“It is not good to settle into a set of opinions. At first 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, September 10, 1716 (a Samurai), 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 come from Paleo/Protein Power sites are being reported at goal and optimal within months of starting TYP from the get go or after 4-5 weeks of tweaking the diet. Often these wonderous results are reported by members, both new and old, with HORRIFIC family histories of premature CAD events.
Yes, all are Paleo or lacto-Paleo. Yes, all are moderate to HIGH dietary saturated fat. No fear of fats! 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.
Yes, they LOWERED THE DOSE OF THE STATIN by extreme measures (sometimes against the advice of their cardiologist... SSSSSHhhhh) because of the, remember, low-Trig-statin- i-n-t-e-r-a-c-t-i-o-n.
Yes, they are not unlike the previous Paleo/semi-Paleo 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? Many cardiologists are starting to speak out about their frank lack of outcomes. How scary is it that the statin industry is trying to peddle these teratogenic drugs to S.A.D. obese children and teenagers?
Lack of regression? Marginal regression? Clinically speaking, 'sucky' lack of clinical reduction in coronary events compared with 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 and all-cause mortality studies, by raising Large HDL2 and lowering small dense LDL? (Figure 1, from the below reference)
Soon I'll be meeting a patient of Dr. Superko's from 10yrs ago before he became busy on the lecture circuit and with Berkeley Heart Lab. It appears this eminent cardiologist 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 appears 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-DM 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 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 effects both HDL and LDL particles.
"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.
Grasp the 'Basics' for Regression (TYP Goals): Vitamin D > 60 Trig < 60 HDL > 60 Small LDL less than 10% or none (LDL-IVb as low as possible and diet works well) Large LDL > 60% Large HDL (2b) > 50%