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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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#481 Kodiak

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Posted 23 July 2019 - 12:37 PM

Sorry, Pamojja, I should've referenced Duke's earlier post...page 11, #321 I believe. He specifically called out those three seeds (See below). If it's an omega-6 thing I get it, but wow, even avoid the seeds, huh?

 

Food-wise:


o Greatly minimize inflammatory fats/oils that have over 10% polyunsaturated fatty acids

o Eliminate (if your serious) all cereal-type grains. (Rice is okay, sorghum and millet are excellent choices.)
o Eliminate all seeds of any kind, even chia, hemp, and flax seeds, widely thought to be healthy

o Eliminate any non-berry type of fruit

o Eliminate any processed food that has corn anything, soy anything, wheat anything in it

o Add resistance starches and prebiotics to your foods and sauces (a good gut biome reduces overall inflammation)


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#482 pamojja

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Posted 23 July 2019 - 12:54 PM

Sorry, Pamojja, I should've referenced Duke's earlier post...page 11, #321 I believe. He specifically called out those three seeds (See below). If it's an omega-6 thing I get it, but wow, even avoid the seeds, huh?

 

Thanks for clarifying, forgot that older post. However, I would check if the advisor in this case not only talks theoretically in terms of very thoughtful prevention. As far as I know, Duke till now did not post any before and after results of imaging studies, showing real reversal of calcification by his interventions. I did (a max. CIMT decrease from 1.9 down to 1 mm within 2 year), and consumed a daily tablespoon of freshly milled flaxseed, chia and hemp seeds occasionally. But on the other side I also supplemented about 4 g/d of omega-3s from fish-oil, and an other gram from diet during the last 10 years.

 

On the other hand: any grain like rice is really poison to me (makes my glucose numbers diabetic), but lecithin from soy wasn't detremental at all. Higher choline also by lecithin improved my liver functions. Otherwise we agree, but overall I believe there isn't a 1-size-fits-all, intakes have to be adjusted by regular lab-testing.


Edited by pamojja, 23 July 2019 - 01:01 PM.

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#483 aribadabar

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Posted 23 July 2019 - 02:11 PM

Thanks for clarifying, forgot that older post. However, I would check if the advisor in this case not only talks theoretically in terms of very thoughtful prevention. As far as I know, Duke till now did not post any before and after results of imaging studies, showing real reversal of calcification by his interventions. I did (a max. CIMT decrease from 1.9 down to 1 mm within 2 year), and consumed a daily tablespoon of freshly milled flaxseed, chia and hemp seeds occasionally. But on the other side I also supplemented about 4 g/d of omega-3s from fish-oil, and an other gram from diet during the last 10 years.

 

On the other hand: any grain like rice is really poison to me (makes my glucose numbers diabetic), but lecithin from soy wasn't detremental at all. Higher choline also by lecithin improved my liver functions. Otherwise we agree, but overall I believe there isn't a 1-size-fits-all, intakes have to be adjusted by regular lab-testing.

 Fully agree with you on this one.

 

The fibers, lignans and omega-3's in flax, chia and hemp make consuming them net positive and the papers and results like yours confirm this. So one can safely ignore any cautions against these specifically as far as CVD health risks are concerned.

Just need not be heated as the omega-3's are very temperature unstable and preferably stored in fridge to retard degradation/oxidation.

 

As far lecithin goes, I would only add one can use sunflower-derived (instead of soy-) and avoid any theoretical or personal sensitivities to soy.

 

On the rice issue - does this spike happen with all and any rice ( brown, black, red) or just the typical white one?


Edited by aribadabar, 23 July 2019 - 02:17 PM.

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#484 pamojja

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Posted 23 July 2019 - 04:37 PM

On the rice issue - does this spike happen with all and any rice ( brown, black, red) or just the typical white one?

 

Yes. On vacations to high carbing India I found I only can tolerate a fermented rice-preparation called Dosa somewhat. As something instead of chapaties or rice, to get the tradtional very spicy curries a bit deluted and down.
 


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#485 smithx

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Posted 24 July 2019 - 05:26 AM

Of interest:

 

Evolutionary gene loss may help explain why only humans are prone to heart attacks

...

Varkis, and Philip Gordts, PhD, assistant professor of medicine, and others report that mice modified to be deficient (like humans) in a sialic acid sugar molecule called Neu5Gc showed a significant increase in atherogenesis compared to control mice, who retain the CMAH gene that produces Neu5Gc.

 

 

https://www.scienced...90723182255.htm


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#486 Daniel Cooper

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Posted 24 July 2019 - 02:03 PM

 

 

Unfortunately it does not appear that supplementing Neu5Gc is the answer.  As the article states it is abundant in red meat and they hypothesizes that an immune response to Neu5Gc makes the situation even worse.

 

At the moment it's interesting information, but does not appear at this point to generate any actionable therapy.  It has occurred to me that if you were really living out on the edge and doing CRISPR Cas9 self experimentation (yes, these people do exist) that you might insert a copy of that gene (should be doable), but seems like you might end up with an autoimmune disorder for your troubles.


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#487 Daniel Cooper

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Posted 26 July 2019 - 02:25 PM

Here's one to throw in the mix.
 
Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

Palmitoylethanolamine (the other PEA) seems like a very low risk supplement. I take it for other issues. Nice to see it might have a positive influence on atherosclerosis.
 

If anyone is interested in the full paper I can post it this evening.

 

 



#488 mikey

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Posted 26 July 2019 - 03:32 PM

Here's one to throw in the mix.
 
Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

Palmitoylethanolamine (the other PEA) seems like a very low risk supplement. I take it for other issues. Nice to see it might have a positive influence on atherosclerosis.
 

If anyone is interested in the full paper I can post it this evening.

 

I happen to take 600 - 1000 mg of PEA for pain twice daily, based on a comparative study with hydrocodone - for about six months now. 
This is a good coincidence.

 

I look forward to seeing the full text of the paper.

 

Thank you, Daniel!



#489 Daniel Cooper

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Posted 26 July 2019 - 05:39 PM

So here's a question for the forum -

 

We the standard model of atherosclerosis is that there are two types of arterial plaques:

 

  • Soft plaques that are composed of pathological macrophages which are engorged with cholesterol (i.e foam cells).
  • Hard plaques that are calcium deposits that form to cover over ruptured soft plaques.

 

Let's say that we had some magic elixir that would make soft plaques vanish overnight.  Does it follow that the calcified plaques would dissolve over time or would they be stubbornly persistent?

 

Not to bias anyone, but my suspicion is that it would be the latter.  This might explain why therapies that are known to reduce IMT thickness don't seem to regress calcium scores.

 

 

 



#490 APBT

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Posted 26 July 2019 - 05:49 PM

Tangentially related, a discussion with Peter Attia and Tom Dayspring:
https://www.longecit...-5-part-series/



#491 aribadabar

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Posted 27 July 2019 - 03:02 AM

I look forward to seeing the full text of the paper.

 

Here it is :)


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#492 pamojja

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Posted 27 July 2019 - 10:27 AM

We the standard model of atherosclerosis is that there are two types of arterial plaques:
  • Soft plaques that are composed of pathological macrophages which are engorged with cholesterol (i.e foam cells).
  • Hard plaques that are calcium deposits that form to cover over ruptured soft plaques.

Let's say that we had some magic elixir that would make soft plaques vanish overnight.  Does it follow that the calcified plaques would dissolve over time or would they be stubbornly persistent?

 

Not to bias anyone, but my suspicion is that it would be the latter.  This might explain why therapies that are known to reduce IMT thickness don't seem to regress calcium scores.

 

Can you give a source for your view, that calcified plaque isn't just a later stage, and therefore almost always present with soft plaque? Since even soft-plaque takes many years to grow along with the later calcification.

 

From the TrackYourPlaque experience we know that calcified plaque often at first increases (by calcifying the soft plaque), before it regresses. Not by a magic elixir, but a number of interventions.
 

American Journal of Therapeutics 16, 326–332 (2009)

 

Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH)

Vitamin D on Coronary Calcium Scores in Asymptomatic Adults

 

William Davis, MD, FACC,1* Susie Rockway, PhD, CNS,2
and Mary Kwasny, ScD3

 

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides 60 mg/dL; high-density lipoprotein 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol 224%, low-density lipoprotein 241%; triglycerides 242%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of 214.5% (range 0% to 264%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%–29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%–71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.



#493 pamojja

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Posted 27 July 2019 - 11:11 AM

A sad study summing up the state of cardiology:

 

JAMA. 2019 Mar 19;321(11):1069-1080. doi: 10.1001/jama.2019.1122.

 
Levels of Evidence Supporting American College of Cardiology/American Heart Association and European Society of Cardiology Guidelines, 2008-2018.
 
 

Abstract

 

Importance:

Clinical decisions are ideally based on evidence generated from multiple randomized controlled trials (RCTs) evaluating clinical outcomes, but historically, few clinical guideline recommendations have been based entirely on this type of evidence.

 

Objective:

To determine the class and level of evidence (LOE) supporting current major cardiovascular society guideline recommendations, and changes in LOE over time.

 

Data Sources:

Current American College of Cardiology/American Heart Association (ACC/AHA) and European Society of Cardiology (ESC) clinical guideline documents (2008-2018), as identified on cardiovascular society websites, and immediate predecessors to these guideline documents (1999-2014), as referenced in current guideline documents.

 

Study Selection:

Comprehensive guideline documents including recommendations organized by class and LOE.

 

Data Extraction and Synthesis:

The number of recommendations and the distribution of LOE (A [supported by data from multiple RCTs or a single, large RCT], B [supported by data from observational studies or a single RCT], and C [supported by expert opinion only]) were determined for each guideline document.

 

Main Outcomes and Measures:

The proportion of guideline recommendations supported by evidence from multiple RCTs (LOE A).

 

Results:

Across 26 current ACC/AHA guidelines (2930 recommendations; median, 121 recommendations per guideline [25th-75th percentiles, 76-155]), 248 recommendations (8.5%) were classified as LOE A, 1465 (50.0%) as LOE B, and 1217 (41.5%) as LOE C. The median proportion of LOE A recommendations was 7.9% (25th-75th percentiles, 0.9%-15.2%). Across 25 current ESC guideline documents (3399 recommendations; median, 130 recommendations per guideline [25th-75th percentiles, 111-154]), 484 recommendations (14.2%) were classified as LOE A, 1053 (31.0%) as LOE B, and 1862 (54.8%) as LOE C. When comparing current guidelines with prior versions, the proportion of recommendations that were LOE A did not increase in either ACC/AHA (median, 9.0% [current] vs 11.7% [prior]) or ESC guidelines (median, 15.1% [current] vs 17.6% [prior]).

 

Conclusions and Relevance:

Among recommendations in major cardiovascular society guidelines, only a small percentage were supported by evidence from multiple RCTs or a single, large RCT. This pattern does not appear to have meaningfully improved from 2008 to 2018.

 


Edited by pamojja, 27 July 2019 - 11:15 AM.

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#494 mikey

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Posted 27 July 2019 - 02:39 PM

Think you read him incorrectly, he only said:

 

 

It's because of the higher omega-6 content. Though with the seeds themself the omega-6 content is much less, and not mentioned to avoid by Duke.

 

Be careful about avoiding (essential) omega-6. If you don't eat much processed or prepared foods - or vegetable oil omega-6 sources - you might find that you have an omega-6 deficiency, like I did.

 

For a number of years I took a tablespoon of Carlson The Very Finest Fish Oil (the best source), to get 3,900 mg of (triglyceride form) omega-3 (EPA/DHA), as one tablespoon of liquid a day. 

 

I avoided omega-6 sources in all regards, in restaurants, in my groceries, etc...

 

My white blood cells were always at the very bottom of normal or just below normal. I didn't get sick, but it was notable in my blood tests over many years.

 

I did a comprehensive fatty acid test by Mayo Clinic and it showed low omega-6. I started taking a tablespoon of Life-Flo organic safflower oil to get a daily supply of omega-6. I've also added Dr. Adorable, Inc. Organic Pumpkin Seed Oil occasionally. 

 

When I have another comprehensive fatty acid test my omega-6 test it was in the normal range. As well, my white blood cells rose into the normal range. So THAT was what was causing my chronic low white blood cells!
 
We need a certain amount of both omega-3 and omega-6 as they are counterbalancing agents.

Omega-6 is required for proliferation and inflammation. Controlled inflammation is necessary for overall health. Too much increases risks of inflammatory diseases. Most Americans get something like ten times more than we need. Thus, we experience inflammatory pathologies, such as cardiovascular disease, cancer and diabetes, etc...
 

Omega-3 is inhibitory and anti-inflammatory. Too much and we might find that we bruise excessively, etc... because it is inhibiting blood clotting by preventing blood platelets from clumping together. A 190 pound doctor friend was taking 6,000 mg a day and noticed increased bruising. He found that an optimal dose for him was about the sames as mine. We weighed the same, too.

Americans typically get about 1/10th omega-3 as much as we need. (1/10th, 1/20th ? - I've seen various numbers of great deficiency.)

Just to share: When I started seeing studies in the '90s that omega-3 could reduce arrhythmia (odd heart beats).

 

I began experiencing serious atrial fibrillation (really bad arrhythmia) when I was 25. For years I found a few things that reduced the incidence of atrial fibrillation, but nothing completely stopped it until I began taking 3000+ mg of omega-3s. I was taking 1,000 mg of omega-3s, but this wasn't enough so I raised my daily dose from three capsule/day (about 1,000 mg of omega-3) to 10 capsules (3,000 mg+). I found the Carlson's liquid to be superior to capsules or any other liquids. Also, it has no fishy taste. No fishy burps.

 

Note that for some people, like people with defibrillators, omega-3 can increase arrhythmia.

 

So this is definitely a read-up-on-it and talk with a KNOWLEDGEABLE healthcare practitioner. (Most US doctors know little about this.)

A best reference book is The Omega-3 Connection by Dr. Andrew Stoll, of Harvard. It's a bit old, so there might be something newer that's better, but it's a great reference work. 


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#495 pamojja

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Posted 27 July 2019 - 07:27 PM

Be careful about avoiding (essential) omega-6. If you don't eat much processed or prepared foods - or vegetable oil omega-6 sources - you might find that you have an omega-6 deficiency, like I did.

 

Very strange and I must assume very rare to occure. I too ceased all omega-6 vegetable oil sources, but calculating my macronutrients for almost 3 years I still got about 19g of omega-6 and 9g of plant based omega-3 from nuts (even by prefering macadamias and hazelnut for their lowest polyunsaturated fat content) and seeds each day. Additional 1g dietary from fish and 4g omega-3 content from fishoil.



#496 Rocket

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Posted 28 July 2019 - 12:34 AM

Is there enough info for a sticky on reversing plaque? Cyclodextrin; taurine; mk7; pauling method; pomegranates? Can anyone say factually there are things that work? For example, I know there are some studies that show pomegranates have a slightly positive affect.

Considering this affects everyone at some point in life, considering how many people go to the hospital each day for this, this is important - very important - for lifespan and quality of life for everyone as we age.
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#497 aribadabar

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Posted 28 July 2019 - 02:09 AM

Is there enough info for a sticky on reversing plaque? Cyclodextrin; taurine; mk7; pauling method; pomegranates? Can anyone say factually there are things that work? For example, I know there are some studies that show pomegranates have a slightly positive affect.

Considering this affects everyone at some point in life, considering how many people go to the hospital each day for this, this is important - very important - for lifespan and quality of life for everyone as we age.

 

I would say only people who had regular and detailed imaging (CIMT, CAC scoring, angiograms etc) after doing their documented protocols can conclusively say one way or another.

And then, there is the individual variability due to our differing genetics.

From the regular contributors so far , I think, only Mikey and Pamojja qualify so we need to defer to them about what works, I guess.

If someone else also fit these parameters please share.



#498 dazed1

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Posted 28 July 2019 - 02:40 AM

Can anyone from the mods tell me why was my post deleted (older not new?) i usually never comment and i let mods do their thing, but its strange since i was not saying anything against the rules?



#499 mikey

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Posted 28 July 2019 - 02:46 AM

Very strange and I must assume very rare to occure. I too ceased all omega-6 vegetable oil sources, but calculating my macronutrients for almost 3 years I still got about 19g of omega-6 and 9g of plant based omega-3 from nuts (even by prefering macadamias and hazelnut for their lowest polyunsaturated fat content) and seeds each day. Additional 1g dietary from fish and 4g omega-3 content from fishoil.

 

Yes, very rare and yes, some consider me strange, like a living laboratory with a sense of humor. Sometimes, being only human, I do make mistakes, such as avoiding omega-6 sources until I do a fatty acid blood test and find out that I am deficient.

 

So you were getting a good amount of omega-3 from fish oil, while vegetable sources of omega-3 as alpha-linolenic acid (ALA) and stearidonic acid (SA), are poorly converted in the human body into the omega-3 (EPA/DHA) that is found in animal foods, such as fish and fully grass-fed beef.

 

So vegetable sources almost doesn't count as an omega-3 source. 

 

Although the sources of ALA/SA, such as macadamia nuts, walnuts, hemp seed oil and many others do provide many health benefits for several reasons.

 

The link below is a good reference work on conversion differences between males, females and infants, vegans and non-vegans, etc... It's complex and sometimes counter-intuitive, so I make sure to take supplemental amounts of both EPA/DHA and now omega-6 as linoleic acid from organic safflower oil.

https://livinginnatu...on-ala-epa-dha/
 


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#500 pamojja

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Posted 28 July 2019 - 09:57 AM

I would say only people who had regular and detailed imaging (CIMT, CAC scoring, angiograms etc) after doing their documented protocols can conclusively say one way or another.

..

From the regular contributors so far , I think, only Mikey and Pamojja qualify so we need to defer to them about what works, I guess.

If someone else also fit these parameters please share.

 

Patrick from k-vitamins.com is an other which, if I remember right had even 18 CAC scores, easily accesible through youtube and his side.

 

In this post I pointed to John, which on his own forum is accessible, and already detailed his intervention too:

 

Compare that picture of an diseased aorta with an others old TrackYourPlaque buddy's regression of calcification in the coronaries (click to enlarge):

 

Found further down a thread, where he also prescribes in great detail all interventions, and rationals for them (forum needs signing up, but is for free). If you read it you will find a different approach to mine, as mine is different to Patrick's, which is again different to Dr. William Davis. As in his study:

 

Which already seem to have worked for 44%, before the time he also added K vitamins, dropped statins and niacin in most cases, and other major changes to the studied protocol.

 

 

 


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#501 aribadabar

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Posted 28 July 2019 - 04:20 PM

Found further down a thread, where he also prescribes in great detail all interventions, and rationals for them (forum needs signing up, but is for free).

 

Thanks, I tried registering but the forum seems broken.

 

 Would it be possible to upload the linked thread as a PDF?



#502 pamojja

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Posted 29 July 2019 - 01:38 PM

Thanks, I tried registering but the forum seems broken.

 

 Would it be possible to upload the linked thread as a PDF?

 

The registration process at http://www.heartlifetalk.com/forums/ is not automatic. It requires admin approval for avoiding spams. When registering there is a message to that effect, and approval is usually within 24 hours (most within minutes). With an email message welcoming to HLT. 
 

It's copyrighted. And though this forum has lost much of its former activity, it has acumulated a lot of valueable health-related information well worth signing up.



#503 mikey

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Posted 04 August 2019 - 05:15 PM

I would say only people who had regular and detailed imaging (CIMT, CAC scoring, angiograms etc) after doing their documented protocols can conclusively say one way or another.

And then, there is the individual variability due to our differing genetics.

From the regular contributors so far , I think, only Mikey and Pamojja qualify so we need to defer to them about what works, I guess.

If someone else also fit these parameters please share.

 

Thank you for the honorable mention. But please don't "defer" to me.

I have been on Longecity since 2012 and have seen enough to know that we each must find out what works for ourselves. I, like any of us, am subject to my specific genetics, which are somewhat unusual, and am subject to occasionally having incomplete information. 

 

For instance, I stated that I had seen a publication that showed no difference in tissue-specific effects between vitamin K2 (MK4) and vitamin K2 (MK7), and so I depend on MK7, because it lasts in the body for three days and is taken in mcg. (I take 300-500 mcg/day) where MK4 is has a short half-life (~2 hours) and is undetectable in the bloodstream within 8 hours. So, MK4 should be taken in much greater amounts as mg (1,000 times as much as mcg). I am working my way through my last bottle of Relentless Improvement "Vitamin K2," which provides 15 mg of MK4 and 90 mcg of MK7, taking one capsule a day. (I get the majority of my MK7 from another product.) 

15 mg of MK4 taken three times a day is recommended.

On a busy day when I only had enough time to scan this forum quickly, someone, I think it was pamojja, noted publication that showed that MK4 produced a beneficial effect in one type of arterial tissue and MK7 benefited another type. I didn't have time to focus and investigate it.

If whoever that was would re-post it I would be grateful and get more understanding of perhaps important differing roles in arterial health regarding MK7 and MK4.

Does MK4 provide an important role in arterial health while MK7 provides another?

Thank you in advance. 



#504 Andey

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Posted 05 August 2019 - 02:43 PM

Let me be a devils advocate here.

Looks like we are concentrated too much on the calcium depositions and treat this as end-all progress bar of a heart disease.

What if this is just a coincidental marker of damage and works only when averaged to the the population level, and doesnt reflect disease progression if individual takes supplements that influence calcium metabolism(or that metabolism genetics is different from average)

Ive just put some average numbers into MESA risk calculator and for 80 yo man with zero CAC score 10 year risk is about 10% which is better then 42% for this age but still.

 

As far as I understand it people with zero CAC are 3 times less likely to suffer hard event https://www.ncbi.nlm...les/PMC2766514/, but its still a significant risk.

And I recall hearing that majority of ruptures happen in noncalcified regions of the arteries.

 

Is it possible that shifting calcium metabolism doesnt help much with heart disease an we are just `fixing`  the test result instead of disease?

Shouldnt we concentrate more on soft plague removal, inflammation markers, endothelial health? 

 


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#505 dazed1

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Posted 05 August 2019 - 02:48 PM

Correct on all points.
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#506 pamojja

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Posted 05 August 2019 - 06:29 PM

Is it possible that shifting calcium metabolism doesnt help much with heart disease an we are just `fixing`  the test result instead of disease?

Shouldnt we concentrate more on soft plague removal, inflammation markers, endothelial health? 

 

For me 'reversing artherial plaque' has always meant all of it, calcified or not. And as someone having experienced remission from a walking-disabilty from a 80% blockage at my abdominal aorta bifuraction, I of course wanted to have this remission confirmed by ultrasound meassurements or available other risk markers (also to know and address what drives arterogenic growth). But the primary goal after has always been remission from disabilty.

 

CAC score is just the least invasive and most predictive test to show the disease is already present, and how much it progressed. Or if it regresses with any choosen intervention. I didn't even needed one, since the 80% blockage was already so obvious with my disabilty (and on MRI). CIMT is probably second best and better at confirming regression than MRI.
 

All 'risk-marker' blood-tests are useless for showing that. They are only good for showing what could be co-factors driving the disease-process, and therefore whats needs to be adressed.


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#507 pamojja

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Posted 06 August 2019 - 11:32 AM

On a busy day when I only had enough time to scan this forum quickly, someone, I think it was pamojja, noted publication that showed that MK4 produced a beneficial effect in one type of arterial tissue and MK7 benefited another type. I didn't have time to focus and investigate it.

If whoever that was would re-post it I would be grateful and get more understanding of perhaps important differing roles in arterial health regarding MK7 and MK4.

Does MK4 provide an important role in arterial health while MK7 provides another?

 

Wasn't me. But guess you meant smithx from a page ago:

 

I was asked for references, and so far haven't located the study which showed MK4 but not MK7 affecting coronary artery calcification. However I did come across this study, which found that Mk4 deficiency predicted aortic calcification, but Mk7 deficiency predicted iliac calcification.

 

https://www.ncbi.nlm...pubmed/22692665

 

Most studies about Mk4 and MK7 on k-vitamins.com.
 

Personally I believe the much shorter half-life of MK4 can't be taken by itself to mean lesser potential. For example the half-life of vitamin C in the body with dietary intake is almost a month. With mega-dosing only 1/2 a hour. But one can't expect the same pharmacological effects from dietary intake and that amazing half-life alone.

 

98% of all K vitamins in the brain are found to be MK4. With such high demand in some tissues, its maybe just soaked up from serum that much faster?

 

Therefore I don't bet and get at least sufficent amounts of all three: K1, K2mk4 and K2mk7.
 

From the study smithx posted:

 

 

Vitamin K1 deficiency was the strongest predictor of vertebral fractures (odds ratio [OR], 2.94; 95% confidence interval [CI], 1.38-6.26). MK4 deficiency was a predictor of aortic calcification (OR, 2.82; 95% CI, 1.14-7.01), whereas MK5 deficiency actually protected against it (OR, 0.38; 95% CI, 0.15-0.95). MK7 deficiency was a predictor of iliac calcification (OR, 1.64; 95% CI, 1.03-2.60). The presence of vertebral fractures was also a predictor of vascular calcifications (OR, 1.76; 95% CI, 1.00-3.08).

 

They all seem to work in concert.


Edited by pamojja, 06 August 2019 - 11:38 AM.


#508 mikey

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Posted 17 August 2019 - 04:23 PM

Lest we not forget, spermidine has shown promise in reversing arterial plaque. Revisiting spermidine I find:
 

Mech Ageing Dev. 2013 Apr 20.

The Autophagy Enhancer Spermidine Reverses Arterial Aging.

Larocca TJ, Gioscia-Ryan RA, Jr CM, Seals DR.
Department of Integrative Physiology, University of Colorado, Boulder, Colorado, 80309.

Arterial aging, characterized by stiffening of large elastic arteries and the development of arterial endothelial dysfunction, increases cardiovascular disease (CVD) risk. We tested the hypothesis that spermidine, a nutrient associated with the anti-aging process autophagy, would improve arterial aging. Aortic pulse wave velocity (aPWV), a measure of arterial stiffness, was
20% greater in old (O, 28 months) compared with young C57BL6 mice (Y, 4 months, P<0.05). Arterial endothelium-dependent dilation (EDD), a measure of endothelial function, was 25% lower in O (P<0.05 vs. Y) due to reduced nitric oxide (NO) bioavailability. These impairments were associated with greater arterial oxidative stress (nitrotyrosine), superoxide production, and protein cross-linking (advanced glycation end-products, AGEs) in O (all P<0.05). Spermidine supplementation normalized aPWV, restored NO-mediated EDD and reduced nitrotyrosine, superoxide, AGEs and collagen in O. These effects of spermidine were associated with enhanced arterial expression of autophagy markers, and in vitro experiments demonstrated that vascular protection by spermidine was autophagy-dependent. Our results indicate that spermidine exerts a potent anti-aging influence on arteries by increasing NO bioavailability, reducing oxidative stress, modifying structural factors and enhancing autophagy. Spermidine may be a promising nutraceutical treatment for arterial aging and prevention of age-associated CVD.
PMID: 23612189  http://dx.doi.org/10...mad.2013.04.004 

 

Full text attached.

A post about spermidine found in food stated:
 

Eat your peas.
Eisenberg et al, 2016. Cardioprotection and lifespan extension by the natural polyamine spermidine.
Nature Medicine. doi:10.1038/nm.4222
Here we show that oral supplementation of the natural polyamine spermidine extends the lifespan
of mice and exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic
function in old mice. Spermidine feeding enhanced cardiac autophagy, mitophagy and mitochondrial
respiration, and it also improved the mechano-elastical properties of cardiomyocytes in vivo, coinciding
with increased titin phosphorylation and suppressed subclinical inflammation. Spermidine feeding failed
to provide cardioprotection in mice that lack the autophagy-related protein Atg5 in cardiomyocytes. In
Dahl salt-sensitive rats that were fed a high-salt diet, a model for hypertension-induced congestive heart
failure, spermidine feeding reduced systemic blood pressure, increased titin phosphorylation and
prevented cardiac hypertrophy and a decline in diastolic function, thus delaying the progression to heart
failure. In humans, high levels of dietary spermidine, as assessed from food questionnaires,
correlated with reduced blood pressure and a lower incidence of cardiovascular disease.
 
In July, 2019 Amazon sold 5 grams of the RPI spermidine product to me and sent it to my home. When I ordered directly from companies such as RPI they always required that it be sent to my business address, a large commercial facility. After I received the RPI product RPI sent a note to me telling me that they couldn't deliver to homes and told me to send it back to them.
 
From what I gather Amazon selling RPI spermidine to ship to homes was not allowed until recently.

This apparently means that Amazon will sell it and ship it to a person's home, and RPI can disclaim responsibility. Otherwise, RPI would lose a lot of business.

 

Is anyone here using spermidine or have you considered using it. Turnbuckle just posted that he is stocked up and, therefore, retains it in his protocol. In moving and such I had lost track of it.
 

 

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#509 pamojja

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Posted 17 August 2019 - 05:09 PM

Beside not being available in Europe, I rather stick with what already worked in humans to reverse artherial plaque. Despite many health problems, blood pressure isn't one of them.


Edited by pamojja, 17 August 2019 - 05:10 PM.

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#510 mikey

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Posted 28 August 2019 - 02:45 PM

Beside not being available in Europe, I rather stick with what already worked in humans to reverse artherial plaque. Despite many health problems, blood pressure isn't one of them.

 

With all due respect, elevated blood pressure is an indication of arterial plaque. Contrarily, blood pressure decreasing indicates the potential that arteries are more flexible, possibly because of a decrease in arterial plaque - or at least an improvement in arterial stiffening.

 

I note that, while I am taking numerous supplements, my blood pressure has experienced a significant decrease after I began using a VMAX Elite 7 PowerPlate (at 38 hz/high-intensity) regularly for 5-6 minutes a day. In a week my blood pressure dropped about 10 points both systolic and diastolic, to being more like it was in my 20's. This effect worked significantly better and faster than cardio and sustains. Less is more.

(The only other time that I experienced a tremendous decrease in BP was after two exposures to Dasatinib with Quercetin. A side-effect of slight fat loss was evident with a wrinkle forming below my lower lip. Daredevil reported several facial fat loss with more use DQ than I did. So, I am reticent to use DQ again.)

 

A pro-level powerplate vibrates in three directions, so if one stands on it, one experiences an increase in muscle perfusion to the lower extremities, which can result in a decrease in arterial stiffness, which can induce a blood-pressure lowering effect.Standing on it for 5-6 minutes set at high-intensity shakes everything in your body. It's quite dramatic. 

 

If this effect is supported by good nutritional status, it supports the potential for reformation of the arterial endothelium caused by exercise. This is just preliminary thinking. I will continue to utilize supplements, such as the K-vitamins, and much more, while abstaining from "garbage" foods to supply the raw materials for regeneration.

I have known one 54-year old person that lived on fast (garbage) food and walked 5-7 miles a day. He had the blood pressure of a teen, indicating that consistent regular exercise is a large part of the equation for a healthy cardiovascular system.


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Also tagged with one or more of these keywords: artery, cardiovascular disease, lipids, matrix gla protein, vitamin k2 mk4, vitamin k2 mk7, xanthohumol, plaque

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