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Reversing arterial plaque

artery cardiovascular disease lipids matrix gla protein vitamin k2 mk4 vitamin k2 mk7 xanthohumol plaque

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#91 Rocket

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Posted 03 April 2016 - 01:33 PM

 

Idk much about this topic... Lipids, but why can some people eat like I do and be in perfect health and others, it would give them heart disease? And, no, I'm not young.... Middle aged.

 

Or me, getting a severe PAD above 40, and having been vegetarian since age 10?

 

In my case there was 2 years of immense occupational stress preceding (actually quit it and right after got diagnosed). What made my lipids immediately look better was quitting any sugars, then grains and generally reducing carbs. And adding eggs and fatty fish back in. Along with ortholomolecular medicine.
 

 

 

Again, IDK much at all about this subject, but why can't someone find out what the biological mechanism is that let's people like myself eat what we eat and not only not suffer from high cholesterol, but to fall within the ideal range for LDL and HDL?  Then they could come up with a drug mimetic for that process.



#92 zorba990

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Posted 04 April 2016 - 02:18 AM

Idk much about this topic... Lipids, but why can some people eat like I do and be in perfect health and others, it would give them heart disease? And, no, I'm not young.... Middle aged.


Or me, getting a severe PAD above 40, and having been vegetarian since age 10?

In my case there was 2 years of immense occupational stress preceding (actually quit it and right after got diagnosed). What made my lipids immediately look better was quitting any sugars, then grains and generally reducing carbs. And adding eggs and fatty fish back in. Along with ortholomolecular medicine.


Again, IDK much at all about this subject, but why can't someone find out what the biological mechanism is that let's people like myself eat what we eat and not only not suffer from high cholesterol, but to fall within the ideal range for LDL and HDL? Then they could come up with a drug mimetic for that process.

Well, at least one theory says it has to do with vitamin k absorption: http://www.k-vitamin...rdiac_Manifesto

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#93 Daniel Cooper

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Posted 11 April 2016 - 09:18 PM

Here's a very neat paper that was just published:

 

Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming

 

http://www.ncbi.nlm.nih.gov/pubmed/27053774

 

 

Abstract

Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol concentrations. Despite ongoing advances in the prevention and treatment of atherosclerosis, cardiovascular disease remains the leading cause of death worldwide. Continuous retention of apolipoprotein B-containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Because cholesterol accumulation and deposition of cholesterol crystals (CCs) trigger 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. We showed 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 antiatherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Because 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.

 

 

From my reading, cyclodextrin appears to be a cyclic oligosaccharide which is a generally recongized as safe food substance by the FDA.

 

Edited by Daniel Cooper, 11 April 2016 - 09:22 PM.

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#94 hav

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Posted 23 April 2016 - 06:05 PM

I've always heard of cyclodextrin functioning as a transport to increase the absorption of something else.


Edited by hav, 23 April 2016 - 06:11 PM.


#95 NoodleHead

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Posted 24 April 2016 - 04:59 PM

 

Here's a very neat paper that was just published:

 

Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming

 

http://www.ncbi.nlm.nih.gov/pubmed/27053774

 

 

Abstract

Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol concentrations. Despite ongoing advances in the prevention and treatment of atherosclerosis, cardiovascular disease remains the leading cause of death worldwide. Continuous retention of apolipoprotein B-containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Because cholesterol accumulation and deposition of cholesterol crystals (CCs) trigger 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. We showed 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 antiatherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Because 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.

 

 

From my reading, cyclodextrin appears to be a cyclic oligosaccharide which is a generally recongized as safe food substance by the FDA.

 

 

 

Hi, I've just been searching the forum here trying to find anything related to Hydroxypropyl-β-Cyclodextrin (HPBCD) as a treatment for atherosclerosis (congrats this is the first mention!). After reading some of the reports on this paper, I was really surprised that there aren't people already taking it already.

 

I found a lot of information regarding safety here: http://addiandcassi....BCD-Summary.pdf

 

It seems it a very safe substance, with up to 16g/day being safe as a oral dose. in 2009 HPBCD was used  to cure 2 twin little girls from a rare genetic disorder involving cholesterol build up in their cells. http://arstechnica.c...-heart-disease/

 

At this point I was ready to order some from ebay http://www.ebay.co.u...-/141965396870?

 

But then I found this paper which made me stop in my tracks:

http://www.ncbi.nlm....les/PMC3532434/

 

Yeah, hearing loss is a possibility, So I would definitely advise against anyone 'feeding their 70kg rats' HPBCD for atherosclerosis at this time until we know more about the risks and dosages needed.

 

I hope someone finds this information useful :)

 

Does any one have full text copy of the paper?


Edited by NoodleHead, 24 April 2016 - 05:12 PM.

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#96 Logjam

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Posted 24 April 2016 - 09:40 PM

There's a good reason.  Cyclodextrin is not orally absorbed.  You need to inject it.  The children actually needed to have it injected via spinal tap to bypass the blood brain barrier.

 

There was some discussion about how IV injection would likely not bypass the BBB, which is similar to the ear's blood barrier (but not the same).  The nice part is that IV isn't even necessary.  Subcutaneous will suffice.  That makes it easier.

 

YMMV, but you'd need to inject it subcutaneously, and nobody is suggesting that here.  Orally ingesting it will probably do nothing, even at 16g/day.

 

I found a link to the paper, but it's usually gated.  You can find it if you try, but I'm trying and I can't find it again yet.

 

 

 

Here's a very neat paper that was just published:

 

Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming

 

http://www.ncbi.nlm.nih.gov/pubmed/27053774

 

 

Abstract

Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol concentrations. Despite ongoing advances in the prevention and treatment of atherosclerosis, cardiovascular disease remains the leading cause of death worldwide. Continuous retention of apolipoprotein B-containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Because cholesterol accumulation and deposition of cholesterol crystals (CCs) trigger 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. We showed 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 antiatherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Because 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.

 

 

From my reading, cyclodextrin appears to be a cyclic oligosaccharide which is a generally recongized as safe food substance by the FDA.

 

 

 

Hi, I've just been searching the forum here trying to find anything related to Hydroxypropyl-β-Cyclodextrin (HPBCD) as a treatment for atherosclerosis (congrats this is the first mention!). After reading some of the reports on this paper, I was really surprised that there aren't people already taking it already.

 

I found a lot of information regarding safety here: http://addiandcassi....BCD-Summary.pdf

 

It seems it a very safe substance, with up to 16g/day being safe as a oral dose. in 2009 HPBCD was used  to cure 2 twin little girls from a rare genetic disorder involving cholesterol build up in their cells. http://arstechnica.c...-heart-disease/

 

At this point I was ready to order some from ebay http://www.ebay.co.u...-/141965396870?

 

But then I found this paper which made me stop in my tracks:

http://www.ncbi.nlm....les/PMC3532434/

 

Yeah, hearing loss is a possibility, So I would definitely advise against anyone 'feeding their 70kg rats' HPBCD for atherosclerosis at this time until we know more about the risks and dosages needed.

 

I hope someone finds this information useful :)

 

Does any one have full text copy of the paper?

 

 


Edited by Logjam, 24 April 2016 - 09:41 PM.

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#97 NoodleHead

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Posted 24 April 2016 - 09:49 PM

 

There's a good reason.  Cyclodextrin is not orally absorbed.  You need to inject it.  The children actually needed to have it injected via spinal tap to bypass the blood brain barrier.

 

There was some discussion about how IV injection would likely not bypass the BBB, which is similar to the ear's blood barrier (but not the same).  The nice part is that IV isn't even necessary.  Subcutaneous will suffice.  That makes it easier.

 

YMMV, but you'd need to inject it subcutaneously, and nobody is suggesting that here.  Orally ingesting it will probably do nothing, even at 16g/day.

 

I found a link to the paper, but it's usually gated.  You can find it if you try, but I'm trying and I can't find it again yet.

 

 

 

Here's a very neat paper that was just published:

 

Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming

 

http://www.ncbi.nlm.nih.gov/pubmed/27053774

 

 

Abstract

Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol concentrations. Despite ongoing advances in the prevention and treatment of atherosclerosis, cardiovascular disease remains the leading cause of death worldwide. Continuous retention of apolipoprotein B-containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Because cholesterol accumulation and deposition of cholesterol crystals (CCs) trigger 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. We showed 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 antiatherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Because 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.

 

 

From my reading, cyclodextrin appears to be a cyclic oligosaccharide which is a generally recongized as safe food substance by the FDA.

 

 

 

Hi, I've just been searching the forum here trying to find anything related to Hydroxypropyl-β-Cyclodextrin (HPBCD) as a treatment for atherosclerosis (congrats this is the first mention!). After reading some of the reports on this paper, I was really surprised that there aren't people already taking it already.

 

I found a lot of information regarding safety here: http://addiandcassi....BCD-Summary.pdf

 

It seems it a very safe substance, with up to 16g/day being safe as a oral dose. in 2009 HPBCD was used  to cure 2 twin little girls from a rare genetic disorder involving cholesterol build up in their cells. http://arstechnica.c...-heart-disease/

 

At this point I was ready to order some from ebay http://www.ebay.co.u...-/141965396870?

 

But then I found this paper which made me stop in my tracks:

http://www.ncbi.nlm....les/PMC3532434/

 

Yeah, hearing loss is a possibility, So I would definitely advise against anyone 'feeding their 70kg rats' HPBCD for atherosclerosis at this time until we know more about the risks and dosages needed.

 

I hope someone finds this information useful :)

 

Does any one have full text copy of the paper?

 

 

 

The information in the pdf I linked suggests that 3-6% is absorbed via the gastrointestinal tract when taken orally. Its a very small amount, but we don't know the dosages used in this paper yet as its behind a paywall. Say if you were taking 5g orally 150-300mg would be absorbed. Taken daily that may be enough to dissolve away your arterial plaques. But with the risk of cumulative hearing damage, its probably far too risky at this time.


Edited by NoodleHead, 24 April 2016 - 09:50 PM.

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#98 Hebbeh

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Posted 24 April 2016 - 11:01 PM

This is your answer:

 

The HPBCD preparation did contain some propylene glycol that was also labeled. The amount of label absorbed corresponded to the amount of proplyene glycol present.

 

 

The information in the pdf I linked suggests that 3-6% is absorbed via the gastrointestinal tract when taken orally. Its a very small amount, but we don't know the dosages used in this paper yet as its behind a paywall. Say if you were taking 5g orally 150-300mg would be absorbed. Taken daily that may be enough to dissolve away your arterial plaques. But with the risk of cumulative hearing damage, its probably far too risky at this time.

 

 

 


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#99 NoodleHead

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Posted 25 April 2016 - 08:38 AM

 

This is your answer:

 

The HPBCD preparation did contain some propylene glycol that was also labeled. The amount of label absorbed corresponded to the amount of proplyene glycol present.

 

 

The information in the pdf I linked suggests that 3-6% is absorbed via the gastrointestinal tract when taken orally. Its a very small amount, but we don't know the dosages used in this paper yet as its behind a paywall. Say if you were taking 5g orally 150-300mg would be absorbed. Taken daily that may be enough to dissolve away your arterial plaques. But with the risk of cumulative hearing damage, its probably far too risky at this time.

 

 

 

Ah yes, good point. That's a shame, perhaps there is a way that HPBCD (or similar safer chemical) can be made to absorb through the gastrointestinal tract.

 

It's still great to know that its possible to reverse atherosclerosis. Maybe at some point in the near future a treatment will become available, even if it has to be injected subcutaneously.


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#100 Logjam

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Posted 25 April 2016 - 11:37 PM

I expect this treatment to go the way of EDTA, but call me cynical.  That's not to say EDTA works.  But this probably won't get tested for efficacy — and then doctors will say it's not tested for efficacy so it must not be efficacious.  Totally circular.  Never mind that plenty of drugs are barely or questionably efficacious for some of their indications.  Never mind that EDTA demonstrably removes calcification in vitro, and some lesions are obviously calcified or the sclerosis is of the medial/Monkeberg variety.

 

At best there would be a use patent on this one, which will not fund the millions of dollars needed to run the (human) studies.  And let us not forget stents are huge business with the newest generation being drug eluting and bioabsorbable.  Bioabsorbable is a pretty remarkable advancement, and some will need stents regardless. 

 

I hope I'm wrong, but it's almost hopeless to get studies done on things that are already in a mayonnaise jar like cyclodextrin.  Plenty of industries will use expensive tools when a cheaper tool will do.  Every day.

 

I don't think I'd hold my breath for the human studies to materialize.


Edited by Logjam, 26 April 2016 - 12:02 AM.

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#101 Daniel Cooper

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Posted 27 April 2016 - 01:43 PM

I expect this treatment to go the way of EDTA, but call me cynical.  That's not to say EDTA works.  But this probably won't get tested for efficacy — and then doctors will say it's not tested for efficacy so it must not be efficacious.  Totally circular.  Never mind that plenty of drugs are barely or questionably efficacious for some of their indications.  Never mind that EDTA demonstrably removes calcification in vitro, and some lesions are obviously calcified or the sclerosis is of the medial/Monkeberg variety.

 

At best there would be a use patent on this one, which will not fund the millions of dollars needed to run the (human) studies.  And let us not forget stents are huge business with the newest generation being drug eluting and bioabsorbable.  Bioabsorbable is a pretty remarkable advancement, and some will need stents regardless. 

 

I hope I'm wrong, but it's almost hopeless to get studies done on things that are already in a mayonnaise jar like cyclodextrin.  Plenty of industries will use expensive tools when a cheaper tool will do.  Every day.

 

I don't think I'd hold my breath for the human studies to materialize.

 

Unfortunately I am also not hopeful.

 

This type of basic, not profit oriented research is a role that our universities used to fill.  Unfortunately, now they too are busy chasing the next billion dollar blockbuster drug.  So, this role now largely goes unfilled.

 

Unless something is likely to result in a strong patent, no one seems to have any interest.


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#102 Daniel Cooper

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Posted 27 April 2016 - 02:31 PM

Logjam,

 

I'm interested in hearing the case for EDTA.  What do you think is the best evidence out there?

 

 



#103 Logjam

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Posted 27 April 2016 - 11:11 PM

http://www.ncbi.nlm....les/PMC4268131/

 

See Figure 4.  Note that they said EDTA without the targeting didn't work, but the duration was short.  It's focusing on medial calcification, and that makes perfect sense also in light of the fact that the TACT study worked best on diabetics — who have medial calcifications very often.

 

Tested in rodents again, but it could probably just be human albumin instead.

 

Logjam,

 

I'm interested in hearing the case for EDTA.  What do you think is the best evidence out there?

 


Edited by Logjam, 27 April 2016 - 11:26 PM.


#104 HomoLudens

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Posted 30 April 2016 - 10:06 PM

 

There's a good reason.  Cyclodextrin is not orally absorbed.  You need to inject it.  The children actually needed to have it injected via spinal tap to bypass the blood brain barrier.

 

There was some discussion about how IV injection would likely not bypass the BBB, which is similar to the ear's blood barrier (but not the same).  The nice part is that IV isn't even necessary.  Subcutaneous will suffice.  That makes it easier.

 

YMMV, but you'd need to inject it subcutaneously, and nobody is suggesting that here.  Orally ingesting it will probably do nothing, even at 16g/day.

 

I found a link to the paper, but it's usually gated.  You can find it if you try, but I'm trying and I can't find it again yet.

 

 

 

Here's a very neat paper that was just published:

 

Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming

 

http://www.ncbi.nlm.nih.gov/pubmed/27053774

 

 

Abstract

Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol concentrations. Despite ongoing advances in the prevention and treatment of atherosclerosis, cardiovascular disease remains the leading cause of death worldwide. Continuous retention of apolipoprotein B-containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Because cholesterol accumulation and deposition of cholesterol crystals (CCs) trigger 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. We showed 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 antiatherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Because 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.

 

 

From my reading, cyclodextrin appears to be a cyclic oligosaccharide which is a generally recongized as safe food substance by the FDA.

 

 

 

Hi, I've just been searching the forum here trying to find anything related to Hydroxypropyl-β-Cyclodextrin (HPBCD) as a treatment for atherosclerosis (congrats this is the first mention!). After reading some of the reports on this paper, I was really surprised that there aren't people already taking it already.

 

I found a lot of information regarding safety here: http://addiandcassi....BCD-Summary.pdf

 

It seems it a very safe substance, with up to 16g/day being safe as a oral dose. in 2009 HPBCD was used  to cure 2 twin little girls from a rare genetic disorder involving cholesterol build up in their cells. http://arstechnica.c...-heart-disease/

 

At this point I was ready to order some from ebay http://www.ebay.co.u...-/141965396870?

 

But then I found this paper which made me stop in my tracks:

http://www.ncbi.nlm....les/PMC3532434/

 

Yeah, hearing loss is a possibility, So I would definitely advise against anyone 'feeding their 70kg rats' HPBCD for atherosclerosis at this time until we know more about the risks and dosages needed.

 

I hope someone finds this information useful :)

 

Does any one have full text copy of the paper?

 

 

 Bypassed the paywall, found the pdf: http://www.meb.uni-b...odextrin.pdf :)


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#105 9lives

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Posted 29 May 2016 - 07:19 AM

I originally did EDTA 8 years ago for heavy metal chelation purposes (a series of 10 treatments). Following that treatment, it was easier for my doctor to do IV's and blood draws. My veins don't roll when he and others try to inject a needle in my vein. My doctor believes it's because of reduced calcification, and I was able to verify this benefit in the scientific literature. I highly recommend it.

 

I would agree that supplementing with vitamin K2 (MK4/ MK7) is also smart to do.


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#106 aconita

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Posted 11 June 2016 - 06:16 AM

Finally do we have someone's arterial scan showing taking high doses K2 lowered calcification?

 

Mikey, it is 3 years now from your first post in this tread and I am sure you did test again, what about the results?

 

Theories and rats are wonderful but of little practical relevance if in vivo in humans doesn't work.


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#107 thedarkbobo

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Posted 11 June 2016 - 06:31 AM

Well I guess we are still waiting for something that works well and is doable on our side. There are some projects going on like this:

https://www.fightagi...erotic-plaques/


Edited by thedarkbobo, 11 June 2016 - 06:32 AM.


#108 pamojja

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Posted 11 June 2016 - 02:01 PM

Finally do we have someone's arterial scan showing taking high doses K2 lowered calcification?

 

One guy on the TrackYourPlaque forum started high dose vitamin K2 already about 6 years ago, by using bulk powders. He did yearly scans which showed repeatedly reduction of his CAC score. In this process he started to produce his own Vitamin Ks product, since it otherwise isn't available at such doses, along documenting his experiences and research:

 

http://www.k-vitamins.com/

 

However, he does take a lot of things as shown in his January 2011 regime.

 

 

 

 



#109 Darryl

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Posted 28 August 2016 - 04:03 AM

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 endotoxemiaNutrition & metabolism10(1), p.1.

To examine the role of lipid rafts in intestinal endotoxin transport, ileum segments from 16 pigs (56 ± 4 days of age) were mounted in Ussing chambers as described above. Segments were pre-treated with or without 25 mM Methyl-β-cyclo dextrin (MβCD, a synthetic lipid raft modifier) for 30 min. Thereafter, the mucosal chamber was spiked with either saline-bile acid (CON) or Coconut oil-bile acid (12.5% v/v) and the FITC-LPS apparent permeability coefficient for each tissue was calculated...

 
As expected, the CO treatment significantly augmented the ileum endotoxin Papp compared to the saline control (P < 0.05). However, the endotoxin Papp was significantly reduced with the MβCD treatment compared to the saline control (1.54 vs. 0.07, P = 0.04). In the presence of MβCD and CO, the ileum Papp was attenuated three fold from the CO alone treatment (P < 0.05). Importantly, ileum integrity and permeability as measured by transepithelial resistance was not altered by either short term coconut oil, MβCD, or the combination compared to the saline control (P = 0.98).
 
Gut derived endotoxins have received considerable attention as mediators of inflammation and endothelial dysfunction from high-fat meals and diets. Most enter systemic circulation via the lymphatic route, as part of the chylomicrons produced by intestinal epithelial cells that transport long-chain fatty acids (incl. laurate, here) to adipose tissue. How are they getting into the epithelial cells? Methyl-β-cyclo dextrin, at a modest 25 mM concentration, reduced fasting transcellular endotoxin transport by 95%, and high-fat postprandial transport by two thirds. For this experiment, it just means the endotoxin import was via a lipid raft mediated process. But one can imagine clinical implications.
 
Granted, this is just a benchtop experiment on tripe, but I want to see a long term atherogenic diet feeding study using methyl-β-cyclo dextrin in the feed in the experimental arm. Shame there's no patent, no prospective money, and hence little private funding.

Edited by Darryl, 28 August 2016 - 04:38 AM.

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#110 albedo

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Posted 30 August 2016 - 04:52 PM

....

My takeaway from a lot of reading: Stay thin, avoid added sugars, fats, and fatty foods (except nuts), especially arachidonic acid from grain-fed animal products, exercise before high-glycemic meals, eat lots of microbiota-accessible carbohydrates (from beans, wheat bran, onions/leeks/garlic, artichokes, asparagus etc. and resistant starch), and moderate inflammation with high polyphenol intake, EPA/fish oil, and baby aspirin. Once that foundation is in place, then its time to concern oneself with decalcification with high-dose K2, ant-inflammatory supplements, aspirin, etc.

....

 

Thank you for your very rich post.

"... exercise before high-glycemic meals ...": what would be the rationale?

 



#111 Darryl

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Posted 30 August 2016 - 06:40 PM

"... exercise before high-glycemic meals ...": what would be the rationale?

 

I may have meant meant exercise before high-fructose meals. Dr. Robert Lustig has received considerable notice popularizing a once obscure aspect of fructose metabolism (which has been known for decades). Fructose is metabolized in the liver almost exclusively, and bypasses the main rate-limiting step in glycolysis, catalysed by phosphofructokinase. Whereas glucose metabolism is tightly regulated by negative feedback from its own products ATP and citrate, fructose can be continuously and uncontrollably metabolised to pyruvate and lactate, precursors to acetyl-CoA (and de novo lipogenesis, triglycerides and VLDL). When the liver is glycogen replete, this may contribute to the modern epidemic of insulin resistance, obesity, hypertension, fatty liver, and atherogenic hyperlipidemia. After exercise or fasting, livers can accommodate more glycogen and fructose. Our primate ancestors were primarily frugivores, but they had to climb trees (and burn glycogen) to get at the fruit.

 

Basically, high-fructose meals eaten by the sedentary are the bad carbs. This profoundly confounds most past epidemiology on carbohydrates and CVD risk in Western populations, and may account for why in Western epidemiology, carbohydrates are associated with greater CVD risk than PUFAs and MUFAs, whereas traditional agrarian societies with 80-85% starch diets (and little added sugars) have almost negligible risk. Stick to starches, with high-polyphenol whole fruit as the main sweets.

 

Yang et al, 2014. Added sugar intake and cardiovascular diseases mortality among US adultsJAMA internal medicine174(4), pp.516-524.

Among US adults, the adjusted mean percentage of daily calories from added sugar increased from 15.7% in 1988-1994 to 16.8% in 1999-2004 and decreased to 14.9% in 2005-2010. Most adults consumed 10% or more of calories from added sugar (71.4%) and approximately 10% consumed 25% or more in 2005-2010. During a median follow-up period of 14.6 years, we documented 831 CVD deaths during 163 039 person-years. Age-, sex-, and race/ethnicity–adjusted hazard ratios (HRs) of CVD mortality across quintiles of the percentage of daily calories consumed from added sugar were 1.00, 1.09 (95% CI, 1.05-1.13), 1.23 (1.12-1.34), 1.49 (1.24-1.78), and 2.43 (1.63-3.62; P < .001), respectively. After additional adjustment for sociodemographic, behavioral, and clinical characteristics, HRs were 1.00 (reference), 1.07 (1.02-1.12), 1.18 (1.06-1.31), 1.38 (1.11-1.70), and 2.03 (1.26-3.27; P = .004), respectively. Adjusted HRs were 1.30 (95% CI, 1.09-1.55) and 2.75 (1.40-5.42; P = .004), respectively, comparing participants who consumed 10.0% to 24.9% or 25.0% or more calories from added sugar with those who consumed less than 10.0% of calories from added sugar. 

 


Edited by Darryl, 30 August 2016 - 07:02 PM.

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#112 albedo

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Posted 30 August 2016 - 08:36 PM

Thank you Darryl for your reply.



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#113 Castiel

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Posted 31 August 2016 - 12:36 AM

 

 

Idk much about this topic... Lipids, but why can some people eat like I do and be in perfect health and others, it would give them heart disease? And, no, I'm not young.... Middle aged.

 

Or me, getting a severe PAD above 40, and having been vegetarian since age 10?

 

In my case there was 2 years of immense occupational stress preceding (actually quit it and right after got diagnosed). What made my lipids immediately look better was quitting any sugars, then grains and generally reducing carbs. And adding eggs and fatty fish back in. Along with ortholomolecular medicine.
 

 

 

Again, IDK much at all about this subject, but why can't someone find out what the biological mechanism is that let's people like myself eat what we eat and not only not suffer from high cholesterol, but to fall within the ideal range for LDL and HDL?  Then they could come up with a drug mimetic for that process.

 

 

A very long time ago it was found a single mutation of hdl  that allows for heavy meat eaters with no clogged arteries and very long lifespans.  
 

...The 38 lucky carriers have a simple mutation in a protein of so-called good cholesterol that lets them eat red meat, sausage and butter without artery-clogging deposits.

They range in age from the teens to nearly 90. And they have never worried about strokes or heart attacks since longevity runs in the family.
"They are almost all smokers. They eat like hell, the worst diet," said the University of Milan's Dr. Cesare Sirtori, who screened residents of Limone for the miracle mutation....

[animal tests were promising back then]

Sirtori said he will publish similar results in December showing "no plaque at all" in rabbits injected with Apo Milano. Shah said he will test monkeys, pigs and mice before considering human trials, a point that could take several years to reach...

"We hope to be able to introduce a treatment to give once a week for somewhere from two to six months, and that treatment would induce regression of atherosclerosis," the common form of artery buildup, Andersson said from Stockholm. "If it works, it would be revolutionary."

 

 

http://articles.lati..._artery-disease

 

 

With chimeric research, the decades it would take for 3d printing an organ to come to market is done away with,  engineer an animal to have neither blood vessels nor a particular organ, and inject human stem cells into the embryo.  You will get a fully compatible organ of your choosing, the embryonic environment within the womb will carry out all the complex cellular signals to develop the organ perfectly.

 

Genetically modify a single cell, verify that it was modified correctly with no unintended changes, and grow the entire organ of your choice.  Then implant.

 

There's also been suggestions by Dr. Fossel, iirc, that the artery can maintain integrity indefinitely, but that telomere depletion precedes the onset of symptoms.   That is if I interpreted his comments correctly, which I may or may not have.



#114 tunt01

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Posted 31 August 2016 - 01:55 AM

One area scientists have been targeting is inhibiting cholesterol ester transfer protein (CETP) in lipid metabolism.  By preventing CETP from rebalancing triglycerides and cholester esters between LDL and HDL particles, it causes HDL counts to remain higher and the atherogenic potential of LDL to be lower.

 

Xanthohumol, a metabolite of beer, is a possible supplement to inhibit CETP and improve lipid metabolism.

 

 

From Hirata, et al.:

 

 

pone.0049415.g002.jpg

 

Effect of xanthohumol on serum cholesterol and CETP activity.

Serum HDL-C concentration in the control group (closed circle), xanthohumol group (opened circle) and Chow group (closed triangle) of CETP-Tg mice (A), and in the control group (closed square) and xanthohumol group (opened square) of wild-type mice (B) over time. © Serum CETP activity after 18 weeks of treatment. (D) Correlation of serum CETP activity and HDL-C/T-Cho (%) in CETP-Tg mice fed HCD after 18 weeks. CE content of serum (E) and HDL-fraction (F) after 18 weeks. (N = 15; CETP-Tg mice control, N = 16; CETP-Tg mice xanthohumol, N = 10; CETP-Tg mice Chow, N = 3; wild-type mice control, N = 8; wild-type mice xanthohumol) Means±SEM. *P<0.05, **P<0.01.

 

 

The appropriate comparative group is CNT and XN (xanthohumol diet) in a transgenic model of CETP (CETP-Tg).  Mice do not have CETP like humans, therefore a transgenic model of expression is used to model humans and show atheroscelrosis.  Xanthohumol seems to materially improve HDL cholesterol levels and inhibit CETP activity.

 

 

NOTE:  Several CETP inhibitor drugs have failed clinical trials.  This is not meant to suggest CETP inhibition is the 'holy grail' of athersclerosis regression.  But, I think we've seen a lot of positive news on beer/alcohol consumption that confers greater lifespan.  Perhaps mild CETP inhibition and xanthohumol is a component of that benefit.

 

 

Hiroshi Hirata, H. (2012). Xanthohumol Prevents Atherosclerosis by Reducing Arterial Cholesterol Content via CETP and Apolipoprotein E in CETP-Transgenic Mice.Plos ONE7(11). Retrieved from http://www.ncbi.nlm....les/PMC3500296/


Edited by prophets, 31 August 2016 - 08:00 PM.

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#115 Castiel

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Posted 31 August 2016 - 10:26 AM

 

One area scientists have been targeting is inhibiting cholesterol ester transfer protein (CETP) in lipid metabolism.  By preventing CETP from rebalancing triglycerides and cholester esters between LDL and HDL particles, it causes HDL counts to remain higher and the atherogenic potential of LDL to be lower.

 

Xanthohumol, a metabolite of beer, is a possible supplement to inhibit CETP and improve lipid metabolism.

 

 

From Hirata, et al.:

 

 

pone.0049415.g002.jpg

 

Effect of xanthohumol on serum cholesterol and CETP activity.

Serum HDL-C concentration in the control group (closed circle), xanthohumol group (opened circle) and Chow group (closed triangle) of CETP-Tg mice (A), and in the control group (closed square) and xanthohumol group (opened square) of wild-type mice (B) over time. © Serum CETP activity after 18 weeks of treatment. (D) Correlation of serum CETP activity and HDL-C/T-Cho (%) in CETP-Tg mice fed HCD after 18 weeks. CE content of serum (E) and HDL-fraction (F) after 18 weeks. (N = 15; CETP-Tg mice control, N = 16; CETP-Tg mice xanthohumol, N = 10; CETP-Tg mice Chow, N = 3; wild-type mice control, N = 8; wild-type mice xanthohumol) Means±SEM. *P<0.05, **P<0.01.

 

 

The appropriate comparative group is CNT and XN (xanthohumol diet).  Xanthohumol seems to materially improve HDL cholesterol levels and inhibit CETP activity.

 

 

 

 

Hiroshi Hirata, H. (2012). Xanthohumol Prevents Atherosclerosis by Reducing Arterial Cholesterol Content via CETP and Apolipoprotein E in CETP-Transgenic Mice.Plos ONE7(11). Retrieved from http://www.ncbi.nlm....les/PMC3500296/

 

 

It appears there are optimal levels of HDL, so any therapies should keep that in mind

 

 

Commonly touted as "good cholesterol" for helping to reduce risk of stroke and heart attack, both high and low levels of high-density lipoprotein (HDL) cholesterol may increase a person's risk of premature death, according to new research. Conversely, intermediate HDL cholesterol levels may increase longevity, according to the research.https://www.scienced...60811190922.htm


 



#116 albedo

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Posted 31 August 2016 - 11:40 AM

I came across CETP when looking at my HDL and nutritional interventions based on genotypes and diet-genotype interaction, so the xanthohumol possible inhibition of CETP and the positive impact on HDL is interesting. However, I admit I was quite overwhelmed by the complexity due to both the complexity of CVD and the nutrigenomics itself. It seems also that looking at the CETP genotype is important when considering statin treatment (1).

 

Two in depth papers in my to-read list are precisely those pointing to the CETP genotype and the HDL association (2) and the nutrigenomics of CVD (3) which for the moment lacks simple recommendations.

 

(1) CETP genotype predicts increased mortality in statin-treated men with proven cardiovascular disease: an adverse pharmacogenetic interaction.

http://www.ncbi.nlm....pubmed/18957472

 

(2) Genetic-epidemiological evidence on genes associated with HDL cholesterol levels: A systematic in-depth review

https://www.ncbi.nlm...les/PMC2730542/

(see in particulat Table 1, “Genetic variants within the CETP gene coding for the cholesteryl ester transfer protein and their association with HDLC concentrations.

 

(3) Nutrigenomics in cardiovascular medicine

http://www.ncbi.nlm....les/PMC2810265/



#117 tunt01

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Posted 31 August 2016 - 02:24 PM

 

 

 

It appears there are optimal levels of HDL, so any therapies should keep that in mind

 

 

Commonly touted as "good cholesterol" for helping to reduce risk of stroke and heart attack, both high and low levels of high-density lipoprotein (HDL) cholesterol may increase a person's risk of premature death, according to new research. Conversely, intermediate HDL cholesterol levels may increase longevity, according to the research.https://www.scienced...60811190922.htm

 

 

 

This is very true and other mechanisms of reverse cholesterol transport, probably via improvement of ABCA1, would likely be better at reducing arterial plaque.

 

The cyclodextrin angle is really interesting to me.  It really should be explored more and possibly evaluated for a group buy.



#118 Darryl

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Posted 31 August 2016 - 10:35 PM

The veterans study (Bowe et al, below) is not the first time a U-shaped association has been found for HDL levels and mortality.

 

Moradi et al, 2014. Elevated high-density lipoprotein cholesterol and cardiovascular mortality in maintenance hemodialysis patientsNephrology Dialysis Transplantation, p.gfu022.

Bowe et al, 2016. High density lipoprotein cholesterol and the risk of all-cause mortality among US veteransClinical Journal of the American Society of Nephrology, pp.CJN-00730116.

 

Anyone who's followed clinical trials and Mendelian randomization studies should have doubts about a causal role for HDL in lowering CVD risk

 

Briel et al, 2009. Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysisBmj338, p.b92.

 

Frikke-Schmidt et al, 2008. Association of loss-of-function mutations in the ABCA1 gene with high-density lipoprotein cholesterol levels and risk of ischemic heart diseaseJama299(21), pp.2524-2532.

Haase et al, 2011. LCAT, HDL cholesterol and ischemic cardiovascular disease: a Mendelian randomization study of HDL cholesterol in 54,500 individualsThe Journal of Clinical Endocrinology & Metabolism,97(2), pp.E248-E256.

Voight et al, 2012. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation studyThe Lancet380(9841), pp.572-58

Holmes et al, 2014. Mendelian randomization of blood lipids for coronary heart diseaseEuropean heart journal, p.eht571.

 

I don't believe these consistent results casting doubt on a causal role for HDL can all be explained by a U-shaped response curve. A number of lifestyle behaviors and dietary elements that increase HDL (aerobic exercise, weight loss, moderate alcohol consumption, monounsaturated fats, long-chain omega-3s, and soluble fiber) are believed to exert protective benefits by mechanisms independent from cholesterol efflux. The past association of low HDL and HDL/LDL ratios with risk may be a coincident marker of their absence. Likewise, some HDL and HDL/LDL ratio elevating fatty acids (laurate and myristate) are known to have negative inflammatory or vascular effects independent from their effects on cholesterol levels. Increased risk at the high end may reflect their intake.

 

There aren't many studies which have found negative effects from elevated HDL, but I always respect studies where the researchers are scratching their heads more than the ones with expected results:

 

Huang et al, 2012. Moderate to high concentrations of high-density lipoprotein from healthy subjects paradoxically impair human endothelial progenitor cells and related angiogenesis by activating Rho-associated kinase pathwaysArteriosclerosis, thrombosis, and vascular biology32(10), pp.2405-2417.

 

 


Edited by Darryl, 31 August 2016 - 10:39 PM.

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#119 RWhigham

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Posted 05 November 2016 - 04:09 AM

In my simplified view,

 

1) HDL wanders around collecting extra cholesterol and other building material from cells that have more than they need (they push it to their surface). The HDL hands off the cholesterol and other building material to LDL. (Other building material includes triglycerides, phospholipids, and various molecules). 

 

2) LDL wanders around offering cholesterol and other building material to any cells that need it.

 

    VLDL becomes LDL after dumping most of its triglycerides into adipose and muscle tissue.

    The resulting LDL contains a lot of left over material from VLDL, then acquires more from HDL.

 

3) After awhile, the liver collects the LDL, and recycles the left over material.

 

4) CTEP inhibitors block the exchange between HDL and LDL.

 

5) This causes HDL to quit functioning. The drop in LDL-C and rise in HDL-C makes cardiologists giddy - but surprise, CETEP inhibitor trials have all failed due to increased mortality. Who wants to volunteer for the next trial?

 

Side note: various train engineers, bus drivers and so forth who take statins may very well have experienced spells of temporary amnesia and as a result lost control of their machines.

 

 https://www.spacedoc.com/articles/amnesia-and-statins

https://www.ncbi.nlm...les/PMC3027897/  "Transient global amnesia associated with statin intake"

 


Edited by RWhigham, 05 November 2016 - 04:25 AM.

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#120 JustGetMeIntoSpace

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Posted 05 November 2016 - 07:33 AM

In my simplified view,

 

1) HDL wanders around collecting extra cholesterol and other building material from cells that have more than they need (they push it to their surface). The HDL hands off the cholesterol and other building material to LDL. (Other building material includes triglycerides, phospholipids, and various molecules). 

 

2) LDL wanders around offering cholesterol and other building material to any cells that need it.

 

    VLDL becomes LDL after dumping most of its triglycerides into adipose and muscle tissue.

    The resulting LDL contains a lot of left over material from VLDL, then acquires more from HDL.

 

3) After awhile, the liver collects the LDL, and recycles the left over material.

 

4) CTEP inhibitors block the exchange between HDL and LDL.

 

5) This causes HDL to quit functioning. The drop in LDL-C and rise in HDL-C makes cardiologists giddy - but surprise, CETEP inhibitor trials have all failed due to increased mortality. Who wants to volunteer for the next trial?

 

Side note: various train engineers, bus drivers and so forth who take statins may very well have experienced spells of temporary amnesia and as a result lost control of their machines.

 

 https://www.spacedoc.com/articles/amnesia-and-statins

https://www.ncbi.nlm...les/PMC3027897/  "Transient global amnesia associated with statin intake"

fyi:  Great post.  Quick comment:  

 

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

 

This may explain these kind of studies:

 

http://www.nytimes.c...heart-risk.html


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