aging in general, especially if like I suggest, you take them at a low dose, intermittently.

Janic et al. have performed 2 or 3 pilot studies on people with sub clinical atherosclerosis and also with diabetics, and had very good results.

[Andey]

You're quite right that chloresterol is not the cause of CVD. But ironically Statins don't work by reducing chloresterol! The fact they do reduce chloresterol (their original intended effect) is not what this helping against CVD, it is a pleitrophic effect - somehow blocking chloresterol synthesis (which also blocks Q10 production) is also inhibiting Rho-kinase, which creates endothelial progenitor cells.

Everyone loves to hate Statins, but they may be one of the best treatments we have against CVD and aging in general, especially if like I suggest, you take them at a low dose, intermittently.

Janic et al. have performed 2 or 3 pilot studies on people with sub clinical atherosclerosis and also with diabetics, and had very good results.

 

  I believe the reduced incidence of the cardiac events in statin studies is proportional to the decrease of cholesterol, is not it? 

Also adding ezetimibe (to statins) which is not a statin but cholesterol reuptake inhibitor also additionally lowering cardiac events.

[QuestforLife]

I believe the reduced incidence of the cardiac events in statin studies is proportional to the decrease of cholesterol, is not it?

Nope, I don't believe it is. Atleast in the studies I quoted, no reduction in chloresterol was required for the improvement in arterial function.

In some cases chloresterol reduction might be desirable, but I think we'll look back at this time and wonder how we got so sidetracked by chloresterol. Glucose levels are far more important IMO, and in the future a clear line from metabolic to cardiovascular health will be established.

[Iporuru]

As far as statins are concerned there is a new meta-analysis:

 

Am Heart J. 2019 Jan 10;210:18-28. doi: 10.1016/j.ahj.2018.12.007. [Epub ahead of print]

 

Comparative effectiveness and safety of statins as a class and of specific statins for primary prevention of cardiovascular disease: A systematic review, meta-analysis, and network meta-analysis of randomized trials with 94,283 participants.

Yebyo HG¹, Aschmann HE², Kaufmann M², Puhan MA³.

Author information

 

Abstract

The current guidelines of statins for primary cardiovascular disease (CVD) prevention were based on results from systematic reviews and meta-analyses that suffer from limitations.

 

METHODS:

We searched in PubMed for existing systematic reviews and individual open-label or double-blinded randomized controlled trials that compared a statin with a placebo or another, which were published in English until January 01, 2018. We performed a random-effect pairwise meta-analysis of all statins as a class and network meta-analysis for the specific statins on different benefit and harm outcomes.

 

RESULTS:

In the pairwise meta-analyses, statins as a class showed statistically significant risk reductions on non-fatal MI (risk ratio [RR] 0.62, 95% CI 0.53-0.72), CVD mortality (RR 0.80, 0.71-0.91), all-cause mortality (RR 0.89, 0.85-0.93), non-fatal stroke (RR 0.83, 0.75-0.92), unstable angina (RR 0.75, 0.63-0.91), and composite major cardiovascular events (RR 0.74, 0.67-0.81). Statins increased statistically significantly relative and absolute risks of myopathy (RR 1.08, 1.01-1.15; Risk difference [RD] 13, 2-24 per 10,000 person-years); renal dysfunction (RR 1.12, 1.00-1.26; RD 16, 0-36 per 10,000 person-years); and hepatic dysfunction (RR 1.16, 1.02-1.31; RD 8, 1-16 per 10,000 person-years). The drug-level network meta-analyses showed that atorvastatin and rosuvastatin were most effective in reducing CVD events while atorvastatin appeared to have the best safety profile.

 

CONCLUSIONS:

All statins showed statistically significant risk reduction of CVD and all-cause mortality in primary prevention populations while increasing the risk for some harm risks. However, the benefit-harm profile differed by statin type. A quantitative assessment of the benefit-harm balance is thus needed since meta-analyses alone are insufficient to inform whether statins provide net benefit.

Edited by Iporuru, 05 February 2019 - 07:59 PM.

[mikey]

As far as statins are concerned there is a new meta-analysis:

Am Heart J. 2019 Jan 10;210:18-28. doi: 10.1016/j.ahj.2018.12.007. [Epub ahead of print]

Comparative effectiveness and safety of statins as a class and of specific statins for primary prevention of cardiovascular disease: A systematic review, meta-analysis, and network meta-analysis of randomized trials with 94,283 participants.
Yebyo HG¹, Aschmann HE², Kaufmann M², Puhan MA³.
Author information

Abstract
The current guidelines of statins for primary cardiovascular disease (CVD) prevention were based on results from systematic reviews and meta-analyses that suffer from limitations.

METHODS:
We searched in PubMed for existing systematic reviews and individual open-label or double-blinded randomized controlled trials that compared a statin with a placebo or another, which were published in English until January 01, 2018. We performed a random-effect pairwise meta-analysis of all statins as a class and network meta-analysis for the specific statins on different benefit and harm outcomes.

RESULTS:
In the pairwise meta-analyses, statins as a class showed statistically significant risk reductions on non-fatal MI (risk ratio [RR] 0.62, 95% CI 0.53-0.72), CVD mortality (RR 0.80, 0.71-0.91), all-cause mortality (RR 0.89, 0.85-0.93), non-fatal stroke (RR 0.83, 0.75-0.92), unstable angina (RR 0.75, 0.63-0.91), and composite major cardiovascular events (RR 0.74, 0.67-0.81). Statins increased statistically significantly relative and absolute risks of myopathy (RR 1.08, 1.01-1.15; Risk difference [RD] 13, 2-24 per 10,000 person-years); renal dysfunction (RR 1.12, 1.00-1.26; RD 16, 0-36 per 10,000 person-years); and hepatic dysfunction (RR 1.16, 1.02-1.31; RD 8, 1-16 per 10,000 person-years). The drug-level network meta-analyses showed that atorvastatin and rosuvastatin were most effective in reducing CVD events while atorvastatin appeared to have the best safety profile.

CONCLUSIONS:
All statins showed statistically significant risk reduction of CVD and all-cause mortality in primary prevention populations while increasing the risk for some harm risks. However, the benefit-harm profile differed by statin type. A quantitative assessment of the benefit-harm balance is thus needed since meta-analyses alone are insufficient to inform whether statins provide net benefit.

[mikey]

As Gomer Pyle might say, “Golly, gee. If I had a nickel for every time I heard an older woman say, “I started taking (some) statin and had all kinds of horrible aches in my muscles. I asked my doctor whether the drug caused the aches and he said “No. it’s just ‘cause you’re getting older.” When I stopped taking the statin the muscle aches went away,” So I might have enough nickles to buy a barrel full of goober peas and be friends with a lot of old ladies. It sure seems like the “studies” understate the amount of myopathy that I am told about or maybe it’s really because we are getting older so we are more likely to be victims of myopathic pain.

[labrat70]

I just finished reading Dr. Jeffery Dach's new book "Heart Book" and it would probably be of interest on this topic.  Bottom line is that the cholestoral theory is BS, and he has a protocol for slowing/reversing plaque buildup using some of our normal things: C, D3, K2, etc... the book is chock full of references too.

[QuestforLife]

A balanced review by Josh Mitteldorf:

 

https://joshmitteldo...nism-of-action/

[Kimer Med]

The Dr that told me EDTA “doesn’t work” was located in LA Koreatown, which the CMA leaves alone as if it’s another country. So he did Prolozone, which the uptown MDs told me would them to lose their license. He always told me exactly what he knew, with no pressure to do otherwise. Therefore, I remain skeptical of EDTA since his credibility was perfect to me. We also talked “shop” since he regarded me as an equal. I also have known Stephen Levine, whose company NutriCology sells oral EDTA for, about 30 years. His credibility is also unimpeachable so this is a quandary to me. I will remain skeptical until perhaps I have the opportunity to speak with Stephen Levine, who is retired from public life. My Prolozone doctor has also retired, and although I have his personal cell phone I won’t bother him since he’s already made his opinion known to me. Perhaps after some have tried and can report their experience it will remain an unknown for me. Please have at it, guys and report your experience, hopefully with scans to support what you have to report. Kind regards.

 

Good luck. I hope it works for you.

 

FWIW, Nutricology, which is the same company as Allergy Research Group, are two brands of supplements that I refuse to take. I had some very bad experiences with multiple products of theirs back in the 90s and 2000s (impurities, contamination, poor solubility, measurably ineffective, etc), so unfortunately my opinion of Stephen Levine isn't a very good one. Hopefully they've improved since then.

[masterlock]

Don't know if this has already mentioned (didn't have to to read ever reply), but Cyclodextrin can cause permanent hearing loss.

https://www.ncbi.nlm...les/PMC5676048/

[Daniel Cooper]

Don't know if this has already mentioned (didn't have to to read ever reply), but Cyclodextrin can cause permanent hearing loss.
https://www.ncbi.nlm...les/PMC5676048/

 
 
Yes, it's almost the entirety of the discussion in the other thread you posted this warning in:
 
Cyclodextrins and Atherosclerosis

[ryukenden]

Anyone has tried statins to reduce atherosclerosis?

[Daniel Cooper]

Statins at best make a barely measurable reduction in arterial plaques.  

 

Their advocates sell them on preventing the progression of atherosclerosis.

 

 

 

 

 

[ryukenden]

Statins at best make a barely measurable reduction in arterial plaques.

Their advocates sell them on preventing the progression of atherosclerosis.

I could recall reading Rosuvastatin help atherosclerosis to regress about 30%.

https://health.cleve...plaque-buildup/

[ryukenden]

Have any of you had MRI angiogram or CT angiogram before using any supplements to compare?

I am thinking of having MRI angiogram if I go back to Bangkok again to see whether the state of my arteries.

[smithx]

I don't know about angiograms, but did do a bunch of research (unfortunately no citations handy) about MRI and CT contrast agents.

 

The upshot is:

• For MRI contrast, macrocyclic gadolinium is the way to go. The heme-type cage around the gadolinium ion shepherds it safely out of the body with little or no damage.
  • Linear or other gadolinium contrast agents may cause kidney damage and may also cause build-up of gadolinium in the brain. Best to avoid.
• For CT scan, there is no safe contrast agent. All contrast agents in common use caused kidney damage in a very significant percentage of patients, when checked in a one-year follow-up.

I know that references are needed for this, but I don't have them handy and don't have time right now to look them up. If anyone else finds these, please reply with them. If you really really have to see citations and somehow can't search on your own, let me now and I may be able to find them again.

 

 

Have any of you had MRI angiogram or CT angiogram before using any supplements to compare?

I am thinking of having MRI angiogram if I go back to Bangkok again to see whether the state of my arteries.

 

[Turnbuckle]

The main problem I have with statins is that they are a mitochondrial toxin. Although the effect can be partially offset with CoQ10, it can't be completely offset. The other problem I have is that they aren't very effective at treating CVD. My view (based on considerable reading and research) is that the idea of high cholesterol causing CVD is largely a hoax perpetrated on the medical community by drug companies.

 

 

Statins are quackery, the modern equivalent of bloodletting. They can help a few people with very high cholesterol levels, but for most it is damaging, for some, the damage can be severe. I was in the latter category, going from the best shape in my life to feeling like I was ninety years only in just a matter of months, and CoQ10 didn't help. The recovery was excruciatingly slow until I realized it was mito damage and fixed it with a fission/fusion protocol. Mitochondria typically have several mtDNA loops that cover for each other, so damaged mtDNA may not be noticeable until they reach a critical level, and then it may take a very long time to resolve without intervention, if ever. So one should not even consider taking this poison for arterial plaque, especially as better solutions can be found, such as carnitine + taurine, which can inhibit and reverse calcification--

 

Vascular calcification in the tunica media of arteries and blood vessels is often observed in the elderly population, in patients with diabetes mellitus and/or chronic kidney disease. Vascular calcifications represent a major clinical problem being in the origin of cardiovascular disease and ultimately mortality.

https://www.ncbi.nlm...les/PMC4247655/

 

 

Calcification is likely driven by high cholesterol levels via inflammation--

 

 

This process is known as inflammatory osteolysis...It is optimistic to conclude, on the basis of this study’ correlation, that cholesterol lowering may prevent or reverse valvular calcification.

https://www.ahajourn...irc.104.16.1881

 

 

 

These calcifications derive from the misplaced expression of vascular smooth muscle cells (VSMCs) , which can be suppressed with carnitine + taurine--

 

L-carnitine and taurine synergistically inhibit the proliferation and osteoblastic differentiation of vascular smooth muscle cells...Vascular calcification, a prominent feature of atherosclerosis, has been considered an organized and regulated process, similar to mineralization in bone tissue. The osteoblastic differentiation of VSMCs is currently considered responsible for the formation of vascular calcification.

https://www.ncbi.nlm...les/PMC4002410/

 

 

Taurine alone can reverse the effect of high cholesterol in rabbits--

 

Effect of a Taurine Treatment on the Regression of Existing Atherosclerotic Lesions in Rabbits Fed on a High-cholesterol Diet

 

These results indicate that the taurine treatment may accelerate the regression of cholesterol-induced atherosclerotic lesions in rabbits without having any effect on the plasma and aorta lipid and lipid peroxide levels.

https://www.jstage.j...5_1035/_article

 

 

Oral EDTA may be helpful when used with taurine/carnitine. Studies show that IV EDTA + high dose oral vitamins (vitamin C in particular) has benefit --

 

EDTA Chelation Therapy Alone and in Combination with Oral High-Dose Multivitamins and Minerals for Coronary Disease: The Factorial Group Results of the Trial to Assess Chelation Therapy

 

In stable post- MI patients on evidence-based medical therapy, the combination of oral high-dose vitamins and chelation therapy compared with double placebo reduced clinically important cardiovascular events to an extent that was both statistically significant and of potential clinical relevance.

 

There are other potential explanations for the observed treatment effect. The chelation solution contains a high dose of vitamin C, an antioxidant vitamin that may help reverse some forms of endothelial dysfunction

https://www.ncbi.nlm...les/PMC4069605/

 

 

 

Bottom line, a therapy might consist of: Taurine, Carnitine, oral EDTA, and vitamin C.

[Ovidus]

 

Bottom line, a therapy might consist of: Taurine, Carnitine, oral EDTA, and vitamin C.

 

I know a precise answer is impossible, but any ballpark figure as to how long such a theraphy would last?

 

Would it be some months, some years.... or a lifelong ongoing commitment?

[aribadabar]

I know a precise answer is impossible, but any ballpark figure as to how long such a theraphy would last?

 

Would it be some months, some years.... or a lifelong ongoing commitment?

 

Chelation is a slow process so I'd say ~6-month initial cycle at the very least to remove deposition (best to re-test via CAC score, CIMT etc to ascertain effectiveness after that) and then 1-2-month repeat treatments every half-year throughout life to maintain house in order.

[pamojja]

Want to Reverse Your Calcification and Heart Disease? Here's How! Podcast Ep21