Sunday, July 19, 2009

Don't Blow Your WOD on Your First Snatch...

...Or First Jerk *ahhhh*
...Or First 2 Rounds of Tabata Torture

I don't know what attracted me to Crossfit first...

How Crossfit diet and health principles are aligned with TYP... The Paleo diet which 80-90% of all members and trainers follow for optimal performance, gains and superior health... Robb and Nicki's gym (ranked top 30 in the U.S. By Men's Health)... the HAWWT people at my gym... my first warrior trainer Luca who could rip your head off if he wanted to... the MLF who keep us safe (military, law enforcement, firefighters)... how T-Muscle (formerly known as T-Nation) tries to knock it but can't like HERE...

Or the raunchy, hilarious inside jokes about our workouts!

So here is my progress (in my tri Zoot suit)...

Finally my insulin is better controlled (no more tooth abscess b/c it was pulled and the synthetic progestin nearly out of my f*&#$(@ system) after a year of Hormone H*LL... and the 6-paks are re-emerging...again...


It can be your friend or your enemy. It can grow great hypertrophic muscles or screw your metabolism, jack your hsCRP and prevent loss of belly fat.

Low carb, mod-high fat Paleo and bursts of anaerobic exercise at Crossfit control insulin.

As does
--avoiding dental infections
--avoiding dental inflammation
--avoiding synthetic/FAKE hormones which increase inflammation and insulin

OK I learned the hard dumb way.

In my experience (and Robb Wolf's), Paleo and Crossfit control autoimmune diseases and chronic inflammation, the crux of today's modern illnesses including heart disease. Our gym has a story of normalization of NASH/fatty liver disease within ONLY 1 month of Crossfit/Paleo, in addition to stories of complete reversal of IBS cases and many fantastic stories of 30-50 lb-weight loss. Robb has a tale of two pharmacists *cough cough* with NASH/fatty liver (which is autoimmune) and resolution with Paleo eating and Crossfit (one case the liver tests were so high, he was on a liver transplant list), and numerous other stories including one painful/burning, autoimmune lower extremity vasculitis (who I met at his b-day party) and another lifelong cutaneous tarda.

Here are my studmuffin Xfit homeys. Our Diablo Crossfit affiliate gym came in 16th out of 100 Xfit gyms. Congrats babes and boys! Y'll R-O-C-K.

Today for Sunday's WOD (workout of the day) we did TABATA... torture... *haa*

Tabata deadlift (135lb men, 95lb women, barbell deadlifts)
Tabata dumbbell push press (men 45lb dbs, women 25lb)
Tabata burpee

A "Tabata" is 20 seconds of work followed by 10 seconds of rest. 8 rounds total (4 minutes). Count reps for each round. Your 'score' for each exercise is the lowest number of reps completed in any one round.

My score: DL 43# 11 times; DB PP 15# b/c I suck 6 times; burpee 4

The key of course to Tabata is to pace yourself. Don't blow your WOD on the first one to two successive rounds.

Sunday, July 12, 2009

Crestor Raises %-Small Dense LDL (Anti-Regressive)

"It takes a wise doctor to know when to prescribe, and at times the greater skill consists in not applying remedies."

B. Gracian
The Art Of Worldly Wisdom

Definition of %-sdLDL ('concentration' of sdLDL)

%-sdLDL = (small dense LDL)/(Total LDL)

Total LDL = large LDL + IDL + sdLDL + Lp(a)

What's Lp(a)? Large Lp(a) + small Lp(a)

Pattern A: Dominance of Large LDL (desirable)
Pattern BAD: Dominance of Small LDL (undesirable)


Judicious use of medications can bring about therapeutic outcomes or can have dire consequences. In medicine, it is truly an art form to balance the two, more than a science. Science however can provide a better understanding of what ancient doctors like Hippocrates or others in the last half century have known as wisdom and deep experience showed them.

'Mindless Statinators'

(Thanks Barkeater for that phrase *WINK*) Growing evidence shows that statins have 'differential' effects on people who take them. The lower the insulin resistance, the less the small LDL particles are reduced. In fact, two studies have shown that the most potent statin Crestor/rosuvastatin in fact raises small LDL concentrations when Triglycerides (TG, Trig) are less than 120 mg/dl (see first table, above, Kostapanos MS et al. Clin Ther 2007).

Or if Trigs are less than 88 mg/dl (1.0 mmol/L)... (see below Caslake MJ et al. Atherosclerosis 2003)

Or if Trigs are less than 177 mg/dl (2.0 mmol/L)... (see below, significant data points sdLDL% increased)


Trigs are low in nearly all low-carb compliant TYP'ers! And definitely 100% of people on low carb PALEO.

Crestor is QUITE potent.

At 40mg daily it is THE most potent statin on the market for sledge-hammering down all the LDL particles (large v. small). Caslake et al (Table 2) found that for normotriglyceridemic individuals LDLIII (small dense) % increased from 15.3% to 21.9% (delta = +6.6% sdLDL%) after 8wks only on the maximum dose Crestor 40mg daily (see below graph with comments, the authors failed to put zero on the So please look at how %-sdLDL increases as the Trigs are less than 88 mg/dl = 1.0 mmol/L and even for a great majority of data points less than 177 mg/dl = 2.0 mmol/L).

What a terrible, counterproduct, ANTI-REGRESSIVE adverse drug effect.

TYP Goal for Regression:

The goal for combatting heart disease and to invoke regression/ reversal/ eradication of plaque is to achieve a lower concentration of small dense LDL. Surprising, regression on EBT is frequently reported even before all TYP goals are met! (Wonderful cases of late -- hillbrow, Lindybill, dcarrns!)

Like dense ignorant people, we want the least amount of density and a transformation to lighter, buoyant, more athero-protective LDL particles.

Statins can hurt people as we know (myositis, peripheral nerve effects, brain damage, depression, accidents, suicide, vision reduction, erectile dysfunction, want me to go and on...?! autoimmune disease, inflammation at the mitochondrial and cellular level, liver/kidney failure related to rhabdomyolysis, death, etc).


Statins in fact can hinder EBT regression I strongly believe and examples unfortunately exist (the REGRESSION 10yr-subanalysis is an example of higher cardiac mortality in the statin-arm in a sub-group that exhibited a phenotype/genotype for low triglyerides). When an individual temporarily stops or backs off on the dose, the large LDL re-appear and the concentration of small LDL decrease. The sdLDL may not be exceptionally great compared to sdLDL reductions promoted by low LOW carb, mod-high fat diets or ketotic diets, but they DO IMPROVE noticeably as a result from 'statin holidays'. An example of statin suppression of large LDL suppression is for instance if one had an %-sdLDL=300/300=100% improve to 200/400= 50% after stopping Crestor for 1-2mos (Trigs always stay low when a TYP'er stops their statin because nearly all TYP strategies are insulin sensitizing).

That makes sense, right? You don't have to be a 20-year trained cardiologist or lipidologist to understand this data. If Trigs are less than 120 mg/dl, then small LDL concentrations are going to start growing. The graph actually shows that the lower the Trigs go, the HIGHER THE SMALL DENSE LDL CONCENTRATION BECOMES.

What is the effect over time?

What is this effect month after month after month.

What is this effect year after year after year of statin-addiction.

I can't even imagine. F*ck aint regression.

EBT Calcification Progression? Y E S .

Iatrogenic, drug-induced coronary calcifications? One study with Lipitor has shown increased coronary calcifications in aortic stenosis patients compared to the placebo. Unfortunately, I see statins as well associated with coronary calcification progression on EBT when individuals continue the statin therapy after Trigs hit Dr. Davis' TYP goal of less than 60 mg/dl. To achieve EBT regression (HATS trial NEJM 2001 91% reduction in coronary mortality/ events in 3yrs NIACIN NIACIN NIACIN + simva 40/d), some reduction in sdLDL concentration is mandatory. Not... necessarily a lot.

Most individuals with severe coronary disease have ALL small dense LDL particles. In fact 100% concentration of sdLDL is not uncommon at all, at the start of the TYP program.

To reach Dr. Davis' goal of 10% concentration of sdLDL, 90% reduction in %-sdLDL would help to achieve regression. It is not the end all, however. It is demonstrated over and over that perfect lipoproteins (esp LDL=60mg/dl) doesn't guarantee SH*T when it's 100% sdLDL. Regression fails to occur in those who persist in over-statinating when the Trigs are excellent less than 120 mg/dl.

Persistently Elevated sdLDL-Concentrations

The signs and symptoms of over-statinating are subtle. They involve persistly high sdLDL-concentrations that do not decrease with TYP strategies, low carb dieting and even the addition of fats which normally remodel sdLDL into large buoyant beautific particles (omega-3, eggs, coconut oil, krill oil, etc). In fact, sometimes (yikes!) the statin effect appears to lead to HIGHER small LDL particle counts and concentrations. Sadly these individuals (to me... IMHO) have disappointing EBT progressions of 10-25% year after year, despite all their wonderful, hard work, good intentions and optimism... Despite spectacular, dramatic reductions in Lp(a).... Unfortunately the Lp(a) is all dense, all small, all drug-related Lp(a) which may actually be accelerating progressive damage.

Would've been better to not be on a statin at all in the first place? Well, perhaps there is value in the first 1-2 wks of the TYP program, but as you can see from post-CAD patients, insulin sensitivity and Trigs are easily controlled with no starch or ketotic diets within only 6 wks (Hays JH Mayo Clinic Proc 2003).

Six weeks... 42 days. Do you have 42 days?

Those who are statin-less at TYP (Mr. 'H', Mr. 'C', Dr. 'K') on the other hand witnessed large %-sdLDL reductions with each NMR or VAP lipoprotein test, perfect increases in large LDL and magnificent reductions in small LDL (even 'NONE') and consequently report EBT regression (Mr. 'C' and Dr. 'K' are pending, I have no doubt). 'Pretty lipoproteins' do not equal regression... it is how the pretty lipoproteins are achieved and the downward trends, with the minimization of iatrogenic, inflammatory drug effects.

Reduction in small dense LDL% is a very important goal to not ignore for atherosclerotic disease regression and eradication because small dense LDL reflects the internal inflammatory status.

ALL Statins Increase %-Small Dense LDL If Trigs Are Low

Crestor is not alone.

The other statins are NOT exempt.

Lipitor does it too.

They are certainly in fine company. The off-patent generic statins do it as well.

No Starches/High-Fat Diet Decreases %-sdLDL By 10%

I will review this in more detail later but this VERY short trial excellently demonstrates the efficacy and safety of a ketotic diet in post-CAD-event men and women, in producing dramatic lipoprotein changes in only 6wks. By eliminating starches and restricting fruit and increasing protein and dietary cholesterol and fat, concentrations of small dense LDL reduced from 35% to 25%. These patients were on lipid-lowering medications and the average LDL was 100 mg/dl (not high whopper doses of statins apparently). During the feeding diet, Trigs diminished from 147 mg/dl to only 88 mg/dl.

Effect of a high saturated fat and no-starch diet on serum lipid subfractions in patients with documented atherosclerotic cardiovascular disease. Hays JH, DiSabatino A, Gorman RT, Vincent S, Stillabower ME.Mayo Clin Proc. 2003 Nov;78(11):1331-6.


A 12-week, prospective, open-label analysis of the effect of rosuvastatin on triglyceride-rich lipoprotein metabolism in patients with primary dyslipidemia. (A significant increase in mean LDL particle size after rosuvastatin treatment (mean [SD], from 26.4 [0.4] to 26.9 [0.4] rim; P = 0.02) was observed only in patients with baseline TG levels greater than or =120 mg/dL.)Kostapanos MS, Milionis HJ, Filippatos TD, Nakou ES, Bairaktari ET, Tselepis AD, Elisaf MS.
Clin Ther. 2007 Jul;29(7):1403-14.
PMID: 17825691

Phenotype-dependent and -independent actions of rosuvastatin on atherogenic lipoprotein subfractions in hyperlipidaemia.
Caslake MJ, Stewart G, Day SP, Daly E, McTaggart F, Chapman MJ, Durrington P, Laggner P, Mackness M, Pears J, Packard CJ.
Atherosclerosis. 2003 Dec;171(2):245-53.
PMID: 14644393

Comparative effects on lipid levels of combination therapy with a statin and extended-release niacin or ezetimibe versus a statin alone (the COMPELL study). (Lipitor raises sdLDL% W T F... Crestor largely does not lower sdLDL concentrations much UNLESS NIACIN IS ON BOARD; Both Crestor and Lipitor wtf raise Lp(a), the most toxic, atherosclerosis-accelerating blood component carried by 17-25% of the general population)
McKenney JM, Jones PH, Bays HE, Knopp RH, Kashyap ML, Ruoff GE, McGovern ME.
Atherosclerosis. 2007 Jun;192(2):432-7. Epub 2007 Jan 19.
PMID: 17239888

Baseline triglyceride levels and insulin sensitivity are major determinants of the increase of LDL particle size and buoyancy induced by rosuvastatin treatment in patients with primary hyperlipidemia.
Kostapanos MS, Milionis HJ, Lagos KG, Rizos CB, Tselepis AD, Elisaf MS.
Eur J Pharmacol. 2008 Aug 20;590(1-3):327-32. Epub 2008 Jun 7.
PMID: 18585701

Effects of maximal doses of atorvastatin versus rosuvastatin on small dense low-density lipoprotein cholesterol levels. (Table 3 shows Lipitor INCREASES wtf sdLDL% +10% and Crestor 40mg makes virtually no change in sdLDL% at this dose (-5%))
Ai M, Otokozawa S, Asztalos BF, Nakajima K, Stein E, Jones PH, Schaefer EJ.
Am J Cardiol. 2008 Feb 1;101(3):315-8. Epub 2007 Dec 20.
PMID: 18237592