591 replies to this topic

[RWhigham]

 

They just found that HDL in those with a certain SNP actually damage arteries instead or repairing them:

 

https://www.nih.gov/...t-heart-disease

Great find!

 

https://www.nih.gov/...t-heart-disease

“The work demonstrates that the protective effects of HDL are more dependent upon how it functions than merely how much of it is present,” Rader says. “We still have a lot to learn about the relationship between HDL function and heart disease risk.”

[JustGetMeIntoSpace]

 

 

They just found that HDL in those with a certain SNP actually damage arteries instead or repairing them:

 

https://www.nih.gov/...t-heart-disease

Great find!

 

https://www.nih.gov/...t-heart-disease

“The work demonstrates that the protective effects of HDL are more dependent upon how it functions than merely how much of it is present,” Rader says. “We still have a lot to learn about the relationship between HDL function and heart disease risk.”

 

 

Who can keep up with all the research pouring out now, eh?  

 

Yeah, I'm interested, because I had a 0 Calcium Score a couple of years ago in my mid 50's.  So I was pretty happy - ecstatic would be a better word - but my LDL-P was a little high a few months ago.  This may correspond to the fact that my HDL was low.  Triglycerides were also low, so I'm not sure how concerned to be about it.  Imo, LDL-P is the biggest gun in all of this.

 

I consume lower fat diets, so they will pull down both LDL-C and HDL.  I have also gamed the system to pull down triglycerides.  But my HDL was too low to feel really good (30).

[Mike C]

They just found that HDL in those with a certain SNP actually damage arteries instead or repairing them:

https://www.nih.gov/...t-heart-disease

Great find!

https://www.nih.gov/...t-heart-disease
“The work demonstrates that the protective effects of HDL are more dependent upon how it functions than merely how much of it is present,” Rader says. “We still have a lot to learn about the relationship between HDL function and heart disease risk.”

Who can keep up with all the research pouring out now, eh?

Yeah, I'm interested, because I had a 0 Calcium Score a couple of years ago in my mid 50's. So I was pretty happy - ecstatic would be a better word - but my LDL-P was a little high a few months ago. This may correspond to the fact that my HDL was low. Triglycerides were also low, so I'm not sure how concerned to be about it. Imo, LDL-P is the biggest gun in all of this.

I consume lower fat diets, so they will pull down both LDL-C and HDL. I have also gamed the system to pull down triglycerides. But my HDL was too low to feel really good (30).

http://www.health.ha...e-2016110210626

The above article indicates the failure of hdl raising drugs is problematic and suggests the higher hdl levels are merely associated with better health practices and not an intrinsic factor

[RWhigham]

 

Darryl post #109

I just came across a reminder of an interesting application of methyl-β-cyclodextrin, pertinent to atherosclerosis, that might function via an oral route.

 

Mani, V et al, 2013. Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia. Nutrition & metabolism, 10(1), p.1.

This shows  methyl-β-cyclodextrin  could stop the transport of LPS into the blood via chylomicrons.

 

We should not want to do this. Chylomicrons are actually protective. They have LPS-binding protein which collects, inactivates, and enhances hepatic clearance of bacterial toxins.

 

     https://books.google.com/books?id=uQB0AwAAQBAJ&pg=PA522&lpg=PA522&dq=how+does+lps+get+into+chylomicrons&source=bl&ots=0m0Vw32vyz&sig=jvG88lkPIfST3yOij20YYUCsOMg&hl=en&sa=X&ved=0ahUKEwie1NepwMXQAhWljVQKHdaWATwQ6AEIRjAG#v=onepage&q=how%20does%20lps%20get%20into%20chylomicrons&f=false  "Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease Mechanisms"

"Most intestinally absorbed LPS is found attached to or within chylomicron remnants in the blood... 

 "..chylomicrons reduce LPS toxicity and enhance its hepatic clearance"

 

https://www.ncbi.nlm...pubmed/12538700 "Lipopolysaccharide (LPS)-binding protein mediates LPS detoxification by chylomicrons"

"Besides a role in the detoxification of bacterial toxin present in the circulation, we believe that LBP-chylomicron complexes may be part of a local defense mechanism of the intestine against translocated bacterial toxin."  (gram positive as well as gram negative).

Edited by RWhigham, 26 November 2016 - 05:17 AM.

[PWAIN]

I've brought 100g of Bete Cyclodrextrin and intend to take 1 gram a day. I have confirmed narrowed small arteries causing angina. I will report back whether there is any improvement or not.

[Daniel Cooper]

I've brought 100g of Bete Cyclodrextrin and intend to take 1 gram a day. I have confirmed narrowed small arteries causing angina. I will report back whether there is any improvement or not.

 

 

Unfortunately I do not believe that cyclodextrin makes it through the gut.  I wanted to do the same thing you're contemplating and found a study showing nil blood levels after ingestion.

 

Check me on that but I looked into cyclodextrin pretty hard at one point because it looked so promising.

 

I think the only means that will be useful is IV or subcutaneous.  

 

Also, be aware, cyclodextrin is ototoxic - it kills cochlear hair cells - however we know it doesn't cross the BBB, and likely doesn't cross the blood cochlear barrier but that is speculation.  They do see ototoxic effects when using it to treat Niemann Pick Disease, however in that application they are injecting it intrathecally - directly into the spinal fluid, effectively bypassing these barriers.  If you wanted to do IV or IM injection, I'd research that very heavily.  Ideally, I'd talk to a doc that is treating Niemann Pick patients as they certainly have the most experience with this substance.

 

I have a mouse study showing that quercetin + dastinib taken once a week for two months may improve cardiovascular function.  I'll try to post it this evening if possible.

 

 

ETA: Indeed the discussion of these issues are on the previous page.  

Edited by Daniel Cooper, 12 June 2017 - 02:52 PM.

[Daniel Cooper]

 

 

Darryl post #109

I just came across a reminder of an interesting application of methyl-β-cyclodextrin, pertinent to atherosclerosis, that might function via an oral route.

 

Mani, V et al, 2013. Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia. Nutrition & metabolism, 10(1), p.1.

This shows  methyl-β-cyclodextrin  could stop the transport of LPS into the blood via chylomicrons.

 

We should not want to do this. Chylomicrons are actually protective. They have LPS-binding protein which collects, inactivates, and enhances hepatic clearance of bacterial toxins.

 

     https://books.google.com/books?id=uQB0AwAAQBAJ&pg=PA522&lpg=PA522&dq=how+does+lps+get+into+chylomicrons&source=bl&ots=0m0Vw32vyz&sig=jvG88lkPIfST3yOij20YYUCsOMg&hl=en&sa=X&ved=0ahUKEwie1NepwMXQAhWljVQKHdaWATwQ6AEIRjAG#v=onepage&q=how%20does%20lps%20get%20into%20chylomicrons&f=false  "Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease Mechanisms"

"Most intestinally absorbed LPS is found attached to or within chylomicron remnants in the blood... 

 "..chylomicrons reduce LPS toxicity and enhance its hepatic clearance"

 

https://www.ncbi.nlm...pubmed/12538700 "Lipopolysaccharide (LPS)-binding protein mediates LPS detoxification by chylomicrons"

"Besides a role in the detoxification of bacterial toxin present in the circulation, we believe that LBP-chylomicron complexes may be part of a local defense mechanism of the intestine against translocated bacterial toxin."  (gram positive as well as gram negative).

 

 

 

What cyclodextin is supposed to do is convert foam cells which are pathological macrophages back into normal macrophages where they can be cleared.  This is pretty much the holy grail for what you need to do to begin to reverse atherosclerosis.

 

Edited by Daniel Cooper, 12 June 2017 - 02:47 PM.

[Daniel Cooper]

Here is the quercetin + dastinib study I mentioned above.

 

 

Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice

 

http://onlinelibrary...acel.12458/full

 

 

If only we were mice we'd have 10 known good ways to reverse atherosclerosis.

 

 

 

[Daniel Cooper]

Hey guys, it seems that there is a new paper on cyclodextrin that has published since the paper on the prior page.  Can anyone get the full text?

 

https://www.ncbi.nlm...pubmed/27241174

 

Preclinical Reversal of Atherosclerosis by FDA-Approved Compound that Transforms Cholesterol into an Anti-Inflammatory "Prodrug".

Mendelsohn AR1,2, Larrick JW1,2.

Author information

 

Abstract

Although atherosclerosis is treatable with lipid-lowering drugs, not all patients respond. Hydroxypropyl-beta-cyclodextrin (CD) is an FDA-approved compound for solubilizing, capturing, and delivering lipophilic drugs in humans. Zimmer et al. report that CD mediates regression of atherosclerotic plaques in two mouse models by solubilizing cholesterol crystals (CCs), and promoting metabolism of CCs into water-soluble 27-hydroxycholesterol, which, in turn, activates anti-inflammatory LXR receptor target genes, promotes active and passive efflux of cholesterol from macrophages, and increases metabolic processing of cholesterol. In effect, CD inverts the role of its cargo, cholesterol, from inflammatory to anti-inflammatory by converting cholesterol into a "prodrug" that when modified to 27-hydroxycholesterol reduces atherosclerosis. This mechanism defines a new class of pharmaceuticals, "inverters": compounds that cause innate biomolecules to act opposite to their normal function. However, chronic CD treatment in animal models damages auditory cells, which must be addressed before CD can be developed as a systemic drug for atherosclerosis.

 

 

Edited by Daniel Cooper, 12 June 2017 - 03:36 PM.

[PWAIN]

 

I've brought 100g of Bete Cyclodrextrin and intend to take 1 gram a day. I have confirmed narrowed small arteries causing angina. I will report back whether there is any improvement or not.

 

 

Unfortunately I do not believe that cyclodextrin makes it through the gut.  I wanted to do the same thing you're contemplating and found a study showing nil blood levels after ingestion.

 

Check me on that but I looked into cyclodextrin pretty hard at one point because it looked so promising.

 

I think the only means that will be useful is IV or subcutaneous.  

 

Also, be aware, cyclodextrin is ototoxic - it kills cochlear hair cells - however we know it doesn't cross the BBB, and likely doesn't cross the blood cochlear barrier but that is speculation.  They do see ototoxic effects when using it to treat Niemann Pick Disease, however in that application they are injecting it intrathecally - directly into the spinal fluid, effectively bypassing these barriers.  If you wanted to do IV or IM injection, I'd research that very heavily.  Ideally, I'd talk to a doc that is treating Niemann Pick patients as they certainly have the most experience with this substance.

 

I have a mouse study showing that quercetin + dastinib taken once a week for two months may improve cardiovascular function.  I'll try to post it this evening if possible.

 

 

ETA: Indeed the discussion of these issues are on the previous page.  

 

Hi Daniel,

 

I did a lot of searching prior to going ahead. I found an extensive paper discussing the amount of absorption. It listed the variations (alpha, beta etc) of Cyclodrexin and their human absorption (it was quite an extensive document). The numbers varied quite a bit with the various types but from memory I think Beta came in at around 6% (it wasn't the highest absorption but beta is the study I read and so I'm going to go ahead with that). Not a great amount but at 1 gram per day, I get around 60mg into me.

 

As for the hearing damage, the hairs in the ear were damages at 8grams per kg and not damaged at 4 grams per kilogram. Those numbers were from mice or rats, can't remember but either way, a human at 70 - 100kg is not going to have problems ingesting 1 gram (thats like 10 mg per kg and only 6% of that is absorbed). The poison is in the dose and I think there is a very safe margin here. On the reverse side of the coin, cholesterol can easily kill me.

 

I wish I could find the paper on the absorption rates but I read through it a couple of times and then closed the tab. I went through my browser history but I have 3 browsers that I actively use and have opened literally hundreds of pages in the last few days.

 

My thoughts on Cyclodrexin is that it is going to be big in the future, it actually removes plaque and has been clinically proven to do so. I don't think there is much else out there that has been shown to do this. I suspect that it not well known because it cannot be patented and that it will take more of a grass roots approach to get this proven and popular. This stuff has been used for about 100 years so is not new, just a new application. It is ironically normally used to help absorption of other chemicals that are not easily absorbed.

 

I've heard of lots of so called plaque removers over time but this is the first that feels like it might be legit. Only way for me to find out is to try it. I think others might like to know about it so I am making my plan to try this known. I don't expect miracle results overnight but over time maybe I'll have something to report.

[Daniel Cooper]

I agree with you on cyclodextrin potentially being a big deal wrt reversing atherosclerosis.  I was very big on this compound last year.

 

I was depressed to find that it wasn't orally available very much, but perhaps you've found that the picture is not so bleak as I might have thought.

 

I agree that I would not be too concerned about taking this stuff orally causing ototoxic effects.  It is classified as "generally recognized as safe" by the US FDA, it is used as a food additive, and the alpha form is used in Europe to add dietary fiber to foods.  Additionally, there seems to be a lot of people using this as a weight loss supplement I believe on the theory that it binds to fats and makes them indigestible.  So that doesn't concern me too much unless you're eating buckets of the stuff.

 

What would be interesting have know is some idea of the plasma levels they were achieving in mice to get the effect noted in the original study.  Presumably you are going to achieve lower levels via the oral route, but perhaps chronic administration will achieve the desired effect.

 

One thing I might suggest .... if you have the funds, I would get a CAC score and/or a carotid ultrasound (ideally both) before starting.  That way you'll have some metric to measure to see if you are doing any good.

 

Keep us posted.

Edited by Daniel Cooper, 12 June 2017 - 07:10 PM.

[APBT]

 

Hey guys, it seems that there is a new paper on cyclodextrin that has published since the paper on the prior page.  Can anyone get the full text?

 

https://www.ncbi.nlm...pubmed/27241174

 

Preclinical Reversal of Atherosclerosis by FDA-Approved Compound that Transforms Cholesterol into an Anti-Inflammatory "Prodrug".

Mendelsohn AR1,2, Larrick JW1,2.

Author information

 

Abstract

Although atherosclerosis is treatable with lipid-lowering drugs, not all patients respond. Hydroxypropyl-beta-cyclodextrin (CD) is an FDA-approved compound for solubilizing, capturing, and delivering lipophilic drugs in humans. Zimmer et al. report that CD mediates regression of atherosclerotic plaques in two mouse models by solubilizing cholesterol crystals (CCs), and promoting metabolism of CCs into water-soluble 27-hydroxycholesterol, which, in turn, activates anti-inflammatory LXR receptor target genes, promotes active and passive efflux of cholesterol from macrophages, and increases metabolic processing of cholesterol. In effect, CD inverts the role of its cargo, cholesterol, from inflammatory to anti-inflammatory by converting cholesterol into a "prodrug" that when modified to 27-hydroxycholesterol reduces atherosclerosis. This mechanism defines a new class of pharmaceuticals, "inverters": compounds that cause innate biomolecules to act opposite to their normal function. However, chronic CD treatment in animal models damages auditory cells, which must be addressed before CD can be developed as a systemic drug for atherosclerosis.

 

 

 

FULL TEXT:

Attached Files

•  Preclinical Reversal of Atherosclerosis by FDA-Approved Compound that Transforms Cholesterol into an Anti-Inflammatory ‘‘Prodrug’’.pdf   75.08KB   17 downloads

[PWAIN]

I thought this paragraph in that study was interesting:

 

A key issue may be unwanted side effects. Even though CD (a) is considered safe, (b) has a very high LD50, © is commonly used in drug formulations, and (d) is in clinical trials for NPC1 (NCT02534844), the compound is not without problems. Chronic treatment of NPC1 cats with CD significantly extends lifespan, inhibits neurological symptoms, and blocks cerebellar dysfunction and Purkinje cell death. However, these benefits are accompanied by hearing loss14 by removing cholesterol from prestin in sensory cells.15 This problem may have solutions. Should CD be developed for treating atherosclerosis in humans, perhaps treatment could be intermittent to limit or prevent irreversible damage to hearing. In that scenario, after regression of plaques, lipid-lowering therapies could be employed to maintain healthy arteries. Alternatively, perhaps it might be possible to use cholesterol-containing ear drops to supplement the sensory hairs sufficiently to afford protection.

 

Would significant lifespan extension be the result of reduced risk of CVD or could there be more to it? I would have thought a msmall or moderate increase due to reduction in CVD.

 

Also thinking that their suggestion of a series of treatments which hopefully results in significant reduction or elimination fo plaque and then just statin therapy or something similar to maintain the arteries.

 

I did look again for the article about absorption but still cannot find it. If anyone else can find it, please link it. There was a lot of tables and they discussed the various routes such as oral, ocular and rectal among others. It was quite a few pages and it might have been from the NIH but not sure, I seem to remember it was from somewhere quite reputable.

[Daniel Cooper]

The thing about cyclodextrin is that it's such a large molecule that (~1400 Daltons) I'm surprised it crosses any of these immuno privileged barriers (blood brain, blood cochlear, etc).  We know it doesn't effectively cross the BBB because in Niemann Pick Disease they have to inject it into the spinal fluid to get any effect.  I wish I knew more about the blood cochlear barrier.  Is it more permeable than the BBB?  Is the BCB different in cats and mice than humans? What is the level of risk?  

 

I wonder if one of our members with the academic background would be interested in opening a dialog with Dr. Mendelsohn from the paper above.  His email is published on his institute's website.

 

 

[Daniel Cooper]

I thought this paragraph in that study was interesting:

 

A key issue may be unwanted side effects. Even though CD (a) is considered safe, (b) has a very high LD50, © is commonly used in drug formulations, and (d) is in clinical trials for NPC1 (NCT02534844), the compound is not without problems. Chronic treatment of NPC1 cats with CD significantly extends lifespan, inhibits neurological symptoms, and blocks cerebellar dysfunction and Purkinje cell death. However, these benefits are accompanied by hearing loss14 by removing cholesterol from prestin in sensory cells.15 This problem may have solutions. Should CD be developed for treating atherosclerosis in humans, perhaps treatment could be intermittent to limit or prevent irreversible damage to hearing. In that scenario, after regression of plaques, lipid-lowering therapies could be employed to maintain healthy arteries. Alternatively, perhaps it might be possible to use cholesterol-containing ear drops to supplement the sensory hairs sufficiently to afford protection.

 

Would significant lifespan extension be the result of reduced risk of CVD or could there be more to it? I would have thought a msmall or moderate increase due to reduction in CVD.

 

Also thinking that their suggestion of a series of treatments which hopefully results in significant reduction or elimination fo plaque and then just statin therapy or something similar to maintain the arteries.

 

I did look again for the article about absorption but still cannot find it. If anyone else can find it, please link it. There was a lot of tables and they discussed the various routes such as oral, ocular and rectal among others. It was quite a few pages and it might have been from the NIH but not sure, I seem to remember it was from somewhere quite reputable.

 

 

It just hit me what else is interesting in that quote.  This:

 

 

Chronic treatment of NPC1 cats with CD significantly extends lifespan, inhibits neurological symptoms, and blocks cerebellar dysfunction and Purkinje cell death. However, these benefits are accompanied by hearing loss by removing cholesterol from prestin in sensory cells.

 

 

I think I have seen this study and if it's the one I'm thinking of, they were looking at CD as a treatment for Niemann Pick Disease, which is why they were using NPC1 cats.  If that is the case, I assume that they were most likely dosing these cats intrathecally.  Either that or they were giving such massive doses IV that the vanishingly small percentage that crosses the BBB was significant enough to be useful as a NPD treatment.  In either case, I don't think it is unexpected that they caused hearing loss since surely either route would cross the BCB.

 

The really interesting question would be is if you give a dose IV or subQ sufficient to reverse arterial plaques, are you in danger of ototoxicity in that situation?

[Rocket]

What about garlic and real niacin? Its what I take.

[zorba990]

An interesting case study, considering....

https://www.ncbi.nlm...pubmed/22392429

Irreversible atorvastatin-associated hearing loss.
Liu M1, Alafris A, Longo AJ, Cohen H.
Author information
Abstract
Drug-associated ototoxicity is a potentially irreversible adverse event. Among the several 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) available in the United States, only atorvastatin is associated with tinnitus, but none are associated with any forms of hearing loss. A search of the published literature (1950-August 2011) revealed no published case reports of ototoxicity associated with statins. To our knowledge, we describe the first case of progressive, irreversible hearing loss in a 32-year-old man 18 months after starting atorvastatin therapy. He began taking atorvastatin 20 mg every evening for treatment of hypercholesterolemia. Six months later, he complained of occasional episodes of tinnitus, which resolved spontaneously. An audiogram was obtained and was normal. By 18 months, the tinnitus became continuous. Another audiogram revealed bilateral "cookie-bite" middle-frequency hearing loss. Atorvastatin was immediately discontinued, and the patient was fitted with hearing aids. Four years after drug discontinuation, his hearing loss had neither progressed nor regressed. Use of the Naranjo adverse drug reaction probability scale indicated a possible (score of 2) temporal and causal relationship between the patient's hearing loss and atorvastatin. Causes of "cookie-bite" hearing loss include chronic exposure to loud noises, presbycusis, genetic predisposition, and drugs. The manufacturer of atorvastatin has received three unpublished cases of deafness, but claims that causal relationships were not established. Despite these claims by the manufacturer, based on this case report, we recommend that clinicians and patients be aware of the risk of atorvastatin-associated tinnitus and permanent hearing loss. Further research is needed to better understand the mechanism and frequency of this adverse event.
© 2012 Pharmacotherapy Publications, Inc.
PMID: 22392429 DOI: 10.1002/PHAR.1040
[Indexed for MEDLINE]

[Daniel Cooper]

I've brought 100g of Bete Cyclodrextrin and intend to take 1 gram a day. I have confirmed narrowed small arteries causing angina. I will report back whether there is any improvement or not.

 

PWAIN -

 

Any updates on your cyclodextrin experiment? 

 

 

 

[Richard McGee]

This is obviously a very important subject. I would venture to say elevated levels of atherosclerotic plaque are near universal in modern populations. Without a doubt, it is a top contributor to shortened life expectancy. I narrowly dodged a bullet with an MI a number of years back.

 

Alas, there is very little consensus on what approaches work the best - or, indeed, work at all.

 

Is it possible to control the creation of new plaque, or to reverse existing plaque deposits? I don't have good answers to these questions. Judging from the responses to this thread, answers appear to cluster around several approaches - each with its own advocates and skeptics.

 

*Diet, exercise, and lifestyle

*Drug intervention

*Chelation therapy (EDTA)

*Pauling-inspired vitamin C megadosing (with aminos)

*Vitamin K2

*Numerous other supplements are occasionally mentioned.

  

One problem is the difficulty of assessing degree of calcification, accurately and inexpensively. Without this information, the individual is severely handicapped tracking the progress (or lack thereof) of his individual regimen.

 

The The Long Saga of Apo-A1 Milano is an instructive cautionary tale for those hoping for a magic bullet substance to treat this disease. The safest bet, as far as I can tell, is adherence to a plant-based diet (as close to vegan as you can stand) with B12 supplementation. I've seriously considered a Koncentrated K regimen, but haven't got up the nerve yet.

[pamojja]

One problem is the difficulty of assessing degree of calcification, accurately and inexpensively. Without this information, the individual is severely handicapped tracking the progress (or lack thereof) of his individual regimen.

 

With very severe symptoms, diagnosis with various means (MRI, ultra sound) and a 60% government certified walking disability revoked again, it looks rather straight forward to me.

 

Though in my case the individual regimen was more universal, and included too many synergies to be able to pin it down to one of these:

 

 

*Diet, exercise, and lifestyle

*Pauling-inspired vitamin C megadosing (with aminos)

*Vitamin K2

*Numerous other supplements are occasionally mentioned.

Whole story here: http://www.longecity...nal-remissions/

[Richard McGee]

With very severe symptoms, diagnosis with various means (MRI, ultra sound) and a 60% government certified walking disability revoked again, it looks rather straight forward to me.

 

 

I wasn't being clear enough. My concern is not necessarily the initial diagnosis (although that's important), but the ongoing tracking of progress in reversing atherosclerotic plaque. This is, in effect, the feedback needed to evaluate the validity of whatever protocol you are following.

 

 

[Daniel Cooper]

 

With very severe symptoms, diagnosis with various means (MRI, ultra sound) and a 60% government certified walking disability revoked again, it looks rather straight forward to me.

 

 

I wasn't being clear enough. My concern is not necessarily the initial diagnosis (although that's important), but the ongoing tracking of progress in reversing atherosclerotic plaque. This is, in effect, the feedback needed to evaluate the validity of whatever protocol you are following.

 

 

The only way I know to effectively track your status is with CAC scores.

 

Coincidentally, there was a paper just released showing that sub-millisievert CAC scans give pretty much equivalent results to the standard 3 millisievert scans most are doing today.  I don't have it handy at the moment.

 

I would not feel bad about repeating a sub millisievert CAC scan every couple of years at all.  A couple of 3 millisievert scans a few years apart would not keep me up at night either.

[Richard McGee]

Daniel, if I ask my cardiologist for a sub millisievert CAC scan, is he likely to know what that is? Is this the same thing as low-radiation dose calcium scoring?

[Daniel Cooper]

Daniel, if I ask my cardiologist for a sub millisievert CAC scan, is he likely to know what that is? Is this the same thing as low-radiation dose calcium scoring?

 

Maybe?  Not sure.

 

I'd just ask what the radiation dose their CAC test generates.  You commonly hear values from 1.5 to 3 millisieverts for a test.  For a point of reference, the "normal" background radiation people receive in the US is about 3 millisieverts per year. But, that can vary by a factor of 2 depending on where you live (higher altitudes, natural radioactivity in the rocks/soil in area).  Some airline crews get an additional 5 - 7 millisieverts a year due to the time they spend at at altitude on some high long routes.

 

So, 3 millisieverts isn't that much.  I wouldn't want to get that every year, but two or three spaced a few years apart .... I wouldn't feel bad about.  And if your facility does one of the lower dose scans ... even better.

[PeaceAndProsperity]

It's really a waste of time getting a calcium score prior to taking vitamin K2. It's proven that K2 can reverse calcification of soft tissue, so go ahead and take it. What the hell do you have to lose besides a few pennies a month, it's a vitamin! After a couple of months you could get a calcium score done to see if you are taking enough (because some get side-effects at low dosages).

 

As for my 71 year old relative, his blood pressure is down from 170-190 systolic to approx. 130 (can go a little bit lower at around 120 but it swings around 120-135, average is around 130) from taking simple supplements that lower lipoprotein(a), as I have already explained exhaustively. Some other user did not respond to the same supplement mix but who cares when a majority who take this combo do get better.

 

There is no excuse not to take the linus pauling combo with nicotinic acid, carnitine and a few other things. I'd go ahead and say that high dose niacin (nicotinic acid) and carnitine, 3-4g of each, is much more superior to any other combo, but I'm going off from mere assumption based upon what I've noticed.

 

I'm hoping that the vitamin k2 my 71 relative started not long ago will be the final nail in the coffin for his arterial plaque.

[Daniel Cooper]

It's really a waste of time getting a calcium score prior to taking vitamin K2. It's proven that K2 can reverse calcification of soft tissue, so go ahead and take it. What the hell do you have to lose besides a few pennies a month, it's a vitamin! After a couple of months you could get a calcium score done to see if you are taking enough (because some get side-effects at low dosages).

 

As for my 71 year old relative, his blood pressure is down from 170-190 systolic to approx. 130 (can go a little bit lower at around 120 but it swings around 120-135, average is around 130) from taking simple supplements that lower lipoprotein(a), as I have already explained exhaustively. Some other user did not respond to the same supplement mix but who cares when a majority who take this combo do get better.

 

There is no excuse not to take the linus pauling combo with nicotinic acid, carnitine and a few other things. I'd go ahead and say that high dose niacin (nicotinic acid) and carnitine, 3-4g of each, is much more superior to any other combo, but I'm going off from mere assumption based upon what I've noticed.

 

I'm hoping that the vitamin k2 my 71 relative started not long ago will be the final nail in the coffin for his arterial plaque.

 

 

How the hell will you know if the K2 is helping if you don't have before and after score?

[Richard McGee]

 

It's really a waste of time getting a calcium score prior to taking vitamin K2. It's proven that K2 can reverse calcification of soft tissue, so go ahead and take it. What the hell do you have to lose besides a few pennies a month, it's a vitamin! After a couple of months you could get a calcium score done to see if you are taking enough (because some get side-effects at low dosages).

 

As for my 71 year old relative, his blood pressure is down from 170-190 systolic to approx. 130 (can go a little bit lower at around 120 but it swings around 120-135, average is around 130) from taking simple supplements that lower lipoprotein(a), as I have already explained exhaustively. Some other user did not respond to the same supplement mix but who cares when a majority who take this combo do get better.

 

There is no excuse not to take the linus pauling combo with nicotinic acid, carnitine and a few other things. I'd go ahead and say that high dose niacin (nicotinic acid) and carnitine, 3-4g of each, is much more superior to any other combo, but I'm going off from mere assumption based upon what I've noticed.

 

I'm hoping that the vitamin k2 my 71 relative started not long ago will be the final nail in the coffin for his arterial plaque.

 

 

How the hell will you know if the K2 is helping if you don't have before and after score?

 

Having gone through a MI, I know from hard-earned experience that subjective impressions can be misleading, if not worthless. The day before my heart attack I was feeling energetic and (subjectively) very healthy. Literally no clue what was about to hit me.

 

So what I worry about is not wasting a few pennies a day. I'm quite willing to make the investment. What I'm really worried about is wasting time, which is my most precious commodity. I can ill afford to waste time on interventions that do not work for me. And I need to be able to objectively verify that they work for me.

 

Insofar as that is possible, of course. Metrics may not always be available, but they should be used when they are.

[pamojja]

 

With very severe symptoms, diagnosis with various means (MRI, ultra sound) and a 60% government certified walking disability revoked again, it looks rather straight forward to me.

 

I wasn't being clear enough. My concern is not necessarily the initial diagnosis (although that's important), but the ongoing tracking of progress in reversing atherosclerotic plaque. This is, in effect, the feedback needed to evaluate the validity of whatever protocol you are following.

 

Yea, with PAD it's that much easier to monitor compared to MI. By just measuring my intermittent claudication: 3-400 meter at the beginning, increasing gradually up to 2 hours along with therapeutic interventions, and evaporating after the 5th year completely.

[mikey]

 

It's really a waste of time getting a calcium score prior to taking vitamin K2. It's proven that K2 can reverse calcification of soft tissue, so go ahead and take it. What the hell do you have to lose besides a few pennies a month, it's a vitamin! After a couple of months you could get a calcium score done to see if you are taking enough (because some get side-effects at low dosages).

 

As for my 71 year old relative, his blood pressure is down from 170-190 systolic to approx. 130 (can go a little bit lower at around 120 but it swings around 120-135, average is around 130) from taking simple supplements that lower lipoprotein(a), as I have already explained exhaustively. Some other user did not respond to the same supplement mix but who cares when a majority who take this combo do get better.

 

There is no excuse not to take the linus pauling combo with nicotinic acid, carnitine and a few other things. I'd go ahead and say that high dose niacin (nicotinic acid) and carnitine, 3-4g of each, is much more superior to any other combo, but I'm going off from mere assumption based upon what I've noticed.

 

I'm hoping that the vitamin k2 my 71 relative started not long ago will be the final nail in the coffin for his arterial plaque.

 

 

How the hell will you know if the K2 is helping if you don't have before and after score?

 

 

After three years of taking 500+ mcg of vitamin K2 (MK-7) my carotid and coronary plaque scores had slightly increased. If the K2 did ANYTHING it might have slowed the progression, but it did not reverse the plaque scores, even at that daily high dose, combined with its required nutrient partners vitamin A and vitamin D.

 

I have studied K2 extensively and conversed with the Maastrickt University team that has been studying K2 for a dozen years and was quite surprised to find that the "after" scans did not show any progress in reversing plaque.

 

The only thing that produced a clear effect, that of lowing of blood pressure significantly, was taking Dasatinib with quercitin, to remove senescent cells. Two exposures to DQ and within a couple of weeks my blood pressure dropped from what could be a high of about 140-150/80-100 to 100-120/60-75, like a 20-year old's.

 

Even during times when I would normally expect my BP to be high, such as after a stressful day, I would measure my BP and find that it was maybe 115/65. This happened consistently for a couple of months.  

 

This was QUITE noticeable, as my BP had been gradually rising over some years.

 

This lasted for about 60 days and then there has been a gradual increase again, but it still hasn't reached the highs that were frequently what I encountered before I used DQ.

 

DQ apparently got rid of sensescent cells in the endothelial lining of my arteries and so the endothelium was able to regenerate with new "young" cells. Thus, arterial flexibility improved tremendously, which showed itself as much lower BP.

 

I haven't used DQ again, because it did cause some facial fat loss, such that I have a line on my face that was not there before and I do not want more loss of facial fat tissue. 

 

I also did not re-do coronary and carotid scans yet.

 

As far as therapies to regenerate everything via clearing senescent cells we will see the emergence of side-effect free therapies, that don't have the potential adverse effects that DQ does.

 

As to single molecules that have some role in arterial health, I have done and am doing many of them from niacin to acetyl L-carnitine to K2 (MK-7). Several of them do have some beneficial effects. But none of them do enough.

 

I figure that if I wait until FOXO4-DRI becomes more available/less costly, I will use that to clear senescent cells globally, without the side-effects of DQ. 

 

That is when we will have the opportunity to regenerate a fresh new arterial system.

 

Edited by mikey, 26 July 2017 - 05:39 PM.

[pamojja]

How the hell will you know if the K2 is helping if you don't have before and after score?

 
After three years of taking 500+ mcg of vitamin K2 (MK-7) my carotid and coronary plaque scores had slightly increased. If the K2 did ANYTHING it might have slowed the progression, but it did not reverse the plaque scores, even at that daily high dose, combined with its required nutrient partners vitamin A and vitamin D.
 
I have studied K2 extensively and conversed with the Maastrickt University team that has been studying K2 for a dozen years and was quite surprised to find that the "after" scans did not show any progress in reversing plaque.

 
Dr. William Davis experience with CAC scoring was, that usually - even while on statins - plaque grows in average by 30% a year nevertheless. Which becomes an exponential growth over the years, and therefore an almost sure death-sentence.
 
With applying multiple strategies - not only high dose K2 - plaque growth decelerates. But with most patients still above 15% yearly plaque growth during the first year. Below 15% yearly growth, according to the clinical experience of Dr. Davis, averse events become very unlikely. He said he hasn't seen even one while practicing. On his old TrackYourPlauque forum many accomplished deceleration, but very few reversal of CAC score with multiple strategies.
 
How much yearly progression did you have with K2 alone?
 

What I'm really worried about is wasting time, which is my most precious commodity.

 
With a serious PAD, like me, or a MI like you, one indeed does not have the time to hesitate and not do everything one can against the usual exponential plaque-growth. And sure death-sentence.

Edited by pamojja, 26 July 2017 - 06:02 PM.