Plaque is the stuff of coronary heart disease. It is CONTROLLABLE, it is STOPPABLE, it is REVERSIBLE.
But you must be equipped with the right information on diet, nutritional supplements, and hopefully the avoidance of medication.
This is the blog that accompanies the 
Here are the results from the latest Heart Scan Blog poll:
What is your dose of omega-3 fatty acids, EPA + DHA, from fish oil? (Add up the total content of EPA + DHA per capsules; multiply times number of capsules.)
The 479 respondents answered:
Less than 1000 mg per day
65 (13%)
1000-1999 mg per day
145 (30%)
2000-2999 mg per day
98 (20%)
3000-3999 mg per day
79 (16%)
4000-4999 mg per day
33 (6%)
5000-5999 mg per day
14 (2%)
6000 mg per day or more
45 (9%)
The poll did not discriminate between who has heart disease, who does not; who is taking omega-3 fatty acids for high triglycerides or for reduction of lipoprotein(a) (which requires high doses), or other indications. So variation is to be expected.
We can say that nearly all respondents are likely receiving sufficient omega-3s to impact cardiovascular risk, since the benefits begin just by consuming fish twice per month. I am especially impressed at the proportion of respondents (53%) who take at least 2000 mg per day of EPA + DHA. It’s clear that people are really embracing the notion that omega-3 fatty acids pack a real wallop of health benefits.
Because different people in different situations and lipid/lipoprotein patterns have different omega-3 needs, there is really no “right” or “wrong” dose of omega-3 fatty acids.
However, there are several factors that enter into knowing your ideal omega-3 intake:
–Higher triglycerides require higher doses
–Lipoprotein(a) can respond to higher doses
–Having coronary or carotid plaque means you desire a “therapeutic” dose of omega-3s, not just a “preventive” dose
Time is a factor, also: The longer you take omega-3s, the higher your blood levels go. You can accelerate the replacement of non-omega-3s with higher doses of omega-3s.
But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL.
Much of the uncertainty about dosing will also be cleared up as we get more experience with the Omega-3 RBC Index, i.e, the proportion of fatty acids in red blood cells that are omega-3s. We are currently aiming for an Omega-3 Index of 10%, given the heart attack reductions observed at this level.
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I take 6000 units daily or more, but I also consume a few tablespoons of ground flax seed daily as well.
AND still eat fish a few times a week, especially oil rich sardines.
Homertobias:
Lots of interesting work being done on pericardial adipose tissue (PAT) and using CT imaging done in conjunction with CAC scoring to more precisely determine the relationship between PAT and the development of CAD and calcified plaques, i.e., in order to more precisely "score" the level of PAT and to determine association and/or causality with calcific lesions.
Dr. Lerber at University Hospital in Munich, Germany has observed that PAT accumulation precedes the development of calcified plaques, that increased volume of PAT are associated with reduced levels of adiponectin and higher CRP. So the idea is that with more precise measurements and concomittant imaging of both PAT and CAC, we might be able to better detect the presence of disease in an earlier stage. There is also some push among those doing such research to link PAT thickness assessment with administering routine echo stress testing but this hasn't gained much traction yet other than in a small circle of folks. The hope though is that PAT can also be used as another surrogate marker for diagnosing preclinical atherosclerosis.
But as of now, I don't think anyone who does a routine CAC scan, whether with MDCT or EBT is doing any form of assessment of PAT, at least not until there is more data on the reliability of using this as a clinical marker of disease.
Personally, I think there's a lot of interesting info that can come from this, and the idea of deposition of fat into muscle tissue and necrosis of that tissue, inflammation and the relation to levels of saturated fats consumed from dietary sources is an area that is just begging to be better researched.
Oh, and by the way, don't believe everything you read here from BG about what foods I consume, how much statin I take, or much else when it comes to me. In fact, I'd prefer that she simply not make references to me in her writings wherever they appear. This will obviate the need for me to continue to correct her misstatements about me, my lipids, and drug and supplement usage, as well as the fact that she continues to misrepresent that I have not achieved plaque stability and/or demonstrated regression through serial MDCT CAC scoring over a period of three years despite very low dose use of rosuvastatin.
A correction…. My serial scan scores show that I have achieved stability and optimally regression of coronary calcium. My point is that Dr. BG continues to claim that those taking rosuvastatin at doses of ~10mg daily cannot possibly achieve regression on EBT/MCDT scanning, and that just isn't so.
I happen to be one of those whom I believe Dr. Davis was referring to with "too much of a good thing" with reference to EPA/DHA dosing. My dose was upped from ~1-2 grams per day (of EPA/DHA) to ~10 grams based on recommendations from Dr. BG. This occurred in or around December 2008 and continued until very recently. Based on five consecutive, quarterly NMR's and VAP's, my sdLDL-P remained at >85% of LDL-P, and my trigs went from ~40 to ~75, and, more significantly, my overall LDL-P rose from ~1000 to ~1300. No other significant impacts were noted, other than CRP dropping to 0.7, which I attribute not to the n-3's, but instead to continued use of rosuvastatin together with combined high dosing of both boswellia and 5-Loxin and large doses of aspirin (taken specifically as an anti-inflammatory due to nerve and muscle pain from a herniated cervical disc in the month immediately prior to the last VAP testing).
The point though is that in some, excess fish oil can convert to higher trigs and higher LDL, and will not improve the concentration or ratios of sdLDL-P/LDL-P.
Yes, n=1, but I'm the n, so that's really most important to me, not what Wolf, Sears or anyone else has to say about this. After all, what we're after is personalized medicine, not epidemiological observations that may be valid in large population studies but which may have no relevance to a particular individual.
Hi JEG,
Thanks for the references. I am truly upset that you andBG seem to be having a cybertiff. She has a big heart, alot of enthusiasm, alot of intelligence and makes me laugh. You are a sincere intellectual, very bright, searching for truth in medicine and are doing a good job of it. I can learn from both of you and want to continue to do so.
As to omega 3 and dosage. I can't seem to find any solid benefit to doses over 4g to maybe 5g per day. This seems to max out tg lowering, ldl improvement in particle size, minimal increase in hdl, bp lowering, improvement in tnf alpha, interleukin 6. Reports on irs effect on HSCRP are conflicting. One interesting report, Thies F, in Lancet 2003 took 188 patients scheduled for carotid endarterectomy and treated them with either DHA/EPA, sunflower oil, or placebo for an average duration of 42 days prior to surgery. There was a significant difference in thickness of the fibrous cap over the plaque,the degree of monocyte infiltration of the fibrous cap, percent DHA etc. This directly addresses plaque stability. I love it.
Homertobias,
That is a great plaque stablization article — will have to ck out!
Jeq,
I must be correct again as indicated by the length and duration of the post!
Let me get this straight — the lipoproteins were less than desirable for both you and JJ/Jim for the past 2008 to 2009 (you reported increased sdLDL?), yet both of you posted regression recently on BOTH of your EBCT/MDCT results….
Gosh… I wonder if the high dose fish oil had anything to do with it?
EPA DHA get infiltrated directly locally into calcified plaque and has immense immeasurable benefits for regression BEYOND lipoproteins. I think you have seen some them, personally IMHO.
-G
Homertobias,
That is a great plaque stablization article — will have to ck out!
Jeq,
I must be correct again as indicated by the length and duration of the post!
Let me get this straight — the lipoproteins were less than desirable for both you and JJ/Jim for the past 2008 to 2009 (you reported increased sdLDL?), yet both of you posted regression recently on BOTH of your EBCT/MDCT results….
Gosh… I wonder if the high dose fish oil had anything to do with it?
EPA DHA get infiltrated directly locally into calcified plaque and has immense immeasurable benefits for regression BEYOND lipoproteins. I think you have seen some them, personally IMHO.
-G
By the way, congratulations to you two gentleman, JJ and Jeg, for achieving regression with Pattern B! I have looked for regression in Pattern B forum posters, but turned up none. You two are the FIRST at TYP that I can find…
Do you think omega-3 had any role in your success since that appears to be the common link as well as major supplement change you guys identified?
I wonder what the omega-6:3 ratio is now off the fish oil?
By the way, congratulations to you two gentleman, JJ and Jeg, for achieving regression with Pattern B! I have looked for regression in Pattern B forum posters, but turned up none. You two are the FIRST at TYP that I can find…
Do you think omega-3 had any role in your success since that appears to be the common link as well as major supplement change you guys identified?
I wonder what the omega-6:3 ratio is now off the fish oil?