Friday, September 25, 2009

'Death Band' = sdLDL on Lipoprotein Subfractionation

Diagrams #1, 2
Modified and Courtesy of some website

Subfractionation of Lipoproteins 101

Let's review some subfractionation techniques. On the market 3 main methods exist. They all work. Dr. Davis highly prefers NMR for its subtleties, scope, and particle counts. Superko and Krauss are affiliated with Berkeley HeartLab which uses GGE (BHL). Density gradient ultracentrifugation is very popular among our members (VAP-II and VAP). Recently, Krauss appears to be introducing a new technology based on ion-mobility.

Basically, the denser the particle, the faster and more mobile 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 = Large LDL-C Predominance

Pattern 'A' is good (all nice large buoyant fluffy particles). LDL particles are not perfectly spherical; they can appear even flat like red blood cells. Large LDL however fit 'perfectly' into LDL receptors on cholesterol-requiring tissues like our sex organs (which produce testosterone and estrogen from cholesterol) and the all-important adrenal glands, tiny triangularlike-walnuts sitting on the kidneys which regulate our blood pressure, tension in the endothelium/smooth vasculature, and minute-to-minute brain functions by issuing cortisol, another cholesterol-based derivative that is mandatory for life.

Pattern 'A' is desirable and highly asscociated with regressive patterns for calcification in the vasculature whether the plaque build up (scar-tissue) is in the renal (kidney) arteries, carotid (neck) arteries, peripheral (legs), coronary (heart), or inner lining of the entire arterial tree (hypertension).

Hypertension? This is just extensive calcium deposition occurring at the smooth muscle, endothelium and vessel wall fibroblast level in the vascular tree. HERE and HERE discuss the role of oxLDL on increasing MMP-9 and arterial stiffening.

What is easier to regress? Dr. D and I agree that the carotids are the easiest (plaque there comes and goes based on full moons or voodoo medicine... no joke, it's so easy). Since the brain is the most important organ... (again, yes, debatable...arguably it might be the... liver...*haa*) the carotids provide blood flow to this GINORMOUS organ. Consequently these arteries are 7-8mm, titanic-sized bilateral highways.

Distribution of blood flow at rest and during flight-fight-fright correlates well with artery lumen sizes IMHO (courtesy of a Rutgers anatomy phys student w/concise pictures HERE).

At rest:a. Brain: 13% (7-8mm)b. Heart 4% (2mm distal LAD; 3-4mm LAD; 4-5mm RCA) (Brown BG et al. Circulation 1992;86;232-246.)
Kidney: 20% (5-6mm)d. Abdominal organs (incl liver): 24% (5-6mm)

During exercise:
a. Skin, muscles and heart increase
b. Remaining tissues either remain same or decrease

Renal is the hardest. I think Dr. T at Nephropal will agree. These are relatively narrow yet receive the greatest majority of tissue perfusion, and have less possibility of collateral growths/angiogenesis than other arterial vasculature. Renal stents notoriously ALL 100% fail. Bypasses are currently unconceivable. Peripheral is not good either (but again, also reversible).

No matter where the plaque is, however, it is ALL potentially reversible.

A L L .

A good 'indicator' of regression is blood pressure normalization < 110/70. Everyone at TYP on the program who maximizes expression of Pattern 'A' with sdLDL as low as possible and HDL2b as high as possible (200-400% increases) notice dramatic reductions in blood pressure. Of course !

In the HATS trial, again where events were prevented by 90% and angiographic regression observed, reductions in blood pressure occurred. We see this in ALL of our successful TYP members as well. Pattern A for A+++ (blood pressure, Large-LDL, HDL2b and sexy hot elastic unstiffened unobstructed vasculature).

Pattern B = Small Dense LDL-C Predominance

Pattern 'B' is clearly BAD.

Dense small stupid cr*ppy stuff.

Small dense LDL quickly and rapidly become oxidized LDL (OxLDL) which do NOT fit into traditional LDL Receptors. They instead are attracted to many non-LDL receptor surfaces and tissues (Galeano NF et al, J Lipid Res. 1998;39:1263-1273). These sites include the endothelium to initiate 'stiffened'/calcified arteries (eg, hypertension), atherosclerosis (plaque burden: CAD ED CVD PVD RAS) or liver to initiate NASH/fatty liver or even our pancreatic islet cells that are highly related to hastening T2DM pathogenesis (Cnop M et al. Endocrinology. 2002 Sep;143(9):3449-53.).


sdLDL is sad news. Especially if one has 50 to 100% sdLDL. Yeah, that is kinda f*cked up and highly associated with prevention of regression. This explains the sad results and outcomes from all statin trials compared with the niacin trials (HATS, FATS, CDP, etc). Recall: Cardio Controversies and Dr. Superko. Pattern ' B ' perpetrated by statins also explains the lack of regression in nearly all EBCT and MDCT clinical trials. Ten out of about 12 to 13 trials that I have reviewed for statins and CT coronary calcifications show no difference between statin and placebo arms.... Or.... even worsening (one lipitor study). Why?
Statins s*ck. (And zetia is worse, eg SEAS, ENHANCE trials... more %-sdLDL... more HDL-3... more cancer... more plaque progression)

Small dense LDL and OxLDL penetrate deeply through several tissue layers.

Tissues involved: any tissue. You name it.

CAD is Autoimmune
OxLDL attract auto-antibodies.

Auto-antibodies are like the 'cleaners' (you know... in Mob terms). Auto-antibodies can go CRAZY.

O-U-T-T-A . . . C-O-N-T-R-O-L . . . (Baby Bash Feat. PITBULL OOOhh... Yeah).

Yes, CAD is an autoimmune process not unlike Hashimoto's/thyroid-insufficiency or NASH/calcified-liver or T1DM or T2DM/pancreatic-insufficiency or Addison's/adrenal-insufficiency

What Promotes Pattern ' B ' ?

Guess what?

Silent and overt celiac disease (gluten intolerances: wheat barley rye) and other food allergies (A1-casein, egg whites, nightshades, nuts, etc)

Excessive dietary carbs (grains, potatoes, peas, corn and fruit). Candy/sweets. Artificial sweetners. Lack of omega-3 fats. Excessive omega-6 refined veggie oxidized refined fats not meant for human or animal consumption.

Lack of s a t u r a t e d fatty acids.

Lack of antioxidants.

Lack of hormones (thyroid, estrogen, testosterone, adiponectin, vitamin D, melatonin, etc).

Synthetic vitamins, hormones or drugs (Lurotin/fake-beta-carotene (used in the HATS AO-arm; ATBC: 7% higher death rate; CARET: 28% higher cancer+mortality); levonorgestrel, Provera/medroxy-progesterone, Premarin/horsey-hormones, oral contraceptives).


S-T-A-T-I-N-S . . . and thus statins +/- Zetia s*ck...

Role of Large LDL in Pattern 'A'

LDL-5 (on VAP) and LDL-6 (on VAPII) are the densest smallest LDL subspecies (devoid of cholesterol content). See below diagram #2. These subparticles oxidize to OxLDL in the metabolic pathway of lipoproteins quickly in the bloodstream, studies show. LDL1 and LDL2 are the Large LDL subspecies which are rich in cholesterol content and extremely resistant to oxidation. Additionally, these magnificently-sized particles are the carriers of antioxidants which provide protection from oxidation, ROS and free radicals, to peripheral tissues after digestion from food. Large LDL transport the great majority of our important fat-soluble antioxidants: coenzyme Q10 (idebenone, etc), carotenoids, vitamin E (tocopherols, tocotrienols), vitamin K1 K2 (menaquinones 4 - 9 chain lengths), et cetera.

Conversion of Pattern 'B' to Pattern 'A' Associated with Regression

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. In the HATS trial where 90% of cardiac death and events were COMPLETELY AVERTED after 3 yrs of niacin ultra-high-dose of 3-4 grams daily (and low low dose of weak-statin 10-40mg/d), conversion to Pattern A occurred in an astounding 70% of the treatment arm. Even niacin alone produces similar outcomes of 60-70% relative risk reduction, compared with statins 17-25%. In other words, niacin alone or in combo is 300-400% better than statins relatively speaking.

What mimics niacin? What binds 'niacin'-receptors?

Ketone bodies.

Generated from intermittent fasting, physical prolonged exercise (low intensity) or... a ketotic diet, eg high protein or high fat and no carbs.

Large LDL Not Associated with Heart Disease

Only 2 studies show Large LDL are remotely associated with heart disease (that I can find) and definitive CAD progression. In each case, the presence of the 'death band', a high peak of LDL-IVb and LDL-IIIa+b (sdLDLs) and an absence of the 'regression peak' HDL-2 occurred (Campos H, Krauss RM, et al. 1995 ATVB. 15;1043-1048.; Campos H et al. 2001 JAMA 286:1468-1474). In 1995, only 3 LDL subspecies were determined. The more infinitely denser, heaveir sub-species -- LDL-IIIb, LDL-IVa, LDL-IVb -- hadn't yet been 'discovered'. 'LDL-III' from Campos/Krauss' article is actually LDL-IIIa.

The 'Death Band' = sdLDL Highly Associated With CAD

See below. LDL-III is considered dense particles. Dense like bullets. In the below graph the 'densest' of the LDL-III is circled. This is not a rock band... I refer to it as the 'death band' since it is associated with coronary events. Peaks corresponding the heaviest, smallest of the LDL-III particles (far left 2 lines at ~1.4%; red) in the CAD group was significantly higher than the control ones (1 line at ~0.5%; pink). If I do some retardo-calculus, then the 'circled' tiny death-band peak is ~2.8% versus ~0.5%. 5.6 times greater in area under the curve.

So, this 'circled' sd-LDL subfraction contained 560% more of the smallest densest 'death-band' particles in the CAD group than compared to control (no CAD).

HDL2 in the CAD group was statistically lower at 10 mg/dl (out of 38 mg/dl, 26%) whereas the control was 50% higher, 15 mg/dl (out of 42 mg/dl, 36%).

Controls (no CAD)... had HDL-2 fifty-percent HIGHER. (Recall, HDL2 increased 60% in the HATS trial in the niacin arm).

In a 'response' to the second Campos study, Krauss wrote an articulate rebuttal to Campos et al discussing the relevance of high sdLDL-Particles and low HDL2-Particles in CAD progression, not Large-LDL-Particles. HERE (sorry, not free yet).

The Denser, The More D A N G E R O U S

How dense is Campos?? How deep do LDL-centric-zealot-statinator-idiots dig?

The Densest Bullet of Them All: LDL-IVb

The bands I circled above were dense. Even denser LDL subparticles exist. These smaller, more atherogenic particles contain even less antioxidants, less transportable-cholesterol and are tremendously prone to oxidation. On NMR these are identified as subclass LDL-IVb and on VAP LDL-5 (VAP-II, LDL-6).

Eight years later after these newer LDL subparticles were identified, Superko and Krauss demonstrated that the mere presence of the SMALLEST, DENSEST LDL sub-species (IV-b) was MOST associated with fastest plaque progression (Superko, Krauss et al. ATVB 2003 Feb 1;23(2):314-21.) Japanese researchers have arrived at the same conclusions as well (Koba S et al. J Atheroscl Thromb 2008,15(5):250-260. Free PDF HERE)

As to be expected, Superko and Krauss, also showed that reduction of the SMALLEST, DENSEST LDL sub-species (IV-b) was highly associated with fastest plaque regression. Therefore, when sdLDL were controlled and reduced to the point where the smallest denset LDL (IVb) were less than 2.5%, a decrease in plaque burden and regression of atherosclerosis was observed. However this observation did not hold true for those with less extensive angiographic plaques where stenosis < 30% (?soft plaque still progressing? yet lower appears better). Diagram from Superko and Krauss 2003.

What Ultimately Lowers 'Death Bands' LDL-IVb The Best?

Saturated fatty acids (all of them: short-chain, medium-chain, long-chain) (Noakes M et al. Nutr Metab Cardiovasc Dis. 2009 Aug 17.; Krauss RM et al. Curr Atheroscler Rep. 2005 Nov;7(6):455-9.; Noakes M et al. Am J Clin Nutr. 2009 Jul;90(1):23-32.)

High-protein, Low Carb Diets (Clifton P, Krauss RM, et al. Am J Clin Nutr. 2008 May;87(5):1571S-1575S.)

Carb restriction (Volek JS et al. J Nutr. 2009 Sep;139(9):1667-76.)

Ketotic Diets (Clifton P et al. Obes Rev. 2006 Feb;7(1):49-58.)

Paleo Diets (Frasetto LA et al. Eur J Clin Nutr. 2009 Aug;63(8):947-55. Hays JH, Editorial 2004. )

Niacin (ultra high dose) (HATS trial, NEJM 2001)

Omega-3 PUFAs: DHA EPA ALA (Schaefer EJ et al. Atherosclerosis. 2008 Mar;197(1):12-24.; Mozzafarian D. J Cardiovasc Med (Hagerstown). 2007 Sep;8 Suppl 1:S23-6.)

What Lowers Blood Pressures Concomitantly Whilst Annihilating 'Death Bands' and Raising HDL2b?

ALL THE ABOVE (see above citations)

(Except for Niacin, A-L-L the above are additionally associated with weight control, body fat loss, improvement in Metabolic Syndrome, T1DM, T2DM, insulin control, hyperinsulinemia)

What Does Not:
--olive oil (monounsaturated fatty acid)
--omega-6 veg/seed/bean oils
--mercury, cadium, heavy metal toxicity; selenium-deficiency (Houston MC. Altern Ther Health Med. 2007 Mar-Apr;13(2):S128-33.)
--low fat/high carb AHA diet
--low fat diets
--low cholesterol diets
--low saturated fat diets


steve said...

Great post! I would like to see what the particle profile of Japanese men and women in Japan look like. Their diet is not very high in sat fats and yet lowest rate of heart disease. Large or small particles? The amount of Niacin you state of 3to 4 grams is quite a bit to take. I tried it and had to stop. The intense itch at random times and questionable incremental dryness it was causing me(eczema sufferer)at 1to 1.5 grams was tough enough. My HDL were 62 per NMR, and still have almost 100% small dense(10% large while on Niacin for 6weeks). On Lipitor 10, and overall particle number with niacin dropped like a lead baloon to 598 from 1305.
Be interested in seeing you post a daily diet recommendation that you think would lead to large LDL profile. I for one think there is a genetic basis to it. I am grain free(except ground flax), sugar and dairy free ex Whey protein which i may eliminate.
I read the Hyman book you recommended. Interesting; he is low fat you know and thinks Sat fats cause inflamtion.
Hard to know what to believe sometimes!
My own experience is that NMR is the best. VAP had me as type A, large LDL, and two years later and no diet change, NMR had me as very high(1795 particle count) and all small dense. Boy was i shocked. have been on TYP diet and still all small but less, except for small amount large during Niacin trial. I think i just need to get small dense as low as possible: genetics sometimes rule.


Dr. B G said...


Centenarians on the traditional Okinawan diet had HDLs of 60 mg/dl (that is a helluva lot better than 90% of Americans) with lard, fatty pork belly and rich goat milk. This is not the case now since Okinawans lost the longevity edge in the 1990s and currently (after canola oil was introduced imho).

The mainland Japanese are rapidly catching up to Americans b/c they are fighting this 'metabo' campaign to reduce Metabolic Syndrome, obesity and pre-/diabetes at this time. I bet their particles don't appear optimal with the increasing intake of refined carbs, n-6 pufas and reduction in exercise and n-3 pufas. Vitamin D deficiency? Yup, they are all deficient as well. Vitamin K2? Likely deficient as well.

Hyman does advocate coconut oil and coconut milk as 'good' saturated fats. He also as you are probably reading strongly advocates grassfed beef, and I'd presume the fat where all the omega-3s, CLA and vitamin A are located.

Recently Dr.Hyman posted on the lack of association betw sat fat and dietary cholesterol with atherosclerosis and other experts take on saturated fats:
Reasons not to fear saturated fat (and it raises HDL and lowers the bad dense LDL):
Saturated Fat is HEALTHY, Mark Sisson elite Primal athlete
Saturated Fat Improves Lipoproteins (lowers Lp(a) + sdLDL, raises HDL), Drs. Mary and Mike Eades, Protein Power series
Why Cholesterol May Not Be Bad For Us, Dr. Mark Hyman MD
Coconut oil = Good Saturated Fat, Recipes Ultrametabolism, Hyman

Do you think you have any food allergies? Perhaps you still consume excessive carbohydrates? Are you hormones incl thyroid whacked out? Genetics determine your insulin sensitivity that is for certain. Pima Indians have the least on earth and perhaps you are similar to them. You cannot even inhale or lick a piece of FRUIT. No oat bran. Exercise, hunt, forage like a traditional Pima Native American. Eat plenty of pemmican, nuts, and FAT (like fat squirrels, rabbits, peasants, etc).

Yes -- it is genetics how we interact with the availability of toxins, gland-killing pesticides/bromides and gluten.

Good luck!


William Trumbower said...

Another great post! I look forward to your posts as much as Dr. Davis. If CAD is autoimmune, then gluten is possibly the initiating cause of the leaky gut that leads to autoimmunity. CAD could then be worsened by malabsorption of essential nutrients (folate, B12, Vit D etc). One of the main causes of decreased sex hormone production in men and women is probably autoimmune attacks on the gonads. WHEAT KILLS Look at my facebook for my new favorite person.

steve said...

dr BG: thanks for response. i will check out HYman on sat fat/coconut oil. Perhaps i am getting to many carbs, but doubt it since i eat no grains no starches or sugars. My blood glucose is 79 at last measure. I don't know insulin, and will check on thyroid,but doubt an issue: lots of energy, never cold(actually prefer cold) Mainly eat grassfed beef,organic chicken, fish from vital choice,omega eggs,99% dark chocolate for snack. Virtually no fruit: only berries, straw and blueberries. Not sure how much more i can tighten diet HDL per NMR is 62 and Large hdl-P is 17.1 so i guess i am getting adequate sat fat: you agree? Will try to lower carbs while avoiding bowels locking up. Whose K2 would you recommend? What dietary sources are best? No food allergies except for nuts. Appreciate your thoughts! May try the niacin at a lower dose.

Dr. T (Nephrologist) said...

Brillant!!! The sad part is that most physicians do not get it. A lot of the continuing education comes from the drug reps or drug sponsored events. The physicians in the hospital think that I am ecentric to advocate a Wheat free/ Paleo diet. But my patients are now getting it and educating their own doctors. Of course! I have my patients reading Animal Pharm.

steve said...

DrBG: Looked at Hyman links and while he says cholesterol is not an issue, he says sat fats are:
One of the biggest cholesterol myths out there has to do with dietary fat. Although most of us have been taught that a high-fat diet causes cholesterol problems, this isn't entirely true. Here's why: The type of fat that you eat is more important than the amount of fat. Trans fats or hydrogenated fats and saturated fats promote abnormal cholesterol, whereas omega-3 fats and monounsaturated fats actually improve the type and quantity of the cholesterol your body produces

Seems to me he does not like sat fat; could not find the approval of coconut oil. Appreciate your thoughts on what Hyman says on sat fats. Clearly he thinks they should be limited. Do you know or have a link to what he says to do to have large fluffy particles?
Note also that in the Krauss studies that while 70% increased particle size, 30% did not. Wonder why? Dr.Davis has said that in some cases genetics rule and small LDL is the result; Eades thinks otherwise, but he is not a cardio doc. Again, appreciate your thoughts. I am searching to see what will get my particles to large,and preclude plaque progression.

Dr. B G said...


Put in 'Good saturated fats include coconut oil' in the google book ref for the Ultrametabolism recipes. My UltraMIND book is in Shanghai right now (with my hubby) otherwise I'd give you a page #.

I think VAP traditionally overestimates pattern "A" and gives false security (not unlike useless gliadin or tTG tests) imho.


Dr. B G said...


Yes -- you are totally RIGHT ON! Thank you, I edited the post. R u kidding? Can I b u when I grow up??

In PubMed there are various articles implicating auto-antibodies against ovaries, endometrium, S-P-E-R-M, etc. with infertility, PMS, fibroids, endometriosis. It is too bad this is the main reason for hysterectomies/ B-oophorectomies now and 50 yrs ago. Indeed very sad. I think we are still in the dark ages for women's health.

*haa* I'll ck out FB...


Dr. B G said...

DR. T!

I have the same experiences! One doc even told my patient that my recommendations are even changing the doctors' diets *haaa*! (it's about TIME)

Honestly I can't refrain from sharing your CKD reversal stories (like wonderful Billy) and the few ones that I have seen on low carb/ wheat-free/ Paleo/ fish oil. The stories are so encouraging!!! The pts seem to get really into it when they observe the SCrs drop from 1.7-2.0 to < 1.1-1.3. I've noticed that six months is where the highest recidivism rate occurs -- gotta catch em around there.

I've told the pts about higher antioxidant values (ORAC) in wild v. tame blueberries... now I can share with them the recommendations for MALBEC (one of my faves)! Thanks again for your awesome posts.


Dr. B G said...


Hyman is mistaken (like many docs). Is he a recovering vegetarian? I have no idea but at least he has come a LONG way.

His rare 'bunkiness' also extends to B-vitamin recomendations. One cannot willy nilly take high-dose folic acid or cyano-cobalamin. Under-methylators make up the great majority of our population (60-70%) and folic acid may actually be harmful. Methylated folinic acid, TMG, methylated- or adenosyl-cyanocobalamin are preferred. I had a prostate CA survivor tell me when his oncologist gave him B12 shots (cyano-b12 form) his PSA increased.

Anonymous said...

People with lots of SMALL LDL particles (Small LDL-P) have a lot of cardiovascular disease and events. Think Metabolic Syndrome and Diabetes. People with lots of LARGE LDL particles (Large LDL-P) also have a lot of cardiovascular disease and events. Think Familial Hypercholesterolemia.

The common theme is that people with high numbers of LDL particles have a lot of CVD risk (even if the particles are large), and people with low numbers of LDL particles have much lower risk (even if the particles are small). In studies considering both size and number of LDL particles, size almost always washes out in multi-variate analysis, but number almost always remains a significant independent predictor of risk. Between LDL-P by NMR and apoB, there is now a very large body of data on this point.

Statins lower LDL-P 18-55%, and there is a huge body of Level I outcomes data supporting the benefits of statin therapy. Niacin lowers LDL-P 10-25%, and there is ZERO Level I outcomes data. The Coronary Drug project failed to acheive its primary endpoint, and the HATS trial, while very interesting, had many limitations (hardly Level I). It will be interesting to see what the AIM-HIGH trial shows - this data will be out in a few years. I suspect that the combination of statin/niacin will be VERY impressive, but that is just speculation until the results are in.

In a nutshell, when you increase the size of LDL particles (i.e. with Niacin), the NUMBER of particles needed to transport a given amount of cholesterol goes down, because larger particles transport more cholesterol than smaller particles (on average). Increasing LDL particle size is associated with plaque regression, but this is likely due to the accompanying reduction in LDL particle number more so than the increase in particle size. NMR data from VA-HIT also supports this notion for fibrates (specifically gemfibrozil).

homertobias said...

Mark Hyman is much more of a salesman than a researcher or a doctor. I sat next to him in a conference last year, watched him preen prior to speaking and take ten minutes choosing which picture of himself to present as his first slide....Free book signing after listening to his talk. He had the pepsident smile down pat. I think he will popularize a favorable trend in personal health well and become rich in the process. Good for him! But I certainly don't consider him an authority on anything.

Dr. B G said...


You heretic! Hyman is better than nothing at this point. He's accessible, mainstream (now -- even the idiots like Oz and Weil are embracing him), and hell... not that bad looking (when he preens himself *HAAAAAA*).

You are TOO FUNNY. My best friend scored tickets to see him in SF in 1wk (after spending an arm and leg to support PBS public TV). If I remember ur comments, I'm going to start cracking up in the audience...


Dr. B G said...


Are you on a statin b/c your logic sounds demented to me?

FHC have high sd-LDL absolute particle-#'s just like the Campos, Krauss article.

The HATS and niacin trials has excellent fulfillment of ALL endpoints:
--all-cause mortality (which statins usually INCREASE by increasing cancer mortality, suicide mortality and accident mortality)
--all cardiac endpoints
--all stroke endpoints

15yrs later after initial niacin Tx in the CDP and subsequent niacin discontinuation, the treatment group continued to see benefits. Reduction in 10% all-cause mortality which was mostly CAD occurred compared with placebo (p < 0.0004; placebo mortality 58.5%, niacin mortality 52.2%).

It is nice that you know the fibrate and statin trials, and make some blatant inferences on LDL-C reduction, but it is actually the change in the quality of the LDL subparticles that statins and fibrates achieve any meaningful reduction in any events (without killing people through cancer or suicides).

In ARBITER-2 the statin alone continued clear, definitive, significant atherosclerosis progression measured by CIMT post-1yr treatment (not unlike all the statin EBCT/MDCT studies). However in the statin + niacin combo, progression was nearly halted. I disagree with everything you've posted.

Are you only reading the summary sheets from drug reps?

I think ur info is bunk. I'd suggest reading the original articles and the subfraction post-analyses if you desire to know the truth.


steve said...

i would have to agree with view expressed about Hyman(and G is correct about B vitamins): he is a salesman(saw him on PBS) like most including Oz,Weil and others who are probably more interested in $$$ than anything else. That said, Dr BG should be commended for looking for the "grains of truth" that appear in many of the writings of these so called experts, and combining it with a close look at the medical lit.
I would have to add that sometimes you neglect to see the failures: for example in Krauss studies how do you explain the 30% who did convert from small LDL to large LDL? That is a statistically significant number, and in a randomly selected population unlikely to be caused by the failures let us say having hormonal imbalances; there must be something else here.
Niacin is great and in combo with low dose statin corrects lipid imbalances real quick. Problem is that it is hard to take for many(ME) due to affect upon dermatological pathways. Dr BG: Want to become a billionaire? Figure out a way to block the naicin from adversely affecting the skin; it will still affect the liver and do its magic! If successful, statin use would decrease dramatically!
Keep digging for us!

Adam Wilk said...

"What Promotes Pattern ' B ' ?

Guess what?

Silent and overt celiac disease (gluten intolerances: wheat barley rye) and other food allergies (A1-casein, egg whites, nightshades, nuts, etc)"

OMG. ...and this is why, I just love it when you put fingers to keyboard and share your brilliance--I know whenever there is a new posting here, I'm bound to learn something not only new, but extremely important in my quest to avoid "the bypass".

I've been low-carbing for years, and unbeknownst to me, whilst ingesting thousands of eggs as part of a healthy diet, I'm finally told by my ENT that I'm allergic to eggs. Of course, G@d forbid they should go a step further and specify what part of the egg I'm allergic to--I had to do my own layman research to find out it's the whites that many are affected by. Of course, not experiencing any overt "allergies" to my beloved eggs, "gee, Honey, what the f@ck are these doctors talking about, I just ate an omelet and I feel just fine..." I never stopped.

This is where I say thank goodness for you mentioning the above--I'm not touching egg whites or perhaps even eggs for awhile--not until I get more information about the whites causing inflammation or raising this "B" pattern. I'm annoyed no doctor ever explained this to me, but I'm glad you told me. 10 solid years of eggs. You want to know why I walk around with anxiety? Grrrrrr

But thank you for seconding that slight suspicion I had lurking in the back of my head.


Dr. B G said...


Actually I like Oz and Weil -- I've given many of Oz's books away as gifts b/c they are well written. Dr. Mike? Oz? Someone is very clever and funny. The illustrator is PHAT!!!! :) Weil on PBS is quite relaxing and educational esp on lifestyles like yoga, relaxation, etc.

I don't know which study you are referring to that remained 30% Pattern B? There is an explanation (I'm sure) b/c I don't prescribe to the 'genetic' theories, which are just theories. Members as you know at TYP 'break down' these genetic so called barriers everyday (Sergad, Dr. Kasing, Harry35, etc). Ketones work for everyone. This is borne out of the niacin and HATS trials for me which achieved astounding outcomes despite:
--insanely low HDLs
--no hormone optimization
--rampant hypothyroidism not unlike population norms at this time
--AHA SAD low-fat, high carb idiocy
--exercise? who knows
--vitamin D deficiency
--omega-3 deficiency
--high n-6:3 ratios
--everything contrary to the TrackYourPlaque program
--30% failed to shift to Pattern B (at TYP we've found that lipoproteins do NOT have to be 'perfect' for perfect stabilization or regression and event eradication)

In truth, I'm not the biggest fan of niacin if there are more natural ways to achieve the same results (ketones, IF, low carb Paleo, exercise 2-4hr stretches, HIIT, etc).

Hopefully Steve you'll find the 'sweet spot' that works for you like other members who have experimented before you! Learn from their posted experiences! Keep reading... My goodness -- you are the best student I have encountered. I really enjoy your curiousity, questions and energy!


Dr. B G said...

Hey Adam,

That is interesting -- I wonder how the ENT suspected eggs? Did you have swollen lymph glands? chronic sinusitis? The elimination diet is apparently the only way to conceivably figure it. Eliminate then re-intro. Fun. You would be surprised how many individuals are allergic to a variety of different foods, even olives/olive oil (coconuts/coconut oil too!), citrus, diff veggies, tree v. legume nuts, etc. Meat on the other hand I've never heard of peple being 'allergic'. Shellfish yeah but not meat!


Adam Wilk said...

Dr. BG,

The ENT told me this from a blood test, but a preliminary one, not the scratch test that ran my insurance company over $3,000 (and people want to know why there's a health insurance crisis in this country?) and indicated I was allergic to grass and trees (whatever). I was suffering from sinusitis, and that's how the egg problem was discovered...
Here's my non-scientifically-untrained-talking-out-of-my-butt mind working here: can you imagine the reason wheat is such a disaster lipid-profile wise for so many could be due to the fact that it's often combined with eggs to make everything from pizza dough to bread to cakes of all sorts?
Just my crazy head spinning again, I can't prove any of this...
Man, am I going to miss my eggs...

steve said...

would going to an allergist help in detecting the food allergies that may contribute to inflamation and possibly small LDL? Pretty hard to otherwise detect as Adam has found out. Your thoughts?
Thanks for the student compliment. Yes, am trying to find what will work. I would be interested in hearing what will help to keep the plumbing working if go very low carb, 50 grams or less. I seem to back up the lower carb i go, and gastro says that may be due to having a very long colon. Go fgure.

William Trumbower said...

Adam If you get leaky gut from gluten, any dietary protein can trigger an immune response depending on your own genetic variability. The question I have is whether the allergic response ever subsides when gluten is eliminated and if so, how long does it take. I also wonder if other dietary modifications that alter your immune response eg. high dose fish oil, might make a difference in the immune response.

harry35 said...

Hi G,

Sorry we haven't seen you at TYP recently - we miss you. Just thought I'd let you know I've got my small LDL down to 10 nmol/L. Large LDL-P is about the same at 277, still perhaps too low. 3 months ago I decided to do everything I could to get HDL up and not worry about LDL. I increased saturated fats, 3 tbsp coconut oil/day, some intermittant fasting, and religious strength workouts. So what happened? HDL stayed about the same, large LDL-P stayed about the same and small LDL-P dropped from 100 to 10. Can't understand why that happened, but its improvement so I can't complain. I'm not convinced that large LDL is beneficial, but we shall see. Since my LDL was a bit low before, and still is, the only thing I can think of that might increase LDL is to stop the Crestor, which you will be happy to know I have done. I'll check the NMR's in 3 months and let you know what happens. I'm hoping you are as right about statins as you were about saturated fats. Cheers, harry35

Dr. B G said...


That is WONDERFULLY great news!!! I am certain you won't be disappointed as you continue on this diet/lifestyle that appears to work best for optimal genetic expression and control of sd-LDL.


I would not be afraid of large LDLs. I do see your hesitation b/c I was once there actually not long ago! I started pounding more saturated fats when I started blogging Feb 2008 but it really wasn't until spring 2009 that I seriously amped it up with coconut oil (cream, half-n-half and full fat dairy weren't cutting it... in fact I was trying to go whole Paleo and dairy was getting cut out). I had already read all the Krauss, Volek and other nutrition/metabolism studies and anecdotal TYP stories (like Doug and Hillbrow), but I hadn't gone totally hogwild yet.

Just 1-2 Tbs is my idea of 'hogwild'. It isn't much but yet you've seen what the results are, right?

Here is a quote from my buddy Tom from Fathead, his blog HERE:
"Mike Eades told me that in their practice, they treated patients with triglycerides of over 2,000. I can’t imagine what you have to eat to be that out of whack. He also said there’s some evidence that large, fluffy LDL has anti-inflammatory properties. I don’t know how strong that evidence is at this point, but it would make sense, since the body produces cholesterol in response to inflammation."

Next year you will finally score regression on EBCT!!!!

Thank you for updating me!


Dr Dan said...

Great article. Im glad you too notice that if you pig out on carbs you feel hungry for up to 72hrs afterwards. I really notice that!!

nielso said...

The Berkeley test is the hardest to get (requires MD participation). Can I identify the "Death Band" adequately from VAP or NMR?

Dr. B G said...


Yes -- I believe NMR with a doctor's order one can obtain that elusive 'page 2' which breaks down the small/med/large count for LDL and HDL (with a nice pretty colored chart graph). On NMR I believe the 'Small LDL' gloms together the dense-LDL + very-dense-LDL: LDLIIIa+b, LDL-IVa+b without distinction.

DR. Davis has a diagram and clearer explanation HERE.

This is what a typical NMR contains:
Small LDL-P
Total cholesterol
LDL Particle size
Large Pattern A
Large HDL-P
Large VLDL-P
'Page 2' (breakdown of LDL and HDL to small med large; see DR. Davis' post)

This is what VAP (DGU) contains:
Total LDL-C direct
Total HDL-C direct
Total VLDC-direct
Sum Total Cholesterol
Trig direct
Total non-HDL-C
Real LDL-C
Sum Total LDL-C
Pattern A/B A B
Sub Class information
HDL-2 (Large Buoyant)
HDL-3 (Small Dense)
Lipoprotein (a)

An example of what Berkely Heart Lab (GGE) contains:
Chol (mg/dl) 1
LDL-C (mg/dl)
HDL-C (mg/dl)
Trig (mg/dl)
Advanced Risk Markers
LDL IVb (%)
HDL 2b (%)
ApoB (mg/dl)
ER Lp(a) (mg/dl)
Apo E Genotype
Advanced Lipid Data
LDL I (%)
LDL IIa (%)
LDL IIb (%)
LDL IIIa (%)
LDL IIIb (%)
LDL IVa (%)
LDL Peak 1
LDL Peak 2
LDL Pattern A B or A/B
HDL 2a (%)
HDL 3a (%)
HDL 3b (%)
HDL 3c (%)
PLAC (ng/ml)
hsCRP (mg/L)
Insulin (µU/ml)

Here is a PDF tutorial from Berk Heart Lab:

Obviously I disagree w/MANY of their 'heart-healthy' goals:
LDL-IVb goal < 5% (no, < 2.5 or even < 0.60% for mod-sev disease)
LDL-IIIa+b goal < 15% (no, < 10%)
fat intake 40% (ok, agree!!)
sat fat 8% (no, >> 18% min)
more olive and canola oil (no)


Dr. B G said...

DR. Dan!

So glad you are back!!

Love hearing about your new Russian insights... my Russian gal pals appear quite Paleo on sauerkraut, soup and dancing... *haa* oy vodka...


O Primitivo said...

Discordance between low-density lipoprotein cholesterol and particle number -

Dr. B G said...

You are busy as usual!

I haven't even had a chance to read this one!!! *winks and hugs*

Josh said...

love this article
i have read more on your stuff about APOE4 too, i am heterozygous APOE e3/4
do you think these rules apply even to e4 carriers?
my aim is always to decrease inflammation and oxidation above all else, however i eat a high fat lo carb diet, and am currently waiting on results from a German lab on oxLDL, sdLDL etc etc


josh @ paleo osteo

Dr. B G said...

Hey Josh,

Have you read my thoughts on apoE4? I like your practice (Paleo Osteo) and the nutrigenomic testing. The value has to be put into the context of evolutionary medicine and the common neoLETHAL contaminants and toxins in our food/lifestyles/environment.

ApoE4 is not the only SNP that increases accumulation and decreased clearance of modern toxins (particularly heavy metals). Have you heard of the work of Dr. Yasko utilizing the identification of SNPs and diet/supplement optimization?

MTHFR, apoE4, metallotheinin, glutathione, etc are among many SNPs which determine our inflammatory status, and thus oxLDL and sdLDL and insulin resistance and tolerability to gluten/casein (because accumulated mercury binds and toxifies DPP-IV enzyme function, the enzyme which degrades gluten/casein).

Please let me know your results. I'd be curious to review them later.