Let's review some subfractionation techniques. On the market 3 main methods exist. They all work. Dr. Davis prefers NMR. Superko and Krauss are affiliated with Berkeley HeartLab which uses GGE. Density gradient ultracentrifugation is also very popular ( VAP-II ). Recently, Krauss also appears to be introducing a new technology based on ion-mobility.
Basically, the denser the particle, the faster and mobile (like sp*rm *haa*) the particle moves through a gel (GGE). The denser the particle, the smaller the diameter (Angstroms or nanometers) as determined via electromagnetic resonance (NMR) or absorbance via density ultracentrifugation (VAP, which are indirectly compared to known sizes).
Pattern 'A' is good (all nice large buoyant fluffy particles).
Pattern 'B' is clearly BAD. Dense small stupid cr*ppy stuff. Guess what causes it? Excessive dietary carbs and/or fruit. Lack of omega-3 fats. Excessive omega-6 refined veggie oxidized refined fats not meant for human or animal consumption. Lack of saturated fatty acids. Lack of antioxidants. Lack of hormones.
The medical literature is rife with studies demonstrating that the conversion of small dense LDL to buoyant LDL is associated with regression of coronary artery disease.
Measuring LDL-Cholesterol Alone is Faulty and a Farce
Why is subfractionation via NMR/gel electrophoresis/UC of lipoproteins the most accurate way to assess cholesterol ? In doing so, the density and particle counts can be determined.
Only the marketing ploy of the statin/fibrate/zetia industries want to measure LDL-C alone without particle sizing. Yes. It is not cheap -- $99 via different labs. Some insurances cover it. Most don't at this time.
LDL-C alone tells nothing. It is like looking at someone's debt. Is it good debt (student loans, low fixed interest)? Or is it all bad debt (variable ARM, no down, several high interest boat/car/house loans)?!? Or No Debt? Or a mix (no debt on car boat house but low good student + low fixed vacation house debt)?
Do you have a good accountant? Do you have a good investor (eg, YOU)? Would you trust your money with a loser? With someone who has no money in the bank? With your statinator cardio-idiot? How many coronary events did he/she avert? Using 'tracking' EBCT/MDCT technology and targeted strategies to raise HDL2 and lower small dense LDL and Lp(a), both Drs. Davis and Blanchett (in Colorado, our colleague) have ancedotally seen single-digit events in their practices that span almost 10 years. HeartHawk likes to refer to this phenomenon as 'no event, no matter what score.' Even if the coronary calcification score is 4-digit, literally no events are seen. The failures they do see are related to noncompliance with the program and calcification scores consistently increasing 10+% or 20+%, respectively.
Well, when you trust your local neighborhood statinator, eg local General Practitioner, internal med LDL-centric drug-rep-pimped-up doc, cardiologist with lipidology credentials and certifications, what do they have in the bank? You must ask them. If they don't provide a good enough answer, seek new advice I would heartily suggest.
What do I look for?
No debt. High safe investments. High money in the B A N K . Demonstrated portofolio performance.
...EBCT regression or no EBCT score at all.
Personally I believe non-physician individuals like Richard Nikoley or Dr. Stephan Guyenet PhD or Dr. Dr. Petro Dobromylskyj (vet) or elite athlete Mark Sisson or Robb Wolf MS (Paleo/Xfit protege) know far more than your local GP statinator ninnyhead who are only focused on NCEPIII-LDL-centric guidelines. Quality of lipoproteins trumps quantity alone. Holds true for economic debt too. Does your statinator know that?!?
Lowering LDL-C Alone Does Not Reverse Heart Disease
Remember Cardio Controversies and Dr. Superko ? LDL-C reduction alone was no better than placebo. Event rates barely were improved when Superko look at the whole picture comparing statin trials v. niacin trials. Yes, he made a variety of inferences. Yes, Niacin trumps all statin trials. Niacin in alone or in combo trumps ALL STATIN TRIALS in all-cause mortality, cardiac-death, and cardiac events. Superko makes educated, non-biased, medical-literature-based inferences.
So what? He is correct.
Statins raise %-sdLDL. sdLDL is oxLDL. See below. Statins create and sustain Pattern B which is predominance of small dense LDL. On statin therapy, often the LDL are 50-100% all small dense particles. sdLDL cr*p. OxLDL. On our TYP forum, the same phenomenon does appear to occur. Statins appear to prevent regression. What? I think Superko is super-right.
On statins, the EBCT progression fails to halt despite niacin, omega-3 fish oil ULTRA high dose, 10-20+ lb fat loss, body recomposition, Lp(a) reduction, HDL2 increases... despite all TYP-directed efforts... EBCT scores increase 10-25+% annualized. Why?
They maintain a high oxLDL concentration which the body cannot escape. It is not unlike bad revolving debt.
This is worse in those with Lp(a) -- anything greater than 3 mg/dl.
Yes. It doesn't matter how much Lp(a) one exhibits. Any amount jacks up the picture. Dr. Hecht, Superko's partner in cardio controversies, has shown that. Hecht, like Drs. Davis and Blanchett, is one of the earliest, most vocal proponents of using CT technology for screening of subclinical coronary atherosclerosis. I'll be going over later how he thrashes the retarded Heart Protection Study which marketing ploys by statin companies attempted to lower the LDL-C health standards. *urrg*
It is a good thing at TrackYourPlaque that we no longer rely on this useless drug class. (BTW fibrates s*ck. BTW zetia s*cks too.)
Niacin and n-3 fatty acids trump them all.
Statins Increase OxLDL For oxLDL to 'transform' to Large fluffy healthy LDL, CETP needs to deposit cholesterol esters into the particles. How can it if statins block cholesterol synthesis? Or if worse Zetia blocks dietary cholesterol uptake from the gut. Frankly the lipoproteins are f*cked. They never seem to attain the large, fluffy particle size associated with regressive Pattern A in the niacin regression trials (70% converted to Pattern A compared with Placebo, HATS trial NEJM 2001).
Mechanism? Lp(a) 'tracks' inversely with analogously with growing and increasing Large LDL and HDL2. Statins s*ck. Statins lower all LDL species, including the good stuff, the buoyant LDL which are necessary for regression. A new marker is the oxLDL/apoB ratio and several trials found an increase in oxLDL proportions related to apoB. Yet another adverse finding was an increase in oxPL (oxidized phospholipids) which bind Lp(a). Does oxPL increase toxicity of Lp(a)? I don't know but it probably does not help and likely explains many of the increases in EBCT scores in statinators. How long are these effects in place? I wish I knew.
Increases in Lp(a) were found with every statin tested.
Krauss and Superko: Only the Densiest Particles Predict CAD
Superko and Krauss found evidence in 2001 that the small dense LDL-III a+b subspecies tracked the best with CAD. However more recently Krauss made note that the smallest, densest fraction out of 7 subspecies actually tracked the most predictable with progression of subclinical and clinical coronary artery disease. I call this band on gel electrophoresis the 'death band'. No, I'm not talking about a rock 'n roll band. The LDL-IVb fraction is the 'death band'. The goal at Berkeley Heartlab is to achieve < 2.5% based on one trial (when angiogram stenosis > 30%). However, this goal is not low enough. We see EBCT and MDCT progression even at > 1.5%. Likely stenosis is < 30% as the trials demonstrate continued progression.
Other researchers have found similar correlations with small dense LDL being superior in predicting CAD (Koba S et al. J Atherothromb 2008).
Berkeley Heart Lab in fact advise for Pattern B a 'high 40% fat diet.' That is pretty progressive! But they fail to specify the components of the fat: monounsaturated, polyunsaturated, n-3 v. n-6 and saturated. Are they afraid of liability? Are they afraid of success? Are they afraid of regression? I dunno.
They do fail to address the carb intake therefore it probably would be fair to say that they can not broach diet unless carbohydrate intake is fairly accurately laid out.
Only two studies exist that I can find that implicate Large LDL in coronary artery disease risk. Krauss wrote the first one in 1995, then re-clarified oh just last month. I briefly discussed HERE. In the clarification, he and other researchers retrospectively analyzed 3 large seminal trials and found no independent correlation between Large LDL and coronary atherosclerosis. One trial included in the review was the Quebec Cardiovascular trial.
CONCLUSIONS: These results indicated that estimated cholesterol levels in the large LDL subfraction were not associated with an increased risk of IHD in men and that the cardiovascular risk attributable to variations in the LDL size phenotype was largely related to markers of a preferential accumulation of small dense LDL particles. PMID: 15618542