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...

Insulin.

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*

Workout:
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.

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)



Over-Medication

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)


WOWO.

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 x-axis...wtf. 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:
small LDL NEAR-ZERO or DOWNWARD TREND

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).

OK.

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 me...it 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.



References

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

Benefits of High-Saturated Fat Diets (Part IV): REGRESSION IN HEART PATIENTS

Few studies review the benefits of high-saturated fat diets in actual heart disease patients. Perhaps, researchers worry about... M A L P R A C T I C E . . . ?

Like urban myths, do such studies exist?

Indeed studies of high saturated fat diets in heart disease patients IN FACT do EXIST.

LA...la la la... I feel on top of the world... (LMFAO)


The diagram exemplifies a normal coronary artery, with a large.. wide diameter... spacious... flexible.. lumen (Courtesy: medicinenet.org). The diameter of the artery can be measured accurately down to fractions of a millimeter via angiography.

It was observed that in post-menopausal women with documented heart disease from the Estrogen Replacement and Atherosclerosis (ERA) trial, a multicenter clinical trial evaluating the effects of hormone replacement therapy on atherosclerotic progression, in the group consuming the highest-saturated dietary fat diet (12.0% Sat Fat), an enlargement in coronary diameter of 0.01 mm and a 0.1% regression in coronary artery stenosis.

Quoted to Men's Health, "In the nutrition field, it's very difficult to get something published that goes against established dogma," said Dr. Dariush Mozaffarian MD MPH, assistant professor, Harvard. "The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence." Mozaffarian says he believes it's critical that scientists remain open minded. "Our finding was surprising to us. And when there's a discovery that goes against what's established, it shouldn't be suppressed but rather disseminated and explored as much as possible."

In a year during my pharmacy student training at Stanford, I worked with Dariush on an internal med rotation for 4wks. I think I learned more about drugs and how to use them than some of my preceptors combined. His teaching approaches were usually articulate, concise and patiently provided. Gosh, can I say, I've had serendipity with many mentors in my little drug journey so far. *haa*

• Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. PDF click HERE. Mozaffarian D, Rimm EB, Herrington DM. Am J Clin Nutr. 2004 Nov;80(5):1175-84. EDITORIAL. Figure 1 below.
  

Dividing the saturated fat intake into quartiles, the individuals at the highest quartile (dietary saturated fat intake: 12.0%) demonstrated the least progression on angiogram of coronary diameter. In fact, this was the only group that exhibited REGRESSION.

This group was also characterized as having the:
--least medications, including lipid-lowering medications
--the least medications and the higher the saturated fat, the more coronary artery widening in coronary artery diameter
--highest LDL (low density lipoprotein) measurements
--highest HDL (high density lipoprotein 'good cholesterol)
--highest HDL2 (the regressive particle)
--lowest Trigs
--MOST PAST AND CURRENT SMOKERS
--highest dietary fat intake (32%)
--highest monounsaturated fat intake
--lowest dietary carbohydrate intake (47.1% v. (!!) 69%)



Improved Anti-Atherogenic Lipoproteins
"A higher saturated fat intake was associated with a more favorable lipoprotein profile, including higher HDL,HDL2, and HDL3 cholesterol; higher apoprotein A-I; lower triacylglycerolc oncentrations; and a lower ratio of total cholesterol(TC) to HDL cholesterol (TC:HDL cholesterol). Women who consumed more saturated fat consumed less carbohydrate and dietary fiber and more total fat, protein, cholesterol, polyunsaturated fat, trans fatty acids, and monounsaturated fat."



Lipid-Lowering Drugs: The Less, The More Regression
The researchers astutely noticed that "among the women not taking lipid-lowering medication at baseline or during follow-up, there was 0.22 mm less progression for each 5% greater energy intake from saturated fat, compared with 0.09 mm less progression for each 5% greater energy intake from saturated fat among women taking lipid-lowering medication (P = for interaction 0.008)."


Omega-6 PUFAs: Highly Associated with Progression
After the Lyon-Diet Heart trial was completed and showed a dramatic reduction in all-cause mortality, cardiac death and events with simple reductions in omega-6 PUFAs and increase omega-3 from fish and ALA sources like olive oil, I think this trial hits it home again that any increase in dietary PUFAs are extremely pro-inflammatory leading to progression of coronary artery diameter reductions. The lowest quartile consumed less than 3.9% PUFA which was positively (see above) associated with less of a decline of average minimal coronary artery diameter (P for trend =0.04) compared with other quartiles. Clearly, a dietary PUFA concentration greater than 3.9% was highly statistically correlated to angiogram progression. The highest quartile that consumed 7.5% PUFA in the diet this was shown to produce the second highest amount of artery diameter constriction in this trial.

FIGURE 1 (divided, above, below). Mean (SE) change in minimal coronary artery diameter according to intake of different nutrients, with adjustments as in Table 2 (see footnote 1), except that total fat was not adjusted for carbohydrate, and carbohydrate and protein were also adjusted for polyunsaturated fat. These models estimate the effect of saturated fat replacing other fats (monounsaturated or polyunsaturated),monounsaturated fat replacing other fats (saturated or polyunsaturated), polyunsaturated fat replacing other fats (saturated or monounsaturated), total fat replacing carbohydrate, carbohydrate replacing saturated or monounsaturated fat, and protein replacingsaturated or monounsaturated fat.

Median intakes(% of energy) for quartiles 1–4 were as follows:
saturated fat*** (6.1, 7.8, 9.5, and 12.0),
monounsaturated fat (6.9, 8.6, 10.7, and 13.0),
polyunsaturated fat** (3.9, 5.2, 6.1, and 7.5),

total fat (17.6, 21.7, 27.0, and 31.9),
carbohydrate* (47.1, 55.6, 60.5, and 68.9)
protein (12.7, 15.8, 18.0, and 21.2).

P for trend = 0.001 (**saturated fat), 0.40(monounsaturated fat), 0.04 (**polyunsaturated fat), 0.48 (total fat), 0.20 (protein), and 0.001 (*carbohydrate).

High Carbohydrate Intake: Associated with Coronary Plaque Progression
The authors also found that "Carbohydrate intake (see above) was strongly positively associated with progression, with a 19-mm greater decline in mean minimal coronary artery diameter in a comparisonof extreme quartiles of intake (P for trend = 0.001)."


Overview
The design of this particular study was novel in examining multiple dietary components against a validated heart disease marker for progression. Obviously, prospective RCTs utilizing high-saturated fat, low carb, low PUFA diets would constitute the best scenarios to show unequivocal heart disease reversal. Am I going to hold my breath?



R e g r e s s i o n
With a high-saturated fat diet in documented heart disease patients... coronary artery stenosis regression occurred shockingly in individuals who took less lipid-lower drugs, smoked more, and basically were hedonistic beyond a conventional cardiologist's belief. Should we live life a little dangerously... disobey the 'rules'?

Show Me Your Lipids!

If you have great HDLs please let me know your HDLs and lipid panel!

If you have an LDL particle size and count, as Robb Wolf suggests getting at his Crossfit Nutrition certifications (yes, I am certified . . . be scared), that would be bangin as well...

Benefits of High-Saturated Fat Diets (Part III): My Paleo Peeps With High HDLs

Wanna know what impresses?

Gambling...? Gawwds, no...got no pokerface... (Lady Gaga)


Tell me your labs. (Or show me ur abs...j/k)

You'll get a reaction.

Yeah, you thought... I was... e a s y. *ahhhaa*

I'm not.



When I hear an HDL cholesterol is off the charts, like triple-digit-over-100 mg/dl... you my dear have my full attention.



HDL Cholesterol: The Higher, The HOTTER

HAWT HDLs.

The goal for health optimization for HDL-cholesterol is 60 mg/dl or higher. Studies like the Four Prospective American Studies by Castelli WP et al found "A 1-mg/dl increment in HDL-C was associated with a significant coronary heart disease risk decrement of 2% in men (Framingham/FHS, CPPT, and MRFIT) and 3% in women (FHS)."

According to master cardiologist Dr. Castelli (who has successfully escaped premature family hx of CAD), if one's baseline HDLs are 30's and one increases this to 80's, this may represent a 100% reduction in relative risk for a coronary event. For girls, if one increases from HDLs 50's to 80's, then also a 100% coronary risk reduction could be relied upon.

Sounds excellent to me!

It is not difficult to raise HDLs.

This is observed all over in the evolutionary/paleo blogosphere, at Bernstein's diabetes, Protein Power Drs.Eades blog, at TYP in only those on high sat fat and/or [no or low-statin+wt-loss] and in clinical practice ALL THE TIME.

Eliminating wheat/d*mn-dirty-GRAINS/carbs, adding some vitamin D, omega-3s, Taurine, and Slo-Niacin 1-2 grams/day. Throwing away the Mazola and any packaged food items. Oh yeah, and add some fat. Individuals may continue their EVO (but not too much b/c it cranks up hepatic lipase, see HERE) but they increase eggs 2-6 daily, add some (organic nitrate-free preferably) bacon and some coconut oil.

And...reduce their statin (if even taking).

I know, s a c r i l e g e . . .

Consider the value of not over-statinating.

Over-statinating stagnates the formation of large particles. wtf. This is observed on the TYP forum frequently in over-statinators -- and easily corrected. The statin or fibrate is withheld or severely dose-reduced (TYPically, I advise 'licking the tablet' and that is a clinical term). See below medscape cases as well.

Yes, statins and fibrates LOWER HDLs ('good chol') for many individuals. Lipitor is the worse. Drugs appear to cause a 'ceiling' effect for HDLs and small dense LDL. Marginally on paper these may improve, however iatrogenically they fail to improve FURTHER beyond the ceiling.

Esp if low sat fat.

Esp additionally if you are an apo E2 carrier (you have lower TC LDL HDLs compared to the general pop). Or... if you eat low fat, low cholesterol, low saturated fatty acids. The interaction is hypothesized to be related to a statin-and/or-fibrate-related apo A1 reduction in activity (and because you are chol/saturated-fatty-acid-deficient).

Please, Ladies and Gents... what nicely raises cardioprotective HDLs (and apoA1) and lowers TOXIC small LDL and Lp(a) ?Saturated fat and C H O L E S T E R O L.


Yeah, even if you are moderately high carb, smoke, and had an event already. We'll go over some post-CAD event trials in the near future to describe yet again some interesting paradoxes. Eat fat to lower body fat. Eat fat to lower bad fat, the sdLDL. Eat fat to raise 'happy' good HDL cholesterol. Hhhhmmm... provocative? Our Paleo experiences and the medical literature will tell us.o Paradoxical Decrease in HDL-Cholesterol With Statin and Fenofibrate Combo: S E V E N Case Reports (medscape.com)

o Castelli WP, et al. High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study. Am J Med. 1977 May;62(5):707–714.

o Castelli WP, et al. High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation. 1989 Jan;79(1):8-15.

----> If you'd like to amuse yourself and see how cardio-stat-idiots attempt to debate themselves out of the above clinical findings, read THIS. "We found no significant association of change in HDL cholesterol with the log risk ratio in any model after adjustment for changes in LDL cholesterol." wtf? Note their funding... 'unrestricted grant from... Pfizer.'




Paleo Maximizes/Magnifies HDLs

Below are my Paleo peeps who have ROCKIN' ghetto-FAB lipoproteins with Paleo (or semi-Paleo) (units are mg/dl):

)Mr. Stephan Guyenet (almost-Paleo)
TC 252
TG 49
HDL 111
Real LDL (n/a)
Calc LDL 131 (wrong, but who cares)


Mr. Scott Miller (BF 9% -- nukem, dude, awesome! Lives the ultimate Paleo expanded lifespan plan...lots of coconut oil/70% dark chocolate, some HIIT 3 min/wk that mimics evo-behavior/hunting...zen-like martial arts. He smokes out his friends on 3hr-vigorous mountain bike rides w/minimal effort.)
TC 223
TG 51
HDL 98 (baseline: 38-ish and BF 26%)
Real LDL (n/a)
Calc LDL 125
Lp(a) 2


Mrs. Anna (Against the Grain GRRRLL! )
TC 230 (2007, still transitioning to sat fat/grain-free)
TG 59
HDL 72 (from 60's)
Calc LDL 146


Ms. Anne (Paleo and grain-free)
TC 255
TG 36
HDL 93
Real LDL (n/a)
Calc LDL 154


Mr. Jimmy Moore
Diet: La-Vida-low carb/70%-high-fat
Small-LDL: nearly big PHAT zero on NMR
Large-LDL: ALL per interview with Dr. Davis
Family hx of premature CAD: YES
EBT score: wish I knew... wanna wager 'zero'? Bummer, said I didn't gamble... right? *ha*
My Labs:
6/2009 (on coconut oil, Paleo, [25OHD]=50 ng/ml)
TC 249
TG 68
HDL 105
Real LDL 125
Calc LDL 130 (wrong by 4% but, again, who's counting)
Lp(a) 2


12/2008 (Paleo/Xfit+15#muscle, [25OHD]=60 ng/ml)
TC 229
TG 82
HDL 89
Calc LDL 124

2/2008 ([25OHD]=80 ng/ml; started X-fit)
TC 190
TG 37
HDL 84
Calc LDL 99

10/2007 (vit D deficient [25OHD]=20 ng/ml)TC 170
TG 51HDL 71Calc LDL 90




TYP Hall Of Fame (Statins Optional)

Many others have HDLs to provoke tremendous envy at the TYP forum:

Mr. 'O' (brilliant brain who understands HORMONES, like the powerful hormonal effects of Sat Fat w/the line 'the AHA low fat diet...will kill your HDL...and eventually kill you as well!' *haa* HDL 65 w/niacin IR 1g/d, 6g/d EPA DHA and small amounts of coconut oil; NO STATINS)

Mr. 'D' (EBT regression 5% w/in only 8mos by adding 1-3 Tbs virgin coconut oil, 4 cage-free eggs/d, niacin 1g/day; Large-HDL tripled from 3.2 to 9 umol/L; ABSOLUTELY NO STATINS)

Mr. 'LindyBill' (EBT regression 33.6% in one year and 21% HDL increase from 38 to 46 mg/dl with major weight loss of several inches off the abdomen which accounts for 5-7% Body Fat recomposition (eg, utilization of stored 25-30# Sat Fat) via walking/ball-rm-dancing/ swimming daily and low carb diet; stopped simva 20/d a while ago due to aches but no updated labs; READ, NO STATINS)

Mr. 'H' in the UK (EBT regression 30.2% in one year by walking 1hr per day fast, 3 g/d EPA DHA, niacin 1.5/d, vitamin D, burning 2.5 stone (=5 kgs or 10#) *saturated fatty acids* off the body, Wt Watchers but unlimited (I read: high fat) treats on holiday, high dose vitamin 'O' and... btw... NO HINT OF STATINS)

Dr. 'K' (HDL 68 Feb but probably higher now; reduction in 100% sd-LDL to only 11% by eating COCONUTS and high sat fat, eggs-n-butter, steak, krill-omelets, gamey duck; 9.0 g/d EPA+DHA doesn't hurt for 100% sucky-sd-LDL-baselines...STATIN-FREE)

Mr.&Mrs. 'A' (low carb, high sat fat -- dramatic reductions in Lp(a) by 38%, raising Large-HDL 11 to 22.4 umol/L, raising HDL 63 to 78 mg/dl, and lowering sd-LDL... STATIN-FREE)

Mr. 'C' (Italian Ferrari w/HDL incr from 50 to 79 and now 'zero' Small-LDL (on VAP; on NMR 3.7% LDL-IVb)! Regressive HDL2b from 10 to 43% or 34 mg/dl... Twenty pound body fat loss... yeah btw NO STATIN and SloNiacin 1 g/d, 8 g/d EPA+DHA, krill oil, kelp...low carb, mod Sat Fat, unlimited vegetables, unlimited EVOO, eggs (organic free range plus omega 3), cheese, avocados, red wine, coconut milk (for smoothie), no or limited fruit, cinnamon,unsweetened natural alkaline free cocoa powder; meditation; IF irregular/ unpredictable cycle; lost 20# BF13%)

Mrs. 'M' (HDL=92 mg/dl and teaches me much about omega-3, bless ur heart...STATIN-FREE? undoubtedly!!! on virgin coconut oil + niacin 500mg/d which also dropped sd-LDL despite major hormone imbalances)

Mr. 'P' petroleum engineer ('Unrestricted fats', low carb, Lp(a) reduction of 80% from 70 to 14 mg/dl; niacin 1.5g/am, dhea, 3 g/d EPA DHA, Pauling protocol (L P C), and low dose Crestor)

Mr. 'PBG' (HDL 71 mg/dl, Lp(a) reduced 76% from 83 to 20 mg/dl; sd-LDL reduced to 23% from 56%; statin-free of course)

Mr. 'J' (27# wt loss! on low carb; HDL 61 from 43 mg/dl in a few mos! 42% HDL increase after being statin-free several wks prior to lab testing)

Mr. 'N' (semi-off-not-really-wheat/ carbs, 'mod Sat Fat/pufa' diet; semi-fasts 'perpetually hungry' long 15-20 days every 2mos; 66# wt loss; Lp(a) dropped 85% from 123 to 18 mg/dl; HDL 49 mg/dl who admits when he takes 'lipitor-10mg/d-free holidays' his energy/ mood/ brain brighten)

Dr. 'R' for regression (young endurance triathlete; HDL incr from undetectable b/c TGs 400s to HDL 64 mg/dl; with a low carb Paleo diet with 6kg wt loss and imminst.org antioxidants; simva reduced from 40mg/d to 20mg/d w/the plan to stop after 3mos d/t leg heaviness; I hypothesize astronomical improvements in Lp(a) and EBT but no baselines to report)

Mr. 'R' (elite athlete stud HDL2b 35% and HDLs 115 mg/dl ~200% increase from 60's wow with lower carb etc...mmmm... (still low sat fat) no further comments at this time)

Mr. 'CP' (you ROCK!! HDL 71 from 57 mg/dl and definitely statin-less; 33% sd-LDL% after remarkable 67% drop previous baseline after only 3 mos...how? 'more butter, more eggs, more meat...' despite a lotta back pain)

Mr. 'H' (my favorite hunter and tracker in PA -- 200% increase to HDL 76 from lipitor-low-31 to 40 mg/dl with a Paleo, low carb diet; HEEYYGGE 94.9% sdLDL reduction to nothing 3.4% for sdLDL% that resembles centenarian phenotypes consume ...statin-free? bummer no but low dose and no longer LDL-suppression from effects lipitor 10-20/d or previous low fat diet as evidenced by how the LDLs bounced up from 48 to now. . . PHAT fluffy . . . 90)

And...many others my ADHD memory fails to recall!





Diet?

They all eat a Paleo, semi-Paleo, or Paleo+dairy (eg, Protein Power) or some version of these.

With no fear of fats.

Esp some Sat Fats and Cholesterol (egg yolks).

And oh by the way mainly statin-free.

Esp in the cases with the grossest, most spectacular lipoprotein outcomes (high HDL, low sd-LDL%, lower Lp(a)).




@The Heart of Darkness Dot Org

At a cardiologist forum where I used to pimp TYP/lurk (when I'm thoroughly bored and want to entertain myself with the latest, greatest thoughts of cardio-geniuses), some silly physicians attempted to persuade Mr. Carey (see below) with FH (familial hypercholesterolemia - high LDLs, low HDLs) to give up Paleo/ meat/ no-grains/ no-legumes and adopt the heart-healthy whole-grains WHOLE-DISEASE Mediterrean diet and... reconsider re-statinating himself . . . *wicked laugh*:

"Mediterranean diet was not enough for me. As an FH with a TC of 340, I followed the Mediterranean diet approach (high fiber vegan + salmon +sardines) for over 12 years, while I was on 40mg Pravastatin (TC= 220, HDL = 35, LDL = 130), but after severe plantar fasciitis and muscle wasting set in from the Prav. (even on a dosage reduction to 2mg from 40mg), I stopped rx and tested all the other statins and more without success.

The Paleo diet has changed my ability to metabolize fats, reduced my blood glucose levels, and dramatically increased my HDLs (84). On the same daily running and biking regimen, my body fat % dropped from 15.5% to 8% during the last 6 months. I eat huge quantities of non-cereal, non-grain foods all day and continue to lose weight while feeling far more energetic. As an added benefit, at the age of 44, I recently ran a road race at a pace I have not been able to match since I was on the high school track team.I loved to eat legumes and healthy grains, but I have seen such a dramatic improvement that I will never go back."

His lipoprotein results with Paleo:

"Paleo diet + exercise + psyllium TRIPLED my HDL to 84. I am a slim FH patient who tried and failed to raise my HDL levels above 40 using a low-fat vegetarian, high exercise lifestyle (My LDL was 240). I could not tolerate ANY statin or Welchol. Now, I eat only lean meat, vegetables, fruits and raw nuts while avoiding all sugar, cereals, grains and legumes. With my unchanged intense exercise regimen, I have lost 10 pounds over 6 months, yet grown stronger and faster. I have reduced my LDLs to 202, while raising my HDLs to 84 from as low as 35.
At 44, I feel like I have turned the clock back st least a decade. "

A M E N brother!

Benefits of High-Saturated Fat Diets (Part II): Centenarians, CETP, TYP Diet Part 3

We've been talking a lot of about increasing dietary saturated fatty acids (SFAs) at TYP. The Part 3 Track Your Plaque Diet was published approximately half a year ago and I've been remiss in not promoting it more sooner.

The NEW Track Your Plaque Diet:
Part 3 Special Issues
-- Lp(a)
-- Apo E
-- Diabetes
-- Pre-diabetes
-- Metabolic Syndrome (MetSyn)

Key Summary from Dr. Davis:
--Liberal fat intake of some saturated fats from eggs, meats (non-cured and processed), dairy; monounsaturated; fish oil
--Completely avoid hydrogenated, “trans,” fats
--Wheat and cornstarch reduction or elimination
[Edit: I don't agree with Davis' remaining 'edicts' because they do not appear to work and raise inflammation per clinical trials... =< 200mg cholesterol per day, =< 20 grams saturated fat per day and 15+% omega-6 vegetable PUFAs daily and LDL =< 60 mg/dl]

The Track Your Plaque Basic Diet Principles

Diet Principle #1: Eliminate wheat and cornstarch, limited dairy
Diet Principle #2: Don’t limit fats, but choose the right fats
Diet Principle #3: Unlimited vegetables, some fruits
Diet Principle #4: Unlimited raw nuts and seeds
Diet Principle #5: Unlimited healthy oils
Diet Principle #6: Foods should be unprocessed

Regression or Stabilization

Pioneering the field of cardiovascular research, regression and plaque tracking, Dr. Davis has been promoting (the below) seven TYP goals for Y E A R S . . . light years ahead of the common conventionalist/ interventionalist. New recent observations made by both researchers investigating atherogenic dyslipidemias and by those conducting long-lived healthy centenarian research are, in fact, aligned with several of these seven TYP goals. Maximixation of plaque control and regression have been observed when these seven goals are optimized (TYP 2.0).

For carotid arteries, achievement of any of the below factors will likely induce entire resolution of atherosclerotic plaque. However for the coronary arteries, regression is slightly tougher for a variety of reasons and achievement of all or nearly all seven will support dramatic coronary calcification regression.

Coronary arteries are thinner and more affected by systemic inflammation and the shearing forces secondary to high blood pressure (whether during physical exertion or at rest).

On the other hand, for stabilization and complete elimination of coronary events (angioplasty, stent, MI, bypass or death), gaining control of only three out seven is right on the money... imo.

We define stabilization as EBT CAC score progression of less than 10-20% annual increase.

The average American increase is 30-60% annually (of course faster in Lp(a), apo E4, diabetes and MetSyn).

Wouldn't you like your investment portfolio to grow as fast as American plaque?



So...Easy. To gain control.

Choose any 3.



1) Small-Dense-LDL =< 10% of total LDL particles (imo irregardless of total LDL on NMR or VAP) (Dr. Davis' TYP Goal)

2) HDL > 60 mg/dl (Dr. Davis' TYP Goal)

3) HDL2 (Large-HDL) > 50% of total HDL particles (Dr. Davis' TYP Goal)

4) Large-LDL > 60% total LDL particles (soft goal)

5) vitamin D = 60-80 ng/ml (Dr. Davis' TYP Goal)


6) Sufficient omega-3 ALA and EPA DHA (fatty acid profile, AA:EPA ratio of 1.5-2.0:1; if we flip the ratio around to EPA:AA, in other words omega-3 to omega-6 ratio of 1:1.5, then we're talking 60% of our RBC/cellular membranes being enriched with omega-3 PUFAs content versus omega-6 PUFAs. We really like 60% for some reason at TYP...go figure.)

7) control of inflammation (unfortunately few 'markers' to TRACK):

• dietary (avoidance of gluten, food allergens, casein, etc; adequate ADE K1 K2 MK4-9 vit C B-vits the right ones and minerals Iodine Mg Zn Se, fiber (if tolerated), saturated fatty acids, CLA, GLA, cholesterol, CoQ10/quinones, plant sterols (esp stigmasterol), etc)
• environmental (stay away from plastics/bisphenols/ heavy metal exposure/ pollution/ pesticides, etc)
• mental /psychosocial (stress, excessive physical training, etc)
• hormonal (optimization of thyroid, vit ADEK1K2, omega-3, SFAs, E T P DHEA preg, insulin, cortisol, melatonin, etc)
• pharmaceutical/xenobiotic (adequate intake of antioxidants/ omega-3/ phytochemicals/ FOOD to thwart toxins; avoidance of synthetic hormones, certain drugs (excessive statins), synthetic vitamins (eg, Lurotin, D2/Ergocalciferol, etc), omega-6-PUFA seed/legume oils, etc))
  

Original TYP Goals for Regression: 60-60-60

HDL = 60 mg/dl or higher
TG = 60 mg/dl or lower (#9)
Vitamin D [25OHD] = 60 ng/ml or higher

Am I a *haa* h e r e t i c . . . ?

(LDL = 60 mg/dl is #8 and IMO optional -- this is the easiest with synthetic drugs but unfortunately it prevents #1-4 for some low chol/low fat folks)




VLCD + Cholesterol + SFAs Support 'Super-TYP' Goals #1 through 4

Dr.Volek has published numerous articles on nutrition and metabolism in regards to the benefits of VLCD (very low carb diets) and ketogenic diets in controlling insulin and other hormones. He has shown in various studies how very low carb diets shift small dense LDL particles (atherogenic) to large, fluffy, buoyant LDL particles (regressive). Cholesterol and SFAs (saturated fatty acids) from eggs were demonstrated by Volek to be particularly effective at promoting larger HDL particles, the 'good' cholesterol associated with plaque regression, longevity and cancer protection.

Below is a diagram illustrating the proposal how low carb diets reduce insulin and how high fat/cholesterol diets increase Large-HDL (HDL-2) particles and increase LDL-receptors on adipose cells (and presumably the 'cholesterol core' of atherosclerotic plaque in diseased coronary, carotid, renal and peripheral arteries).

Again, obtaining the lowest proportion of small dense LDL is the holy grail of plaque victims (eg, anyone with a positive (+) EBT coronary calcification score).

Modification of lipoproteins by very low-carbohydrate diets.
Volek JS, Sharman MJ, Forsythe CE.
J Nutr. 2005 Jun;135(6):1339-42. PDF here.

Eggs distinctly modulate plasma carotenoid and lipoprotein subclasses in adult men following a carbohydrate-restricted diet. Mutungi G, Volek JS, et al. J Nutr Biochem. 2009 Apr 13.

Dietary cholesterol from eggs increases plasma HDL cholesterol in overweight men consuming a carbohydrate-restricted diet. Mutungi G, Volek JS, et al. J Nutr. 2008 Feb;138(2):272-6.








Healthy Centenarians Attain ~4 of 7 TYP Goals

Long-lived centenarians, also known as probands, had lipoprotein analyses performed via NMR. Of the markers tracked, four out of seven TYP goals were achieved. Interestingly, centenarian data shows that they still display vitamin D deficiency like the rest of us.

See picture (top)

Figure 2 displaying the Percentage of Large and Small HDL and LDL Particle Sizes in Long-Lived Probands, Offspring, and Ashkenazi and Framingham Controls HDL indicates high-density lipoprotein; LDL, low-density lipoprotein. *P less than .001 for probands vs Ashkenazi and Framingham controls and P less than .001 for offspring vs Ashkenazi and Framingham controls for both large and small HDL and LDL particle sizes.

1) Small-Dense-LDL =< 10% of total LDL particles (irregardless of total LDL on NMR or VAP) (TYP Goal)

2) HDL ~ 60 mg/dl (Table 1: women HDL=56 (SD 15); men HDL=50 (SD 17)) (TYP Goal)

3) HDL2 (Large-HDL) > 50% of total HDL particles (TYP Goal)

4) Large-LDL > 60% total LDL particles (soft goal)


Barzilai N et al. JAMA 2003. Oct 15;290(15):2030-40. Unique lipoprotein phenotype and genotype associated with exceptional longevity.


Apparently this sub-population of Ashkenazi Jewish have a genotype variation on the CETP gene which regulates and controls HDL-particle sizes. HDL-cholesterol is an antioxidant and they have the genetic ability to upregulate Large-HDL particles more than the rest of us. Their offspring may have version as well. The offspring (and controls, who were the spouse of the offspring) who were free of any chronic conditions (no hypertension, no metabolic syndrome, no cardiovascular disease) incidentally displayed similar high HDL particle counts, large HDL and LDL particle sizing and buoyancy, and reached the TYP goals of greater 60% Large-LDL and greater than 50% Large-HDL. Their counterparts with chronic conditions failed to meet these goals.



Polymorphism in CETP Gene and Phenotype of Exceptional Longevity

Can we exert control on our gene expression? We already know by altering omega-3 and vitamin D blood levels, we can alter gene expression of the various components of our immunity and cardiovascular health (Weaver KL J. Biol. Chem 284: 15400-15407; Biocarta; DeLuca HF PNAS 1993 90(20):9257-9260).

Volek et al have demonstrated how one can achieve control of small dense LDL via inhibition of CETP activity by a very low carb diet/HIGH-FAT DIET with additions of dietary eggs/cholesterol/SFAs.

Can we obtain similar sd-LDL less than of 10% lipoprotein profiles as long-lived heart-disease-free, cancer-free centenarians? We may not have the genetic programming/genotype but I certainly believe with our current understanding and technology, achievement of the centenarian phenotype is a definable undertaking.


Previous animal pharm posts:

• Saturated Fats as Potent Anti-Atherogenic Drugs: Lauric Acid Diets Decrease CETP, Increase PLTP
• Lauric Acid Diets (Sat Fat) Reduce Small Dense LDL (atherogenic) MORE THAN Oleic Acid Diets (Olive Oil)

Benefits of High-Saturated Fat Diets (Part I)

Results above -- click to enlarge.

What's a 46% fat diet?

Perhaps what our stone-age ancestors consumed during happy, reproductive, fertile times?


The diet compared 6% Sat Fat (low fat) to 18% Sat Fat (high fat) in a little discussed publication by Krauss et al, one of the founders of NMR lipoprotein density technology here in the Bay Area.

Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men.
Krauss RM et al. Am J Clin Nutr. 1998 May;67(5):828-36. Click HERE for PDF.

• The low-fat diet contained 24% of energy as fat (6% saturated, 12% monounsaturated, and 4% polyunsaturated) and 59% as carbohydrate, with equal amounts of simple and complex
  carbohydrates and 17% as protein.
• The high-fat diet contained 46% of energy as fat (18% saturated, 13% monounsaturated, and 12% polyunsaturated) and 39% as carbohydrate and 15% as protein.

STUDY DESIGN: They tested whether nutrient intakes estimated from 4-d diet records were associated with plasma lipoprotein subclasses in 103 men who were randomly assigned to a low-fat (24% fat) and a high-fat (46% fat) diet for 6 wk each in a crossover design. Carbohydrates (~20% of energy) were basically substituted out for dietary fat intake.

Outcomes can be summarized as the high SFA (saturated fatty acid) diet inducing multiple positive regressive lipoprotein changes:

• raised Large LDL-I 42.6%
• raised Large LDL-II 14.9%
• reduced sd-LDL, LDL-III 26.4%
• reduced sd-LDL, LDL-IV 39.1%
• raised the regressive particle most associated with longevity, niacin and omega-3 benefits, HDL-2 49.9%
• lowered VLDL 38.6%
• lipoprotein lipase (LPL) activity increased with high fat
• hepatic lipase (HL) activity decreased with high fat

The above high fat diet comprised of mostly myristic acid (14:0), palmitic acid (16:0) and stearic acid (18:0). See Table 1.


CONCLUSIONS:

• The results indicate significant associations of dietary saturated fat intake with plasma LDL-particle distributions.
• An increase in saturated fat, and in particular, myristic acid, was associated with increases in larger LDL particles (and decreases in smaller LDL particles).
• Studies of the relation between LDL subclasses and CAD have, in contrast, established that a predominance of small, dense LDL particles (LDL subclass pattern B) is associated with increased risk of myocardial infarction (47, 48) and angiographically documented CAD (48–50). Some studies have also shown that small LDL particles are potentially more atherogenic than larger LDL because of increased susceptibility to oxidation (51, 52) and increased promotion of intracellular cholesterol ester accumulation (53). In addition, reductions in small LDL particles, not in larger LDL particles, have been associated with decreased CAD progression (54, 55).

So the authors do discuss the value of reducing sd-LDL, the holy grail of heart disease sufferers. The discussion on the benefits of a saturated fat intake of 18% however seemed to be quite curt and short though.

In fact, I couldn't even find it.

What we know about lipoproteins at TYP is that the bigger, the better. And the statements made by Krauss definitely confirms our current understanding.

The profound enlargement of Large-LDL (I and II) and HDL-2 in healthy men is quite extraordinary ad remarkable in only 6 weeks. No drugs involved, diet alone. In one the next few posts, we'll examine a heart disease population, including post-CABG men and women, and the benefits, again, of a high saturated fat diet.



Dietary Sources of SFAs Myristic and Palmitic Acid

• Cephalopods -- squid, octopus, cuttlefish -- which are extremely high in omega-3 fatty acids as well. Click here for more info (Ozugul Y. Food Chemistry 2008. 108(3):847-852).
• Wild Fish (Periago MJ. Aquaculture 2005. 249 (1-4):175-188.)
• Grassfed Beef (Leheska JM, J. Anim Sci. 2008)
• Grassfed Beef + FO Supplementation: Even higher SFA/ palmitic/ myristic quantity when fed fish oil omega-3 supplementation! (See Table 5. Moloney AP. Proceedings of the Nutrition Society (2001), 60, 221–229.)
• Grassfed Bison (Marchello MJ. Great Plains Research 11 (Spring 2001): 65-82.)
• Free-Range Chicken (Jahan K. 2005 Poultry Science 84:158–166)
• Free-Range Chicken Egg yolks (not 'organic'-wheat-feed, see above citation)
• Pasture-raised Lamb
• Pasture-raised Pork
• Pasture-raised Diary, Cheese, Ghee, Butter Oil (casein-free, greenpastures.org) (Nestel J Am Coll Nutr.2008; 27: 735S-740S)
• Lard
• Beef Tallow

Vegetarian Sources

For vegetarian sources, virgin coconut oil is a good sub, containing shorter SFAs (medium-chain) lauric and caprylic acid. Sat Fat 18% of a 2000 Kcal/d diet would be equivalent to 40 grams of coconut oil (fat is 9 kcal/g).

Or 2.8 Tablespoons VCO daily.



My HDLs Increased 18.0% With Coconut Oil
Like many Paleo fans, I have observed an increase in my HDLs from 89 mg/dl back in 12/2008 to now 105 mg/dl. It's now almost ~12 mos gluten free, baby. Wow. What a year.

About 6-8 wks prior to the blood test, we started cooking with VCO, virgin coconut oil (+smearing it all over my body after showers...no studies to back justification *haa* but it's nice cheap and works, eg less wrinkles, better healing, maybe better HDLs).

TGs came down from 80s to now 60s mg/dl.

Both the LDL is now higher 120s mg/dl (directly measured, not Friedewald) and TC in the 240s like some long-living healthy female elderly and centenarians.