591 replies to this topic

[smithx]

Have you tried Activated charcoal?
http://www.ncbi.nlm..../pubmed/2612535

This looks really interesting. What are the downsides?

[mikey]

 

Have you tried Activated charcoal?
http://www.ncbi.nlm..../pubmed/2612535

This looks really interesting. What are the downsides?

 

 

Charcoal affects blood lipids that I have no problem with.

[Daniel Cooper]

Reviving this old thread.  I'm curious if those of you that were supplementing with high doses of K2 (m4 and m7) in 2013 have done any calcium scores subsequently that show a reversal of arterial calcium deposits?

 

As you might guess, I recently had a calcium score that came out higher than I might like (64).

 

Any real world experience in reversing arterial calcium deposits would be most welcome.

 

 

[zen]

Take a look on Dr. Greger's presentation below.

 

 

If you want to know more consider reading his recently published book http://www.amazon.co...=how not to die

 

 

 

Reviving this old thread.  I'm curious if those of you that were supplementing with high doses of K2 (m4 and m7) in 2013 have done any calcium scores subsequently that show a reversal of arterial calcium deposits?

 

As you might guess, I recently had a calcium score that came out higher than I might like (64).

 

Any real world experience in reversing arterial calcium deposits would be most welcome.

 

Edited by zen, 11 March 2016 - 07:29 PM.

[Daniel Cooper]

Thanks Zen.

 

A little update.  So, I went to see a cardiologist yesterday to talk about the results from my calcium score.  I was hoping to hear, something like "you're not in any immediate danger, but you need to make some lifestyle modifications so you don't have trouble down the road".  Instead what I heard was, "well, your lipid panel looks good and your blood pressure is fine, but 60 of the 64 score is all in your left anterior descending artery which is not a good place for a blockage.  You've had some chest pains that are probably GERD, but I'd like to do a CT angiogram just to be sure.  And here's some Lipitor, start taking these.". 

 

This has got me a bit freaked out.

 

I've starting taking the LifeExtension Super K (1500mcg K1, 1000mcg K2mk2, 200mcg K2mk7). 

 

Do any of you experience flushing from this supplement?  I'd say about 30minutes to an hours after taking this I have protracted flushing - red hot ears, red hot face, etc.  This flushing seems to last for about 4 hours.  Anyone else get this on a moderately high does of K complex?

 

 

 

Edited by Daniel Cooper, 11 March 2016 - 08:19 PM.

[Supierce]

No flushing here, but I use Vitacost "Ultra Vitamin K with Advanced K2 Complex" and highly recommend it.

Better luck with your future results!

Edited by Supierce, 11 March 2016 - 09:06 PM.

[zorba990]

No flushing ever from Koncentrated K.
Vitamin K2 (MK-4)
(Menaquinone 4) 25 mg
Vitamin K1
(Phylloquinone) 5 mg

Vitamin K2 (MK-7)
(Menaquinone 7) 0.5 mg

Astaxanthin
(from Haematococcus pluvialis extract)

2 mg

***

[Daniel Cooper]

Great info guys.

 

I'm still interested in hearing stories from people that had a higher cardiac calcium score, starting supplementing with K2, and then a year or two later retested.

 

I'd like to hear the results, positive or negative.

 

 

Edited by Daniel Cooper, 12 March 2016 - 01:05 AM.

[Adaptogen]

kyolic aged garlic extract is worth looking into too. there is a lot of research demonstrating that it can reduce or halt the progression of atherosclerosis

[Daniel Cooper]

Another question:  Is there any concern that these high doses of vitamin K might promote excessive clotting?  One would guess that excessive clotting would be a *bad thing* if you have partially blocked coronary arteries.

 

 

 

[niner]

Another question:  Is there any concern that these high doses of vitamin K might promote excessive clotting?  One would guess that excessive clotting would be a *bad thing* if you have partially blocked coronary arteries.

 

That shouldn't be a problem.  Warfarin, a well known anti-coagulant, acts by inducing a vitamin K deficiency.  Vitamin K is needed in order to modify certain proteins that are involved in clotting, and when there isn't enough K around, they don't work properly.  Vitamin K is therefore an "antidote" to Warfarin.  However, having extra K around does not make your blood clot more.  Once the proteins are modified, they're done.  They won't get more carboxylated no matter how much K is on board.  The Wiki entry on vitamin K says this about it:

 

 

Blood clotting (coagulation) studies in humans using 45 mg per day of vitamin K₂ (as MK-4)^[53] and even up to 135 mg/day (45 mg three times daily) of K₂ (as MK-4),^[54] showed no increase in blood clot risk. Even doses in rats as high as 250 mg/kg body weight did not alter the tendency for blood-clot formation to occur.^[55]

[Daniel Cooper]

 

Another question:  Is there any concern that these high doses of vitamin K might promote excessive clotting?  One would guess that excessive clotting would be a *bad thing* if you have partially blocked coronary arteries.

 

That shouldn't be a problem.  Warfarin, a well known anti-coagulant, acts by inducing a vitamin K deficiency.  Vitamin K is needed in order to modify certain proteins that are involved in clotting, and when there isn't enough K around, they don't work properly.  Vitamin K is therefore an "antidote" to Warfarin.  However, having extra K around does not make your blood clot more.  Once the proteins are modified, they're done.  They won't get more carboxylated no matter how much K is on board.  The Wiki entry on vitamin K says this about it:

 

 

Blood clotting (coagulation) studies in humans using 45 mg per day of vitamin K₂ (as MK-4)^[53] and even up to 135 mg/day (45 mg three times daily) of K₂ (as MK-4),^[54] showed no increase in blood clot risk. Even doses in rats as high as 250 mg/kg body weight did not alter the tendency for blood-clot formation to occur.^[55]

 

 

 

Thanks Niner.  Good to know.

 

It's interesting that Warfarin is used to generate a rat model of atherosclerosis.

 

Incidentally, I asked the cardiologists that I saw if he knew anything about vitamin K being effective at slowing or even reversing calcium plaques.  He looked at me like I was from Mars.  His comment was "why would anyone think that would work?".  My reply was "well since warfarin antagonizes the recycling of K1 and it can cause atherosclerosis somebody probably got the idea that there might be a link there".  

 

So, anyone think that an AGE breaker like ALT-711 might be useful at reversing arterial calcium plaques?  Did Alteon ever conduct any trials for that?

 

 

[zen]

Hi Daniel,

​I forgot to mention that the part of Dr. Greger's presentation (see my post #64) which might be of interest to you starts at 40min 30sec.

I have changed my diet about 6 weeks ago and my personal experience so far is:
​a) I have lost about 10 lb of body weight,
​b) my blood pressure which was in the range ~ 140/90 dropped to ~125/80.

​Finally, I take LEF Super K daily without any noticeable side effects.

​HTH

 

Thanks Zen.

 

A little update.  So, I went to see a cardiologist yesterday to talk about the results from my calcium score.  I was hoping to hear, something like "you're not in any immediate danger, but you need to make some lifestyle modifications so you don't have trouble down the road".  Instead what I heard was, "well, your lipid panel looks good and your blood pressure is fine, but 60 of the 64 score is all in your left anterior descending artery which is not a good place for a blockage.  You've had some chest pains that are probably GERD, but I'd like to do a CT angiogram just to be sure.  And here's some Lipitor, start taking these.". 

 

This has got me a bit freaked out.

 

I've starting taking the LifeExtension Super K (1500mcg K1, 1000mcg K2mk2, 200mcg K2mk7). 

 

Do any of you experience flushing from this supplement?  I'd say about 30minutes to an hours after taking this I have protracted flushing - red hot ears, red hot face, etc.  This flushing seems to last for about 4 hours.  Anyone else get this on a moderately high does of K complex?

 

Edited by zen, 13 March 2016 - 04:04 PM.

[Daniel Cooper]

 

Could you list the specific supplement brands you're taking. I have been looking for a decent vitamin K formula for a while.

Some of the Track Your Plaque crowd use:

1. Koncentrated K at www.K-vitamins.com with a 30.5mg Vit K pill (25mg MK4, 5mg K1 and .5mg MK7. I use this one. I haven't checked my calcium score yet( probably in Dec I will), but total cholesterol dropped from 237 to 200.

2. Osteo-K is found on Amazon and it carries a 3 pill serving that has 22.5mg of Vit MK2 (<MK7 and MK4). TheThis pill is designed to support two servings totaling 6 pills with a total of 45mg of Vitamin K. That is the dose used with success in Japan.

 

 

Are any of you on the Track Your Plaque website?  

 

I bought the book and looked at the website.  It seems super commercial, heavily oriented around selling me things.  I haven't given them any money yet.  Just wanted to see if anyone else recommended it (or not).

Edited by Daniel Cooper, 16 March 2016 - 09:32 PM.

[pamojja]

Are any of you on the Track Your Plaque website?  

 

Have been a member of the old TrackYourPlaque forum for a number of years, since that time it has been replaced with http://www.cureality.com/. Though the old side is still up and mirrors the forum content of the new, but for it's biggest part isn't functioning and updated anymore. At the new side you could take a look at the first forum posts (and replies not longer than 250 characters) to get an idea of what's going.

 

I've never purchased anything than the quarter yearly membership fees for the excellent community support at the forum. Then, because the lack of moderation, one member took over the conversation with very bad manners, that's why many left to have a free and moderated version of the forum at http://www.heartlifetalk.com/.

 

Not long after, the disrupting member was finally banned, therefore I can recommend the new Cureality forum for community support again.

[david ellis]

 

 

Could you list the specific supplement brands you're taking. I have been looking for a decent vitamin K formula for a while.

Some of the Track Your Plaque crowd use:

1. Koncentrated K at www.K-vitamins.com with a 30.5mg Vit K pill (25mg MK4, 5mg K1 and .5mg MK7. I use this one. I haven't checked my calcium score yet( probably in Dec I will), but total cholesterol dropped from 237 to 200.

2. Osteo-K is found on Amazon and it carries a 3 pill serving that has 22.5mg of Vit MK2 (<MK7 and MK4). TheThis pill is designed to support two servings totaling 6 pills with a total of 45mg of Vitamin K. That is the dose used with success in Japan.

 

 

Are any of you on the Track Your Plaque website?  

 

I left the website.  It cost more than it was worth to me.  In 2009 I got a CT- scan of my calcium in my coronary arteries.  The score was about 100 mg.    I tried to get a similar scan so I would have an idea about which way the wind was blowing.   I asked for a basic calcium scan and I got a calcium scan called Agaston.   Instead of a simple calcium total, I got a calcium score that reported a risk number, which was a combination of calcium content and its location to determine risk.    The $100 basic calcium CT-count  has disappeared from website price lists.   The Agatston score is there and it is expensive.   I found one 

 

Koncentrated K has interesting research on his website about what he has learned. (www.k-vitamins.com)

 

 

 Koncentrated K has a good recap of his experience on his website.  

 

 

Edited by david ellis, 17 March 2016 - 10:19 PM.

[zorba990]

What about chondroitin sulfate?

From
https://drrichardsta...roitin-sulfate/

"simple nutrient: chondroitin sulfate (CS) – was proven to reduce plaque formation in atherosclerosis. In fact, it had been demonstrated to remove plaque from arterial walls. I was astounded that it was not in general use, since the information has been in the medical literature since the 1970’s and 1980’s. The gentleman who did the research comes with the highest medical credentials, as well. He was Dr. Lester Morrison, Chairman of the Department of Atherosclerosis Research at Loma Linda University. His discovery was truly life-saving. In one long-term study lasting 6 years, only 7% of the patients receiving CS died from cardiovascular disease, compared to 23% in the control group. Nonfatal cardiac events were similarly decreased. An animal study conducted at the same time demonstrated that cardiovascular disease was reversed in monkeys with oral administration of CS."

[bocor]

Look into studies on blueberries it reversed atherosclerosis in mice it also increases gag levels in veins and arteries and also obviously tocotrienols

[Tom Andre F. (ex shinobi)]

stop consuming fluoride and dairy and consume:

 

magnesium, vit D, vit K2 (MK7 forms is compulsory, do not go for the mk9), omega 3s parent forms in order to totally manage the calcium and decalcify the artery. Dont forget also that old cells also produce the calcium.

Edited by Tom Andre F. (ex shinobi), 18 March 2016 - 01:55 AM.

[Ohm]

Look into studies on blueberries it reversed atherosclerosis in mice it also increases gag levels in veins and arteries and also obviously tocotrienols

 

 

 

Here are a few,

 

 

J Nutr. 2010 Sep;140(9):1628-32. doi: 10.3945/jn.110.123927. Epub 2010 Jul 21.

Dietary blueberries attenuate atherosclerosis in apolipoprotein E-deficient mice by upregulating antioxidant enzyme expression.

Wu X1, Kang J, Xie C, Burris R, Ferguson ME, Badger TM, Nagarajan S.

Author information

 

Abstract

Protective effects of blueberries (BB) against atherosclerosis and potential underlying mechanisms in reducing oxidative stress were examined in apoE-deficient (apoE(-/-)) mice. ApoE(-/-) mice were fed an AIN-93G diet (CD) or CD formulated to contain 1% freeze-dried whole BB for 20 wk. The mean lesion area for apoE(-/-) mice fed BB was reduced by 39% (P < 0.001) in the aorta sinus and 58% (P < 0.001) in the descending aorta compared with CD-fed mice. These atheroprotective effects were independent of the serum lipid profile or total antioxidant capacity (as measured by oxygen radical absorbance capacity). The concentration of a biomarker of lipid peroxidation, F(2)-isoprostane, was lower in liver of BB-fed mice (P < 0.05). Genes analyzed by RT-PCR array showed that 4 major antioxidant enzymes in aorta [superoxide dismutase (SOD) 1, SOD2, glutathione reductase (GSR), and thioredoxin reductase 1] were upregulated in BB-fed mice. Enzyme activities of SOD and GSR were greater (P < 0.05) in liver and/or serum of BB-fed mice than those of CD-fed mice. In addition, serum paraoxonase 1 activity in serum of BB-fed mice was also greater than that of CD-fed mice (P < 0.05) at the end of the study. These results suggest a protective effectiveness of BB against atherosclerosis in this apoE(-/-) mouse model. The potential mechanisms may involve reduction in oxidative stress by both inhibition of lipid peroxidation and enhancement of antioxidant defense.

PMID:   20660283   [PubMed - indexed for MEDLINE]   

 

 

 

Food Funct. 2011 Oct;2(10):588-94. doi: 10.1039/c1fo10136f. Epub 2011 Sep 28.

Lowbush blueberries inhibit scavenger receptors CD36 and SR-A expression and attenuate foam cell formation in ApoE-deficient mice.

Xie C1, Kang J, Chen JR, Lazarenko OP, Ferguson ME, Badger TM, Nagarajan S, Wu X.

Author information

 

Abstract

Blueberries have recently been reported to reduce atherosclerotic lesion progression in apoE deficient (apoE(-/-)) mice. However, the underlying mechanisms are not fully understood. The objective of this study was to determine whether lowbush blueberries altered scavenger receptor expression and foam cell formation in apoE(-/-) mice. ApoE(-/-) mice were fed AIN-93 diet (CD) or CD formulated to contain 1% freeze-dried lowbush blueberries (BB) for 20 weeks. Gene expression and protein levels of scavenger receptor CD36 and SR-A in aorta and thioglycollate-elicited peritoneal macrophages (PM) were lower in mice fed BB (P < 0.05). In the second experiment, apoE(-/-) mice were fed CD or BB for 5 weeks. PM were collected and cultured. Gene expression and protein levels of CD36 and SR-A were found to be lower in PM of BB fed mice (P < 0.05). In PM from BB fed mice, fewer oxLDL-induced foam cells were formed compared to those from mice fed CD. Gene expression and protein levels of PPARγ were lower in the PM of BB fed mice (P < 0.05). Detectable isomers of hydroxyoctadecadienoic acids (HODEs) and hydroxyeicosatetraenoic acid (HETEs) were also lower in the PM of BB fed mice (P < 0.05 or P < 0.01). In conclusion, BB inhibited expression of the two major scavenger receptors CD36 and SR-A in PM of apoE(-/-) mice, at least in part through down-regulating PPARγ and reducing its endogenous ligands HODEs and HETEs. We proposed that BB mediated reduction of scavenger receptor expression and attenuation of oxLDL-induced foam cell formation in PM of apoE(-/-) mice are important mechanisms of the athero-protective effects of BB.

PMID:   21952555   [PubMed - indexed for MEDLINE]

 

The decreases in systolic and diastolic blood pressures were greater in the blueberry-supplemented group (− 6 and − 4%, respectively) than in controls (− 1.5 and − 1.2%) (P lt 0.05), whereas the serum glucose concentration and lipid profiles were not affected. The decreases in plasma oxidized LDL and serum malondialdehyde and hydroxynonenal concentrations were greater in the blueberry group (− 28 and − 17%, respectively) than in the control group (− 9 and − 9%) (P lt 0.01). Our study shows blueberries may improve selected features of metabolic syndrome and related cardiovascular risk factors at dietary achievable doses.

 

http://www.ncbi.nlm....les/PMC2924596/

[mikey]

stop consuming fluoride and dairy and consume:

 

magnesium, vit D, vit K2 (MK7 forms is compulsory, do not go for the mk9), omega 3s parent forms in order to totally manage the calcium and decalcify the artery. Dont forget also that old cells also produce the calcium.

 

Hello Tom,

What data do you base using the "parent forms" of omega 3's, meaning alpha linolenic acid (ALA) - that is the one parent form precursor to EPA/DHA.

 

I've read Peskin's thoughts on parent forms of omega's.

 

While 4,000 mg/day of EPA/DHA from fish oil stops me from having dozens of years of acute chronic atrial fibrillation - 10-15 events a year - no vegetable sources of ALA help at all.

 

So, Perkin's theories don't work in my personal experience.

 

Many blessings,

Michael

[Tom Andre F. (ex shinobi)]

 

stop consuming fluoride and dairy and consume:

 

magnesium, vit D, vit K2 (MK7 forms is compulsory, do not go for the mk9), omega 3s parent forms in order to totally manage the calcium and decalcify the artery. Dont forget also that old cells also produce the calcium.

 

Hello Tom,

What data do you base using the "parent forms" of omega 3's, meaning alpha linolenic acid (ALA) - that is the one parent form precursor to EPA/DHA.

 

I've read Peskin's thoughts on parent forms of omega's.

 

While 4,000 mg/day of EPA/DHA from fish oil stops me from having dozens of years of acute chronic atrial fibrillation - 10-15 events a year - no vegetable sources of ALA help at all.

 

So, Perkin's theories don't work in my personal experience.

 

Many blessings,

Michael

 

 

Hi Michael,

 

Actually we need the full spectrum fatty acids and mainly: ALA, LA, AA, DHA

 

Concerning fish oil there is a paradox, they help people prone with heart disease but make health people prone for these disease on the long run.

 

I also think we have to avoid the oxygen exposure to oils (pv value increase) and make sure to consume the foods in their raw forms or in capsules

 

the topic is too complexe i think to be taken like that, and im not an expert unfortunately, its just what i may remember.

 

EDIT: I think the ideal is to mix some ingredients and do not forget saturated fat such as coconot oil

 

Spirulina, coconout oil, flax seed, purslane, sunflower..

 

 

Edited by Tom Andre F. (ex shinobi), 27 March 2016 - 07:34 PM.

[Ohm]

Concerning fish oil there is a paradox, they help people prone with heart disease but make health people prone for these disease on the long run.

 

Reference?

[Darryl]

The thickening of the artery intima & media isn't what causes infarctions, its the rupture of plaques and downstream thrombosis. Those ruptures largely occur due to inflammation, as innate immune cells release matrix metalloproteinases and radicals that degrade collagen in the fibrous cap of plaques.

 

The number one thing to prevent endothelial inflammation/dysfunction and prevent ruptures appears to be avoiding postprandial lipemia, and the associated proinflammatory chylomicron fragments and endotoxin transport. The Esselstyn-diet trials, despite their flaws (small samples, no blinding, no randomized controls), provide a pretty convincing argument that endothelial inflammation and plaque rupture can be largely avoided with extremely low-fat diets, with angina resolving in weeks, and plaque regression in a few years.

 

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.

 

Some low-fat diet trials that reversed atherosclerosis:

Ornish D et al., 1990. Can lifestyle changes reverse coronary heart disease?: The Lifestyle Heart Trial. The Lancet, 336(8708), pp.129-133.

Esselstyn CB. 1999. Updating a 12-year experience with arrest and reversal therapy for coronary heart disease (an overdue requiem for palliative cardiology). American Journal of Cardiology, 84(3), pp.339-341.

Esselstyn CB et al. 2014. A way to reverse CAD?. Journal of Family Practice, 63(7), pp.356-364.

 

Relevant papers/reviews focussing on the postprandial state and endothelial inflammation/dysfunction.

Shah PK et al. 1995. Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture. Circulation, 92(6), pp.1565-1569.

Aikawa M et al. 1998. Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma a potential mechanism of lesion stabilization. Circulation, 97(24), pp.2433-2444.

Roche HM & Gibney MJ, 2000. The impact of postprandial lipemia in accelerating atherothrombosis. European Journal of Cardiovascular Risk,7(5), pp.317-324.

Newby AC. 2005. Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture. Physiological reviews,85(1), pp.1-31.

Alipour A et al. 2007. Postprandial inflammation and endothelial dysfuction.Biochemical Society Transactions, 35(3), pp.466-469.

Wallace JP et al. 2010. Postprandial lipaemia, oxidative stress and endothelial function: a review. International journal of clinical practice, 64(3), pp.389-403.

Vafeiadou K et al. 2012. A review of the evidence for the effects of total dietary fat, saturated, monounsaturated and n-6 polyunsaturated fatty acids on vascular function, endothelial progenitor cells and microparticles. British Journal of Nutrition, 107(03), pp.303-324.

Schwingshackl .L and Hoffmann G. 2013. Low-carbohydrate diets impair flow-mediated dilatation: evidence from a systematic review and meta-analysis. British Journal of Nutrition, 110(05), pp.969-970.

Herieka M and Erridge C. 2014. High‐fat meal induced postprandial inflammation. Molecular nutrition & food research, 58(1), pp.136-146.

 

Postprandial endotoxins/lipopolysaccharide (LPS): emerging as a central causal agent in postprandial endothelial inflammation/dysfunction and cardiovascular disease. Dietary interventions to reduce endotoxemia revolve around increasing FODMAP/prebiotic and polyphenol/hormetin intake.

 

Wiedermann CJ et al, 1999. Association of endotoxemia with carotid atherosclerosis and cardiovascular disease: prospective results from the Bruneck Study. Journal of the American College of Cardiology, 34(7), pp.1975-1981.

Stoll LL et al. 2006. Endotoxin, TLR4 signaling and vascular inflammation: potential therapeutic targets in cardiovascular disease. Current pharmaceutical design, 12(32), pp.4229-4245.

Triantafilou M et al 2007. Lipopolysaccharides from atherosclerosis‐associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2‐induced inflammatory responses in human vascular endothelial cells.Cellular microbiology, 9(8), pp.2030-2039.

Pussinen PJ et al 2007. Endotoxemia, immune response to periodontal pathogens, and systemic inflammation associate with incident cardiovascular disease events. Arteriosclerosis, thrombosis, and vascular biology, 27(6), pp.1433-1439.

Erridge C et al. 2007. A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. The American journal of clinical nutrition, 86(5), pp.1286-1292.

Reifenberg K et al. 2009. Endotoxin accelerates atherosclerosis independent of complement activation.Thrombosis research, 123(4), pp.653-658.

Ghoshal S et al. 2009. Chylomicrons promote intestinal absorption of lipopolysaccharides. Journal of lipid research, 50(1), pp.90-97.

Wiesner P et al. 2010. Low doses of lipopolysaccharide and minimally oxidized LDL cooperatively activate macrophages via NF-κB and AP-1:a possible mechanism for acceleration of atherosclerosis by subclinical endotoxemia. Circulation research, 107(1), pp.56-65.

Pendyala S et al. 2012. A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology, 142(5), pp.1100-1101.

Harte AL et al. 2012. High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects. Diabetes care, 35(2), pp.375-382.

Moreira APB et al. 2012. Influence of a high-fat diet on gut microbiota, intestinal permeability and metabolic endotoxaemia. British Journal of Nutrition, 108(05), pp.801-809.

Yi P et al. 2013. The endotoxin/toll-like receptor-4 axis mediates gut microvascular dysfunction associated with post-prandial lipidemia. BMC physiology, 13(1), p.1.

Schilling JD et al. 2013. Palmitate and lipopolysaccharide trigger synergistic ceramide production in primary macrophages. Journal of Biological Chemistry, 288(5), pp.2923-2932.

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

Aravindhan V et al. 2013. Increased levels of endotoxin core antibodies and decreased Levels of sCD 14 indicate chronic endotoxemia in coronary artery disease. Journal of Clinical & Experimental Cardiology, 2013.

Neves AL et al. 2013. Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk. Journal of molecular endocrinology, 51(2), pp.R51-R64.

Shen W et al. 2014. Influence of dietary fat on intestinal microbes, inflammation, barrier function and metabolic outcomes.The Journal of nutritional biochemistry, 25(3), pp.270-280.

Liu H. et al. 2014. A rabbit model of spontaneous thrombosis induced by lipopolysaccharide. Journal of atherosclerosis and thrombosis,21(10), pp.1075-1086.

 

 

[Tom Andre F. (ex shinobi)]

 

Concerning fish oil there is a paradox, they help people prone with heart disease but make health people prone for these disease on the long run.

 

Reference?

 

 

as explained, for that topic i should take lot of time to enter in again and i have not.

 

However, you can start from some author who spent time to study the question https://chriskresser...tial-after-all/

 

and then of course: http://brianpeskin.c...ts/PEO-Info.pdf that i respect even more

 

Its really make sense since for instance (from wikipedia with attached references below..):

 

"

Collins et al. 1970^[9] were the first to demonstrate linoleic acid deficiency in adults. They found that patients undergoing intravenous nutrition with glucose became isolated from their fat supplies and rapidly developed biochemical signs of essential fatty acid deficiency (an increase in 20:3n-9/20:4n-6 ratio in plasma) and skin symptoms. This could be treated by infusing lipids, and later studies showed that topical application of sunflower oil would also resolve the dermal symptoms.^[10]Linoleic acid has a specific role in maintaining the skin water-permeability barrier, probably as constituents of acylglycosylceramides. This role cannot be met by any ω-3 fatty acids or by arachidonic acid.

The main physiological requirement for ω-6 fatty acids is attributed to arachidonic acid. Arachidonic acid is the major precursor of prostaglandins, leukotrienes, and anandamides that play a vital role in cell signaling. Metabolites from the ω-3 pathway, mainly from eicosapentaenoic acid, are mostly inactive, and this explains why ω-3 fatty acids do not correct the reproductive failure in rats where arachidonic is needed to make active prostaglandins that cause uterine contraction.^[11] To some extent, any ω-3 or ω-6 can contribute to the growth-promoting effects of EFA deficiency, but only ω-6 fatty acids can restore reproductive performance and correct the dermatitis in rats. Particular fatty acids are still needed at critical life stages (e.g. lactation) and in some disease states.

."

 

9 "Plasma lipids in human linoleic acid deficiency.". Nutr Metab 13 (3): 150–67. 1971. doi:10.1159/000175332. PMID 5001758.

10 Prottey, C; Hartop, PJ; Press, M (1975). "Correction of the cutaneous manifestations of essential fatty acid deficiency in man by application of sunflower-seed oil to the skin.". J Invest Dermatol 64 (4): 228–34. doi:10.1111/1523-1747.ep12510667. PMID 1117180.

11 Sanders T and Emery P. The Molecular Basis of Human Nutrition, Taylor Frances, London, 2003 ISBN 0-748-40753-7

 

So sorry to not reply directly to the question but its because for that we have to understand about what we are speaking about: first w3/w6 has to be taken with grain of salt, second difference have to be made between processed and not, and then the fact that parent essential oil are maybe far better than their derivatives.. EFA works well as short term I still believe. In the past i seen lot of people also complaining about how bad effect krill oil was on them after some time (just after the hype around this product)
 

Edited by Tom Andre F. (ex shinobi), 28 March 2016 - 12:02 AM.

[Daniel Cooper]

I found this an interesting read:

 

 

 

New Alternatives for Atherosclerosis Treatment Based on Immunomodulation

http://www.hindawi.c...rn/2012/785094/

 

 

I'm be interested to hear anyone with a bit more background in the subject take on it.

 

 

 

[mikey]

 

 

stop consuming fluoride and dairy and consume:

 

magnesium, vit D, vit K2 (MK7 forms is compulsory, do not go for the mk9), omega 3s parent forms in order to totally manage the calcium and decalcify the artery. Dont forget also that old cells also produce the calcium.

 

Hello Tom,

What data do you base using the "parent forms" of omega 3's, meaning alpha linolenic acid (ALA) - that is the one parent form precursor to EPA/DHA.

 

I've read Peskin's thoughts on parent forms of omega's.

 

While 4,000 mg/day of EPA/DHA from fish oil stops me from having dozens of years of acute chronic atrial fibrillation - 10-15 events a year - no vegetable sources of ALA help at all.

 

So, Perkin's theories don't work in my personal experience.

 

Many blessings,

Michael

 

 

Hi Michael,

 

Actually we need the full spectrum fatty acids and mainly: ALA, LA, AA, DHA

 

Concerning fish oil there is a paradox, they help people prone with heart disease but make health people prone for these disease on the long run.

 

I also think we have to avoid the oxygen exposure to oils (pv value increase) and make sure to consume the foods in their raw forms or in capsules

 

the topic is too complexe i think to be taken like that, and im not an expert unfortunately, its just what i may remember.

 

EDIT: I think the ideal is to mix some ingredients and do not forget saturated fat such as coconot oil

 

Spirulina, coconout oil, flax seed, purslane, sunflower..

 

 

Like Ohm, I'd like to see a reference to the statement "Concerning fish oil there is a paradox, they help people prone with heart disease but make health people prone for these disease on the long run."

[zen]

Just a quick follow up.
Yesterday my wife got her blood lipid test results after following the vegan diet for about 8 weeks, all without any cholesterol lowering drugs.

 

The before diet results from Jan 14, 2016 were:

 

Cholesterol Total: 257
HDL: 83
Triglycerides: 51
VLDL: 10
LDL (Calculated): 164

 

The new results from March 29, 2016

 

Cholesterol Total: 158
HDL: 62
Triglycerides: 57
VLDL: 11
LDL (Calculated): 85

 

 

Hi Daniel,

​I forgot to mention that the part of Dr. Greger's presentation (see my post #64) which might be of interest to you starts at 40min 30sec.

I have changed my diet about 6 weeks ago and my personal experience so far is:
​a) I have lost about 10 lb of body weight,
​b) my blood pressure which was in the range ~ 140/90 dropped to ~125/80.

​Finally, I take LEF Super K daily without any noticeable side effects.

​HTH
 

 

Edited by zen, 02 April 2016 - 03:19 PM.

[Rocket]

Just a quick follow up.
Yesterday my wife got her blood lipid test results after following the vegan diet for about 8 weeks, all without any cholesterol lowering drugs.

The before diet results from Jan 14, 2016 were:

Cholesterol Total: 257
HDL: 83
Triglycerides: 51
VLDL: 10
LDL (Calculated): 164

The new results from March 29, 2016

Cholesterol Total: 158
HDL: 62
Triglycerides: 57
VLDL: 11
LDL (Calculated): 85

Hi Daniel,

​I forgot to mention that the part of Dr. Greger's presentation (see my post #64) which might be of interest to you starts at 40min 30sec.

I have changed my diet about 6 weeks ago and my personal experience so far is:
​a) I have lost about 10 lb of body weight,
​b) my blood pressure which was in the range ~ 140/90 dropped to ~125/80.

​Finally, I take LEF Super K daily without any noticeable side effects.

​HTH

I'm happy for your wife. But this goes to show how genetics really dictate health and life span. Your wife's AFTER results are about what my levels are on a high protein (200g or greater) diet full of meat, eggs, nuts, and healthy carbs with far,far too little veggies.

I'm on a self imposed diet (for mass gain) that would really negatively affect a lot of people's health and my genetics just shrugs it off.

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.

[pamojja]

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.