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


Anonymous said...

What were the studies? Pubmed ID? Thanks.

Anonymous said...

may I ask an off topic question? I seem unable to get enough calories eating a low carb diet unless I eat LOTS of fatty meats on a daily basis. do you think there is a healthy limit (per day, or per week) of eating unprocessed, nitrate free meat? thanks, Dave

Jake said...

Important information that could save many lives.

Dr. B G said...


Sorry -- had some guests today and finally finished. Thank you for your patience!


Dr. B G said...


What is your complaint? Are you losing too much weight? If so (most grrrls would KILL you for that problem) you can consider adding fats (coconut oil, nuts, eggs, avocado, EVOO, avocado oil, etc) and protein (whey powder -- Jay Robbs is casein free; eggs). For hypertrophy, some carbs before or after the workout helps -- yams, sweet potatoes don't increase inflammation.

I don't see any problems with grassfed beef and free range poultry and eggs. Unfortunately wild seafood can have dioxins, PCBs, flame retardants, and heavy metals (mercury, lead, etc) concentrated in their flesh and body oils. If the meat is not grassfed, the omega-6 pufa's and inflammatory markers may be inherent in the meat/eggs despite the 'organic' labelling. They can be fed 'organic' corn or wheat. So deceptive, eh!?



Dr. B G said...


We can only hope, I think... paradigm shifts can be tectonic or microscopically slow like glaciers melting...

I pray we don't hear the same bummed out stories next year. This DATA came out Y E A R S ago. We're all so oblivious (me too). I'm glad for the discussions b/c I would've never found this information. For a long LONG time, I've had suspicions, but no idea how simple the answer was.


onewaypockets said...

I honestly fear for the future of CAD treatment. Modern "cheap" medicine looks for simple tests....TSH and LDL for example. But the evidence more and more shows that lipid management is complicated and not "one shoe fits all". Processed food producers, grain growers, and pharma will fight the non pharma, whole food and supplement approach all the way.

Statins are very primitive, I think in 50-100 years they will be viewed the way we look at "blood letting" or leach treatment. Crestor does a total trip on me. Just 5mg Crestor shot my glucose as high as a very sugary meal or giant desert portion. Crestor at 10mg and I could barely think. Lovastatin never has done that.....

A short while back I disco'ed my Lisinopril/HCTZ combo pill because of Dr. Davis's note on HCTZ being the cause of feeding small particle LDL (I always find these things late....duh). Do you have a "pick of the litter" for a high blood pressure med that does the least messing with lipids (generally speaking, of course)? When I run new NMR labs soon, hopefully I will get a better small LDL count. That seems to be my problem (two stents here) despite having a LP(a) of 5, and trigs of 38. If I still have a small LDL problem, perhaps I can pick your brain?? Currently on Lovastatin 10mg/Slo-Niacin 1500mg and 7,200mg EPA+DHA. I'm actually afraid to quit the Lovastatin...gotta keep a toe in the water, you know?? lol

You have mentioned ketotic diets several's time for me to (once again) lose more weight. I need the strict structure of a diet plan, any favorites? The recent death of Billy Mays (the Oxyclean and Orange Oil dude) really hit home to me. The "Pockets" family looks just like Billy....a bit thick. My favorite Uncle Burt that dropped dead at the age of 52 was a dead ringer for Billy (with a personality to match)'s time for me to diet!

Thanks for your positive spirit and posts G...keep up the fight! :-)


Anonymous said...

It is different than what is talked about in this post, but I've always suspected statins as not being much good. My thinking was, how can something that is known to damage muscles be good for the heart? Despite what my statinator doctor wanted, that is a main reason why I stayed away from them.

Thanks for the statin and small LDL information. Just adds more reasons to avoid them.

billye said...

To follow up on Daves off topic question, if I may. I have absolutely turned my life around and am now a life long low carber. The only problem left to me is grain fed beef. This is the the big sticking point in converting the public to LC. I just can't stand the taste of GF beef,except for the liver. Besides this I am now existing on GF lamb from New Zealand and Australia. I eat organic kosher chicken and beef, but It seems that you just can't get around the farmers feeding animals with grain. Will supplementing with high dose omega 3 in it's various forms, be enough to bring the omega 6 to omega 3 ratio to an acceptable level? For the health of the nation, I hope we can figure this problem out.

David said...

WOW, G! This is amazing information. I've been struggling with what to do with my dad for awhile. He had bypass surgery awhile back, and he's been on 40 mg of simvastatin (doctor's orders, of course!). I've never been comfortable with this, but don't know what the right thing to do is in a post-heart attack, post-bypass patient. Do statins ever have a benefit in a case like his? He takes niacin, fish oil, vitamin D, and all the other goodies, etc., and eats totally wheat free, low carb. His trigs are well under 100, but his Lp(a) has been slow coming down (he'll be doing an NMR pretty soon, here, but his last Friedewald calculation showed an LDL of around 130). I've been wanting to tell him to cut his statin dose down, but have hesitated for some reason. Normally, I'd say a statin is totally unjustified in light of his blood work, but I just have no idea if it's different somehow with him being a post-MI, post-bypass guy. Any thoughts?


Drs. Cynthia and David said...

Very interesting stuff. And so sad that this information gets buried in the mountain of ignored research! My guess is that negative data is certainly not pushed by the pharma companies, and there are no sexy press releases that say how great these findings are. What they want is for people to fixate on LDL or the total cholesterol:LDL ratio since this is a regime where statins seem to do something (even though we know better). The affect on small dense particles are not helpful to their product sales, so they design the studies to look for the endpoints that support their product line, not patient health! Plus, if you read the literature, you see that researchers in the area of atherosclerosis say outright that it is not a lipid storage disease or due to lipid accumulation, but an inflammatory disorder! The public has no idea though, along with most doctors apparently, because the only source of information most people have is provided by those with product to sell! It's kind of like what happened last year with the Jupiter trial claiming that rosuvastatin decreases CRP and hence further decreases CVD risk in nonhyperlipidemic people. Giving a drug to reduce levels of a surrogate marker (CRP) is a good excuse to sell more drug, even though it's not shown to actually prevent disease. A recent study poses doubts about any causative role of CRP in CVD (See recent JAMA, Elliot article), but I doubt you'll hear much about it since it won't be pushed by any vested interests.

Sorry for the rant. Please keep up the good work informing us!


Peter said...

Hi G,

Excellent post again, I've stumbled across a number of papers along these lines... Ties in well with the J-LIT study showing increasing CV mortality at very low LDL levels on simvastatin. But we move Tuesday, so bloggin' is not happening!


Anonymous said...

interesting, but i am on lipitor and my small dense particles have fallen in the face of triglycerid leve of only 30. I maintain a low carb diet and take niacin

Dr. B G said...


Thank you for your insights and thoughts on the forum. Your words always somehow warm my heart...

My least favorite BP drugs are the sulfur-moiety containing ones. I've listed the ones off the top of my head here -- if you email me I can give a more thorough list.

Yes ACE-Inhibitors and the thiazide diuretics are the worst because the can cause autoimmunity which we want to quell, control, and avoid with synthetic entities. These probably extensively increase ROS, oxidation as well as deplete our important redox quinones like Coenzyme Q10.

The best BP drugs are:
ARBs (Diovan, Cozaar, etc)
Coreg (effective but swelling and edema at higher doses)

Natural methods are OPTIMAL
--hormone optimization
--taurine, arginine, leucine
--low low carb diet (Yes -- the ketogenic, grain-free works)
--moderate to high fats
--moderate protein
--thyroid (yours are GOOD)
--yoga, mental stress control
--adequate sleep
--high potassium veggies -- carrot and celery juices, leeks, coconut water, etc
--ultra high dose omega-3; elimination of toxic omega-6
--antioxidants... pycnogenol, alpha lipoic acid, etc

I agree, statins are primitive and for susceptible folks who have anti-statin genetics, the statins trigger autoimmunity in a BIG way. Hopefully that is not the case for you? Crestor increases the risk of Diabetes and I suspect it has a neutral/increasing effect on CETP activity when the Trigs are depleted as the studies on this blog entry evaluated. So much we don't know but enough to know about their obvious toxicity and lack of effectiveness.

Show me your L-A-B-S ! Then later show me your ABS OWP -- you can do it :) I know you can. Looking and feeling physically and spiritually strong I think gives us the key to where we want to go in life.


Dr. B G said...


As you know with Lp(a), if that is the cause, then that needs to be the FOCUS of therapy.

Lp(a) mg/dl mass will DECREASE if the particles are getting


The particle count nmol/L are equally important to track for heart disease reversal.

Count needs to decrease
Mass needs buoyancy (so may actually increase in some cases).

From what these studies show, the higher the dose, the faster the concentrations of sdLDL increase.

I'd question the value of the simvastatin after 2 mos of clean diet and lifestyles and when the Trigs are low without simvastatin. Simva lowers Trigs by 30-50% so whether it's drug effect or low carb effect, Trigs less than 120-150 mg/dl appear to be associated with an overall increase in sdLDL concentration ALL statins.

This becomes problematic at some point. For Lp(a), the pattern A with a dominance of large LDL are absolutely necessary mandatory for CAD and EBT regression.

On the TYP forum, I have not observed ANY case of EBT regression with statin + Lp(a) yet for the last almost 2yrs. It's a big prob.

Progression on EBT of 20-25% is typically the case in the over-statinators who are Lp(a) carriers, IMO.

If your father who has Lp(a) is compliant, please DO NOT let him fall into this category.

The only regression stories on TYP are the statin-less ones. See Dr. Davis recent post "A statinless life". Excellent stuff!


Dr. B G said...


Right on. Thank you for the RANT!!!

Exactly, my friends work for Pharma and it is unbelievable how info is 'planted' with NO TIES back to Pharma. *ha*

Better believe it...


Dr. B G said...


Good luck with your move! Hope the baby and cat don't mind the upheaval (and you as well). Sorry you will be leaving such a beautiful place...

I'll be on this topic for a bit... Take your time coming back!


Dr. B G said...


That is wonderful.

However what are your large LDLs now???!?! Niacin does help but they cannot counter the strong statin SLEDGEHAMMERING/ killing of the large LDLs over time for many individuals. If you have Lp(a), then that will be MAJORLY problematic.

That is the whole point of the post.

Don't be ignorant of the concentrations of large v. small LDL.

Low carb and niacin are the WAY TO GO... Keep up the strong work.


Dr. B G said...


Exactly. I see absolutely NO reason for statins... unless one truly has yellow xanthomas and on apheresis.

Or... on the low fat CR*PPY AHA diet... and fails to see the value of the Paleo low carb diet.

90% of the world are insulin resistant and carb sensitive and semi/silent celiac. Statins actually don't help them because of the risk of mitochondrial toxicity and autoimmunity.


Dr. B G said...


One other thought. All causes of inflammation should be controlled if possible for reduction in sdLDL.

Have you considered food allergies? Contact graywhale who knows a lot about it.

The story about how your wife was improved in her health. You are a great husband to help her to figure it all out.

Consider reading Dr. Mark Hyman, MD. He reminds me of your anti-aging doc!

Mark Hyman MD, Heavy Metal Poisoning and Food Allergies


Dr. B G said...


I have to thank you profusely for commenting on Dr. Davis blog (and mine) otherwise I would never have found your amazing turnaround story!! Congratulations!!! Strong work and continue to keep it up!


You and he make a great PAIR.

OK -- lamb is awesome -- I eat at least once a week in a chinese 'hot pot' (not sure if ours is grass or grain fed but I hear that most of New Zealand lamb is grassfed). I recently bought a 1/4 grassfed cow from Paso Robles (where all the FANTASTIC wine comes from). You don't like it? Overcooking can ruin it...

Dr. Sears, the toxic fact and omega Rx zone researcher, promotes a fatty acid profile test to truly evaluate the omega-6 to omega-3 ratio in the lipid bilayers of the erythrocytes (red blood cells). Minimizing consumption of GRAIN-fed meats/dairy is of course prudent to lower the omega-6 in our bodies.

Easy test... tells you if the AA: EPA ratio is ideal 2.0 for Dr. Sears. For Track Your Plaque, I believe, 1.5 is more optimal for regression because this mimics the Okinawans. The Inuits have slightly more hemorrhagic strokes if the ratio is 0.5 (not good).

Hope that helps and THANK YOU SO MUCH AGAIN! I may even collaborate with Dr. T. Seriously. He is WORTHY. As r u totally.



David said...


Thanks for your thoughts about the Lp(a)/statin issue. I've been going over the literature more for myself and am pretty convinced that this is a big problem. In fact, the more I read and think about it, I'm not sure if I can think of any case where statins would be a good thing.

-If LDL is way high, but the particles are large, then who cares? Large LDL is our friend.

-If LDL is way high and the particles are small, then you certainly wouldn't want to take something that had no effect (or worse yet, a malicious effect) on sdLDL.

-And of course there's the Lp(a). If statins make LDL small, then that sdLDL is what's gonna be combining with the apo(a), and the resulting Lp(a) is going to be just that much more dangerous.

What are we left with? Seems like taking statins is a huge risk, especially when there are safer, more effective lifestyle and supplement alternatives.

My dad is the most compliant person I've ever seen. Eats the right stuff, avoids the bad stuff, takes his pills faithfully. He's like a machine. I think it's definitely time to start getting away from the statin...

Anonymous said...

All NZ lamb is grass fed. We are very good at growing grass here. :) Couldn't sweat to all export beef being grass fed, though.

Michelle in New Zealand

JohnN said...

Thanks for the crusade against one of the more deadly enemies of mankind.

The market for Statins was $26B last year and growing. That's the magnitude of the crime being perpetrated by the drug industry.

Expect more unwitting victims as patents on the drugs expire and cheaper generics become available (and pushed hard).

The "Statinth" wonder of the world: a panacea for all illnesses or a bubble about to burst.

Nusrat Shafiq, Samir Malhotra, Promila Pandhi, Anil Grover
Journal of Negative Results in BioMedicine 2005, 4:3 (23 March 2005)

Dr. B G said...


Brilliant! My assessment as well... Your dad is fortunate to have a warrior son who also aces physics exams and understands more than 99.9% of all cardiologists out there.

Michelle from NZ!

Thanks for the tip!! MMMMmmmm now I love my lamb even more!!!


Thank you very much for the link and your insights. You cannot believe the statinators out there who will NOT RELEASE their white-knuckled grip on a statin like a baby stuck on their pacifier... Everyone wants a MIRACL in a pill... life aint work that way... You are absolutely correct. Nope.

-G said...

You said:
"Are you losing too much weight? If so (most grrrls would KILL you for that problem) you can consider adding fats (coconut oil, nuts, eggs, avocado, EVOO, avocado oil, etc) and protein (whey powder -- Jay Robbs is casein free; eggs)."

I'm low-carbing, but I still have very serious doubts about all animal fats. Of the things you mentioned, I prefer nuts, avocado, and extra virgin olive oil, all together, usually with a lot of chopped celery.

Anonymous said...

and yet its been proven beyond a shadow of a doubt that statins lower risk of heart attacks and lower risk of death. why wasnt that mentioned in this one sided article ?

Anonymous said...

what a surprise if someone leaves a comment that makes your summation look stupid you don't have the guts to print it. Keep up the free flow of ideas lmao said...

"Anonymous" said...
"and yet its been proven beyond a shadow of a doubt that statins lower risk of heart attacks and lower risk of death. why wasnt that mentioned in this one sided article?"

Now that's an extremely arrogant statement, unsupported by any references to research studies, made by an anonymous troll. I guess he's too busy shouting at health care town halls. This is just "anecdotal," but statins cause me a lot of problems.

Dr. B G said...

Jim Purdy!

Are you being as heretical as MOI? Are we only presenting a one-sided view from DEEP deep experience?



I like a lot of one-sided views including...

Dr. Davis MD, my superhero
--the Statin-Free LIFE
--his quotes from our TYP forum "I continue to use statins on occasion when necessary to reduce LDL to target levels. They are not my first choice, but a choice in people who do everything right yet continue to express high LDLs. When people start at 240 mg/dl, for instance, (verified by LDL particle number), then I do believe that a statin is helpful. Don't forget how helpful thyroid normalization can be for LDL reduction, however... When I meet somebody on high-dose statin, e.g., Lipitor 80 mg or Crestor 40 mg, then I will try to reduce the dose by reducing LDL with other means."
--more quotes from our TYP forum (how statins SUCK) "I look at statins with a very simplistic view. I view them just like antibiotics. Say you have a fever of 104 degrees, your coughing up thick, yellow sputum and you can't breathe because you have pneumonia. Perhaps we despise the drug companies for their heavy-handed marketing tactics, but you will likely take an antibiotic. Statins are the same: They bail us out when all else fails. They should not be used casually, nor for every little indication, contrary to the enormity of the drug company-paid "research." They're good to have around, like when the cellulitis from the spider bite gets out of hand. But just taking them for 10 years without solid justification is no better than taking an antibiotic because you sneezed."

Mark Sisson, Mark's Daily Apple
--Big Pharma thoughts esp about how statins SUCK
--And again how statins SUCK

Dr. Eades MD
--how statins SUCK

Our lovely Peter of Hyperlipid, most brilliant THINCer of them all
--how statins SUCK
--how statins increase oxLDL (which is just sdLDL)
--how statins kill people b/c we require cholesterol
--how statins SUCK and SUCK and SUCK (J-Litt, ASTEROID/Nissen, and JUPITER, respectively)


Anonymous said...

I live in Milwaukee Wis. and I am a patient of the great Dr. Davis who is without a doubt THE BEST Dr. I have ever had. You gentlemen are correct that statins cause problems for some people and lots of people don't like to use them however that doesn't change the fact that they have been proven to reduce the number of heart attacks ( the good Dr. has on a number of occasions mentioned the Hats Trial to me ). Dr. Davis has me on Zocor for that reason, he has told me that in his opinion statins don't prevent heart attacks and prolong life because they lower cholesterol but probably because they reduce inflammation but THEY DO lower the incidences of heart attack without a doubt. But who knows maybe he's wrong.

Dr. B G said...


Dr.Davis is wonderful. Stick with him!! I am one of his biggest groupies...

It is niacin that is mainly beneficial in the secondary prevention heart trials. Simvastatin is only MARGINALLY helpful (if one is not totally intolerant or semi-intolerant to or or develop some degree of cellular myositis or myolysis). Statins to me only appear to aid those Metabolic patients who eat a bunch of carbs (eg, 'the AHA low fat diet'). Invariable the post-MI patients in the n=~100 patients in the tiny HATS trial were all Metabolic Syndrome patients with hyperinsulinemia and baseline Trigs greater 200-300s. I do love the HATS trial though like Dr. Davis -- it exemplifies regression and stability of plaque when the HDLs are raised sufficiently. Essentially no one developed cancer (anecdotally per Dr. Abram Hoffer MD) or progression of CAD to death or second coronary event or surgery.

Metabolic patients have Trigs greater than 150-200s and Apo B greater 120. Goal at TYP (without drugs if possible) is 60 and 60-70, respectively.

The relative risk reduction for statins is better in diabetics at 18-22%. In clinical studies, usually NO CHANGE IN ALL CAUSE MORTALITY is observed (or even an INCREASE is seen statin-taking arms due to more suicides, accidents, depression, cancer death, etc, depending on the trial that is examined closely)

Do you know that the relative risk reduction with diet or niacin trials are?

HATS niacin + simva 20-40/d
FATS trial (niacin + colestid) (73%)
Lyon-Diet (more omega-3, less omega-6) (71%)

RR of all-cause mortality were equally good as well, in the above diet or niacin trials!