putting forth great effort to be sure that you have
grasped the basics, then practicing so that they may
come to fruition is something that will never stop for
your whole lifetime. Do not rely on following the
degree of understanding that you have discovered,
but simply think. . . This is not enough.”
Hagakure, Yamamoto Tsunetomo (a Samurai)
September 10, 1716
Quoted by Dr. Superko, MD
Often at TrackYourPlaque I've been curious as to why regression on CT isn't admittedly easy as pie... like one-two-three... ?? A-B-C...??
Routinely now I would say all the lipoproteins I've been coaching or those that refer to us from Paleo/ Primal/ Protein Power sites are being reported at goal and optimal within months of starting TYP or after only 4-5 weeks of tweaking the diet. These wonderous and spectacular results are reported by members, both new and old, with HORRIFIC family histories of premature CAD events. Lp(a) is a risk factor for 90-100% of these individuals, the toxic vascular plaque accelerant.
Yes, all are Paleo or lacto-Paleo.
Yes, all are moderate to HIGH dietary saturated fat.
Yes, all are lower carb or VLC (very low carb).
No, they do not necessarily lose weight.
No, no changes in the $200+ supplements per month. (or...even better taking virtually none)
No, it was not hard. (OK, maybe... !debatable, but hey members pay $80/yr to learn how to live the 'spartan' *ironic laugh* tasty, high fat life where you feel younger, more vital, enjoy better skin/hair and at the same time beat subclinical CAD and stroke risks!??)
Yes, some LOWERED THE DOSE OF THE STATIN by extreme measures (sometimes against the advice of their LDL-centric-fool-cardiologist... SSSSSHhhhh)
because of the, remember, low-trig-statin- i-n-t-e-r-a-c-t-i-o-n.
Yes, repeat, they lowered the stupid-statin-red-pill and obtained BETTER RESULTS.
Or... unequivocally better no statins at all.
Yes, they are not unlike the previous Paleo/semi-Paleo (statin-free) peeps I profiled earlier HERE including Doug/dcarrns regression story.
Why do statins ruin results often? Maybe because they are actually ineffective in this world of 'whole grain happiness' and veggie oil madness? Maybe because Lp(a) is not responsive to statins and, in fact, statins raise Lp(a)? Maybe because IDL, another frequent and overlooked cause of premature and subclinical atherosclerosis, is not responsive to statins? Maybe because statins completely fail to shift lipoproteins to the desirable Pattern 'A'? Maybe because statins do not lower coronary calcifications on EBCT or MDCT in over a dozen of trials that I've reviewed? Maybe because statins block wound-healing which may not exclude plaque lesions? Maybe because statins cause muscle tissue breakdown, mitochondrial defects and coenzme Q10 depletion? Maybe because statins inhibits nerve ending re-myelination of our nervous system?
Maybe because statins prevent the formation of Large LDL which are the primary/only transport units in our circulatory system for cancer- and heart-protective antioxidants like Vitamin K2 (MK-4 through MK-9), Carotenoids (Astaxanthin, Lutein and the 200+ others), Vitamin E tocopherols tocotrienols, and cholesterol which comprises 20+% of our nervous system, integral to every cell membrane and the provides the backbone structure to ALL our vital hormones necessary for life, survival and reproduction?? (Vitamin A, another fat-soluble 'hormone-like' nutrient, on the other hand is so important it has its own transporter known as retinol binding proteins.) For regression and hard clinical event reduction, Dr. B.G. Brown showed in the landmark 3-yr HATS trial in post-CAD men and women (see below graph), the treatment group achieved a high rate of large buoyant LDL (~70% of participants) and HDL2 increased by 61% (total HDL increased 30% from baseline low-30's mg/dl). About 25-30% of participants had Lp(a).
Many cardiologists are starting to speak out about statins' frank lack of outcomes and even their dangerous side effects. Stanford doctor Dr. Mark Hlatky, MD is no exception in an NEJM editorial HERE. How scary is it that the statin industry is trying to peddle these teratogenic Category 'X' drugs to S.A.D. obese teenagers (who might have s*x and might get pregnant)? Obese children are their targets too, children who have rapidly growing brains and nervous systems which require cholesterol?
How about... Lack of regression? Marginal regression? 'Sucky' lack of clinical reduction in coronary events when comprehensively compared to niacin trials and omega-3 trials? Do cardiologists even know regression if it smacked them in the knee? Like those that sit on committees? In the AHA?
Question: Which drug/vitamin, which mimics ketosis, trumps statins in comparisons of CAD outcomes, all-cause mortality, AND angiographic-regression studies, by raising Large HDL2, lowering small dense LDL and controlling toxic Lp(a)? (Figure 1, from the below reference)
Lipid management to reduce cardiovascular risk: a new strategy is required.
Superko HR, King S 3rd.
Circulation. 2008 Jan 29;117(4):560-8; discussion 568. Free PDF
"Myopic Focus on LDL"
Soon I'll be meeting a patient of Dr. Superko's from 10yrs ago; this gentleman was on niacin and doing NMR subfractionation of cholesterol lipoproteins before it became en vogue at places like TrackYourPlaque. I find it be a quite a coincidence because I've been reading much of Dr. Superko's work the last few weeks. Dr. Superko was no longer his physician after he became busy on the lecture circuit and with Berkeley Heart Lab. It appears this eminent cardiologist, prolific researcher, and author is still pretty busy and now earnestly trying to prevent more Americans from dying from the coronary artery disease epidemic. Will it be enough?
"Although this level of success in the fight against heart disease is laudable, a great danger for our patients’ future health lies in the assumption that cholesterol reduction alone will stem the tide of coronary heart disease (CHD). It is wise and prudent to remember the words of Yamamoto Tsunetomo that “this is not enough.” The purpose of this article is to challenge healthcare workers to consider the possibility that the cholesterol-lowering program has in large part failed to stem the epidemic of CHD and that the well-meaning focus on LDL-C reduction has deflected interest in other therapeutic aspects of lipoprotein treatment that provide equal or greater benefit. This myopic focus on LDL alone is not surprising because, so far, guidelines have not adequately addressed other evidence."
"Statistical Significance Does Not Necessarily Mean Clinical Relevance"
Which strategies appear to lower CAD risk the most? It appears from Superko's provocative assertions that raising Large HDL2-cholesterol is the most critical according to current secondary prevention studies (niacin: HATS HATS-MetSyn FATS FATS-10yr CDP CDP-15yr CLAS-I CLAS-II ARBITER). With trials like the well-designed secondary trial in post-MI men and women, the Lyon Diet Heart, it was observed how mildly re-balancing the n-6:3 ratio resulted in 73% reduction in CAD events as well nearly an equally impressive 70% reduction in all-cause mortality (cancer, accidents, suicides, etc). In fact, in the Lyon Diet trial, LDL increased 1.7% and HDL decreased (yikes) 3%. Could the improvements in death rates be from increases in the Large HDL2? Subfractionation of the lipids were not done (or at least I can't find them) but that is necessary to see below the surface how omega-3 fatty acids work. Omega-3 PUFAs, like saturated fatty acids, bind PPAR and effectively lower small LDL (which are toxic) and raise Large HDL (which are regressive). Quite literally, in clinical trials, fish oil does not change total HDL-Cholesterol hardly at all but instead invokes dramatic, TECTONIC shifts in HDL2, sometimes even increasing by 150-300%. Niacin has a similar shifting effect on subfractions enlarging and enriching small particles into larger, buoyant, fluffier particles. Like omega-3 PUFAs and saturated fatty acids, niacin improves both HDL and LDL particle content and functionality.
"Statistical, or mathematical, significance is a tool useful in calculating how likely it is that the results of an experiment are due to chance alone and not really due to the intervention. Achieving statistical significance generally means that the results observed probably were not due to chance alone and probably were the result of the intervention used in the clinical trial. A value of P=0.05 indicates that there is still a 1 in 20 chance that the results were due to chance alone and not the intervention. Thus, statistical significance is a mathematical tool to test the hypothesis that the results observed were probably due to the intervention, but it does not necessarily mean the results are clinically significant or even meaningful..."
"The potential harm in the assumption that mathematical significance is equivalent to clinical significance is that many public and professional individuals have the misleading impression that if they just get their LDL-C low enough, they will be free of CHD risk. The results of 5 large statin trials show that this is a dangerous misconception in that it leaves large numbers of patients still at risk for cardiovascular events."
Statins and LDL reduction... 'This is not enough.'
Niacin . . . m a y b e .
Diet is definitely the best. Trumps them all.
At TrackYourPlaque we agree with Superko and have taken it further.
Grasp the 'Basics' for Regression (TYP Goals):
1. No statins
2. Vitamin D > 60
3. Trig < 60
4. HDL > 60
5. Small LDL less than 10% or none (LDL-IVb as low as possible and diet works well, again, very VERY well)
6. Large LDL > 60%
7. Large HDL (2b) > 50%
Regression is associated with Large HDL (Krauss RM et al, ATVB 1996).
Progression is associated with Small LDL, notably LDL-IVb (Superko HR, Krauss RM et al, ATVB 2003).
Answer: Niacin (which mimics ketotic diets, coming up in Benefits of High-Saturated Fat Diets, Parts VI and VII)