Problem is I'm not quite sure how to read it. I am only at the beginning of this Low Carb journey, so I think it has a lot of room for improvement.


LDL Particle Number
LDL-P 2166
Small LDL-P 1469

Cholesterol Total: 209
LDL-C 142
HDL-C 49
Trigl 88

LDL Particle Size 20.7
Large HDL-P 4.7
Large VLDL-P 0.7

But what does it all mean? ;-)

Hey berserkertooth, I'm happy to help interpret your NMR LipoProfile findings.

First, the good news:

Your HDL is decent and your triglycerides are below 100. The triglycerides/HDL ratio is less than 2...very good news for you.

Now to the not-so-good news:

Your LDL particle size shows some issues. You show a LOT of LDL-P with that 2166 number. By contrast, my LDL-P is 1453 and I have a higher total cholesterol than you do. But your small LDL-P is 1469 which is over two-thirds of your LDL particles...not ideal at all. Compared with my small LDL-P of 30, you've got a lot of work to do.

But like you said, you're just getting started on the low-carb lifestyle and those numbers will DEFINITELY improve if you stick with a high-fat, moderate-protein, low-carb approach. Expect your small LDL-P to drop like a rock, your HDL to rise above 60, and your triglycerides to continue to plummet. You have a great baseline of numbers to see the improvements livin' la vida low-carb will provide to you.

YOU CAN DO THIS!!

Here's a quote from Jonny Bowden's website that should make you feel really good about your starting point.

"We would be so much better off looking at blood measures like triglycerides, homocysteine, CRP (a measure of inflammation) and the ratio of triglycerides to HDL cholesterol, a ratio which- in an published article in the journal Circulation- was found to predict heart disease 16 times better than cholesterol. (To find your ratio take your triglycerides and divide by your HDL cholesterol. For example if you've got triglycerides of 100 and HDL cholesterol of 50, your ratio is 2, which is a vanishingly low level of risk. Five, on the other hand is high risk. You can lower that ratio by simply bringing down your triglycerides, something relatively easy to do with a lower carb, no-sugar diet!)"

So it seems you are already at less than "vanishing low level of risk" even with the extra room for improvement.

Thanks guys. I figured those LDL-P's weren't too good. But I'll keep at it. At least as you say my Trig/HDL isn't too bad.

Besides eating low carb I am also taking 4 capsules (whatever size the large OTC ones are) of Fishoil and 5000iu Vitamin D3.

I guess I'm more motivated than normal now. ;-)

Berserkertooth:

Grab a cup of coffee and pull up a chair. This is going to be a LONG (but hopefully interesting) post!

I can help you with interpretation of the NMR LipoProfile test. Let's start with your traditional lipid values, and then we'll move on to the lipoprotein particle data:

Your Total Cholesterol (TC) is 209. This is slightly elevated according to the National Cholesterol Education Panel Adult Treatment Panel III (NCEP ATP III) guidelines, which specify TC above 200 as "high." NCEP ATP IV should be out early next year, but I doubt if the TC recommendations will change.

Your LDL-C (the cholesterol contained within low density lipoproteins) is 142. This means that you have more LDL-C than 60% of the population. If you are a "low risk" patient, then you would not qualify for treatment. If you are a "moderate risk" patient, then your LDL-C goal would be <130. If you are a "high risk" patient, then your goal would be <100. NCEP issued an addendum to ATP III in July of 2004 establishing an OPTIONAL goal of LDL-C <70 for a new category of patients deemed to have VERY high risk. The American Diabetes Association, American College of Cardiology, and some other guideline-issuing medical societies have performed independent reviews of medical literature, and generally concur with these LDL-C recommendations.

Your HDL-C (the cholesterol contained within high density lipoproteins) is 49. This is "decent" (but not great) if you are male. If you are female, then this is a borderline value. American Heart Association guidelines consider HDL-C below 40 to be "low" for men, and HDL-C below 50 to be "low" for women. Many lipidologists are uncomfortable with HDL-C <50 in men and <60 or in women, but please understand that low HDL-C is primarily viewed as a risk ASSESSMENT lab value. It is not a risk MANAGEMENT lab value like LDL-C (and non-HDL-C, and apoB, LDL-P, etc). NCEP, ADA, ACC, AHA, among others, have all concluded that there is "insufficient data" to establish a specific goal for HDL-C. Low HDL-C is a major predictor of risk, but the guidelines recommend lowering LDL-C (and non-HDL-C, apoB, and LDL-P) as the targets of therapy to reduce risk. This is a very important point - and one that many doctors don't understand.

Your Triglycerides (TG) are 88. This is a pretty good value. The current NCEP guidelines consider TG to be "borderline" if they are 150-200, "high" if they are 200-500, and "very high" if they are >500. When TG are >500, they become a goal of therapy, because very high TG can lead to pancreatitis (not a good thing). When TG are <500, LDL-C is the primary goal of therapy, but if the TG are >200, non-HDL-C becomes a secondary target of therapy. In your case, we have LDL-P data, so I'm going to gloss over non-HDL-C since LDL-P is more predictive. As I mentioned, current guidelines "allow" for TG as high as 150 (and ATP II was ok with TG up to 200). I hope ATP IV lowers the "acceptable" TG down to 125, or preferably 100. A physiologic TG value ranges from 10 to 80, with a mean of ~40. Anything above 80 (or certainly 100) is a potential problem. Why? Because TG are carried within Very Low Density Lipoprotein particles (VLDL). When excessive VLDL particles are present (especially Large VLDL), they interact with LDL particles and HDL particles, and cause these particles to become cholesterol-depleted, and/or smaller. Small HDL particles don't carry as much cholesterol as large HDL particles, and so HDL-C drops. Small HDL particles can also be passed through the kidney and renally excreted (so you start peeing out your HDL-C!). If your LDL particles are small and/or cholesterol depleted, then you have to have a HIGHER NUMBER OF THEM TO CARRY A GIVEN LEVEL OF LDL-C. Here's an important analogy, but first let's debunk a pervasive myth:

There is no such thing as "good cholesterol" and "bad cholesterol." Cholesterol is cholesterol is cholesterol. We call the cholesterol being transported inside High Density Lipoproteins (HDL-C) "good," and we call the cholesterol being transported within Low Density Lipoproteins (LDL-C) "bad." But the cholesterol itself is the same! It's the LIPOPROTEIN PARTICLES that are "good" or "bad!"

Here's the analogy:

Cholesterol is an OIL and blood is WATER-BASED. Oil and water don't mix, so in order for cholesterol to be transported through the bloodstream, it must be carried inside a hydrophyllic lipoprotein particle. Think of the cholesterol molecules as "passengers" riding inside lipoprotein particle "vehicles." If I have an LDL-C of 100 (100 passengers), how many vehicles are they in? I CAN'T KNOW! There could be 20 vehicles with 5 passengers each, or 50 vehicles with 2 passengers each, or 100 vehicles with 1 passenger each. Why do I care about the discordance? Because it's the number of VEHICLES on the road that causes the traffic jam, not the number of PASSENGERS riding inside the vehicles!

As simplistic as this analogy sounds, it is biologically accurrate. Atherosclerosis is a gradient-driven process (as are traffic jams). If you have a high number of LDL particles (LDL-P), then a strong gradient exists, and this strong gradient will force LDL particles to diffuse through the endothelial lining of the arterial wall - in other words, the LDL particles will carry cholesterol into the wall of your arteries, where they can then be retained and oxidized. The lipoprotein "vehicle" will mostly disappear, and the cholesterol that the particle carried into the artery wall will turn into foam cells, and then fatty streaks, and then atherosclerotic plaque. If the plaque ruptures, then you will have a very bad hair day - but keep in mind that it is the LDL PARTICLES (LDL-P) that messed up your hair in the first place!

So if it's the particles that are so danged important, then why are we so focused on the cholesterol inside the particles? Because technological limitations have long-prevented reliable particle number assays, so cholesterol has been used (for decades) as a surrogate marker for lipoprotein particles. We've been using cholesterol for SO LONG that we are now selling Cheerios to people on the basis of lowering their cholesterol - cholesterol is a paradigm - cholesterol is a set of blurry goggles through which most patients (and most doctors!) view cardiovascular risk. The picture becomes clearer when when cut out the surrogate and look directly at lipoprotein particle numbers (i.e. apolipoproteins such as apoB and apoA1, or the NMR LipoProfile test).

With these preliminaries out of the way, we can rapidly move through the NMR lipoprotein particle data:

Your LDL-P is 2166. This is not good. [Mine was 2009, so I can relate.]

LDL-C of 100, 130, 160, and 190 correspond to the 20th, 50th, 80th, and 95th percentiles of the U.S. population. As discussed above, your LDL-C is at the 60th percentile (you have MORE LDL-C than 60% of folks in the U.S.).

Similarly, LDL-P of 1000, 1300, 1600, and 2000 correspond to the 20th, 50th, 80th, and 95th percentiles of the population. Your LDL-P is >95th percentile. As stated above, this is not good. Numerous studies show that LDL-P is a VERY STRONG predictor of cardiovascular risk, even after multi-variate analysis including many other risk factors (including lipid measurements and ratios). A couple of studies have shown that LDL-P is not really much better than TC/HDL-C ratios, or the combination of LDL-C, HDL-C, and TG, but these studies were on people whose LDL-P was "concordant" (similar to) their LDL-C. Your LDL-P is quite a bit higher than your LDL-C would suggest (>95th percentile compared to 60th percentile), so you are "discordant," and LDL-P has a solid track record of out-predicting lipid measurements and ratios in discordant patients. This track record has been acknowledged by THREE different Expert Panels who are all advising that lipoprotein particle number measurements be added to our existing cholesterol guidelines (and all three of these Expert Panels recognize LDL-P by NMR).

I will discuss what to DO about your LDL-P at the end of this post.

Your Small LDL-P is 1469. This has clinical relevance, but NOT in the way that most people think. I will discuss this at the end of the post.

Your LDL Particle Size is "Pattern A." This means that your the average of all of your LDL particle diameters falls into the "large" category (barely). But you have a lot of Small LDL-P too, so how can this be? It's simple. You have a lot of technically "Small" LDL-P, but they're probably not "teeny tiny" - and you have enough Large LDL particles to skew the average LDL size into Pattern A (barely). None of this matters in the way that most people think, as I will discuss shortly.

Your Large HDL-P is 4.7. This is at the low end of "intermediate." If Large HDL-P drops below 4.0, then it is a more predictive marker of Metabolic Syndrome than HDL-C. [Note: There are a few different definitions of "Metabolic Syndrome," but generally speaking a person must have 3 out of 5 parameters in order to have a Metabolic Syndrome diagnosis. HDL-C is one of the 5 parameters, but low levels of Large HDL-P is actually more predictive than HDL-C. "Official guidelines" have not yet recognized this. FYI.] Either way, Large HDL-P is not a goal of therapy - LDL-P is. Worry about your LDL-P - not your Large HDL-P.

Also, data on HDL-C, HDL-P, and HDL size is all over the map. Don't get caught up in any particular "HDL" theory! HDL is a VERY confusing topic, and most doctors don't appreciate the complexities!

Your Large VLDL-P is 0.7, and this is pretty good! It's actually the best lipoprotein particle value you've got, AND it indicates that your low carb diet (and/or exercise) are working! Keep in mind, however, that having a low level of Large VLDL-P is desirable, but it is NOT a "goal of therapy," and it does NOT preclude LDL-related risk.

SO WHAT DO WE DO WITH THESE LAB VALUES?????

1. First the easy stuff. I don't care about your TC, HDL-C (even if you're female it's only 1 point low - and it's not a goal of therapy), your TG are good, Large HDL-P is ok (not great - but not a goal of therapy), Large VLDL is actually quite good (but again, not a goal of therapy).

2. Second, the confusing stuff. You've got a lot of SMALL LDL particles, and I don't care. That's right - I DON'T CARE ABOUT YOUR "small" LDL. What?!!? I'M SUPPOSED TO CARE about those evil little bastard SMALL LDL particles? Right?!!? DOESN'T SIZE MATTER????

Ummm, no.

Anyone who has read this far must clearly have an interest in learning something, so here we go:

As I tell my wife all the time, SIZE DOESN'T MATTER!

But seriously, think about these two groups of patients:

- People with diabetes and metabolic syndrome - As a group, these folks have HIGH NUMBERS of SMALL LDL particles, and they have a lot of risk!

- People with Familial Hypercholesterolemia (FH) - This is a genetic disorder that affects 1 out of 500 people. As a group, these folks have HIGH NUMBERS of VERY LARGE LDL particles, and they have a lot of risk!

The commonality is HIGH LDL PARTICLE NUMBER - not size!

THREE Expert Panels have published data in the last 30 months on this topic, and ALL OF THEM focus on LDL particle NUMBER, not size! (ADA/ACC Consensus Statement, AACC Position Paper, 30-person/10-country panel).

Repeat after me: Size doesn't matter, Size doesn't matter, oh, but it sort of matters....bear with me....

Ok, so what do we DO with an LDL-P of 2100+????

If you recall my earlier statements, LDL-P of 2000 = 95th percentile. In other words, 95% of folks have fewer LDL particles bombarding their arterial walls. LDL-P this high is BAD. Period. End of story.

I don't care about the well-meaning-but-ill-informed folks who want to post "their special theory" about lipids or inflammatory markers (i.e. hs-CRP) or imaging techniques like CIMT, EBT, MRI, CT, etc. LDL-P of 2100+ is a PROBLEM. PERIOD. END OF STORY.

Do lipid ratios and/or non-HDL-C predict risk better than LDL-C? Yes!

Do inflamatory markers like hs-CRP or the PLAC-test provide additive risk prediction? Yes!

Do imaging techniques like CIMT, EBT, MRI, and CT have some usefullness? Yes!

Do any of the aforementioned tests give you a get-out-of-jail-free-card for an LDL-P of 2100+? NO!!!!

Jimmy is correct that a low carb diet will improve your LDL particle number, and that is the good news. The BAD news is that you probably need to reduce your LDL-P by ~35% (if you are a moderate risk patient) or by ~55% (if you are a high risk patient). Your risk status should be determined by your doctor.

Low carb diets DO improve lipoproteins, but you are unlikely to get a 35% reduction in LDL-P by diet alone (possible - but not common). And if you are a "high risk" patient, then it will be virtually impossible for you to get your LDL-P <1000 by diet alone.

With an LDL-P of 2100+, I recommend either Vytorin (10/20 or 10/40), or Crestor 10 (with a possible titration to 20). If you doctor is a die-hard Lipitor fan, then ask him to start you with the 20mg dose (although this would be my third choice based upon my review of the outcomes data).

IF you are taking a decent dose of a potent statin such as Crestor (preferred) or Lipitor, or a statin/ezetimibe combination like Vytorin (preferred), and your LDL-P is STILL TOO HIGH, THEN SIZE MATTERS!

If you're taking an above-listed product, and doing your diet and exercise, and you still have a high LDL-P, AND a high Small LDL-P, then add niacin or a fibrate. If you still have a high LDL-P but your Small LDL-P is not high, then titrate the statin, or switch to a more potent statin, or add Zetia or WelChol.

In other words, LDL particle size helps to predict Metabolic Syndrome, and also helps with selecting appropriate pharmacotherapy. LDL particle NUMBER is a goal of therapy - particle SIZE helps to inform treatment decisions.

Now keep reading while I take Jimmy to task:

JIMMY - Your LDL-P of 1400+ is NOT GOOD! I love what you're doing by promoting the low carb lifestyle, but please realize that LDL-P of 1400+ STILL CONFERS A LOT OF CARDIOVASCULAR RISK! Try generic simvastatin 20mg for $4 per month from Wal-Mart or other competitive pharmacies - please! This low-dose, generic, affordable, SAFE and well-tolerated statin is supported by a HUGE number of outcomes studies. Low carb diets DO IMPROVE LIPOPROTEINS, but a lot of folks need more than just diet and exercise. Please don't talk people out of statins! (and no, I don't have any financial interest in statin sales - I just know the medical literature!) BOTH diet AND pharmacotherapy are important!

In closing, this is an IMPORTANT TOPIC, and I am happy to speak with anyone who has questions. Just call me at the number listed below (between 9am and 9pm EST).

Best Regards,

Marc
804-437-3559

Mark, thanks for your input and welcome to my forum! However, I refuse to go on a statin drug because it has caused real harm to my body in the past. Sure, the drugs were Crestor and Lipitor and not this "low-dose" version, but I'm not interested in that. I disagree that people HAVE to take a statin to improve their lipids. I've discussed my own personal numbers with a noted low-carb researcher and practitioner at Duke University in Durham, NC named Dr. Eric Westman. While he noted the LDL-P is higher than normal, the small LDL-P being a minuscule 30 along with HDL over 50 and triglycerides under 100 said there is nothing to be alarmed about at all.

Several other of the world's best health experts I have interviewed on my podcast show agreed with this analysis, including Dr. William Davis, Dr. Jim LaValle, Dr. John Salerno, and Dr. Mary C. Vernon, among many others. While there are plenty of medical professionals who would agree with your analysis of my situation as well as berserkertooth, like Dr. Dean Ornish and my upcoming podcast interview guest Dr. Michael Ozner, I don't think telling people they have to resort to taking a statin drug with their low-carb lifestyle is the answer. I'd be happy to talk to you today, so feel free to e-mail me at livinlowcarbman@charter.net so we can arrange a time to chat.

THANK YOU again for your addition to the discussion and I look forward to speaking with you.

Marc, welcome to the forum and thanks for your input. However, I would like to add to this discussion that statins provide only a small reduction in heart disease risk and only for middle aged men who have already had a heart attack. I would still go back to the data and absolute risk reduction. Maybe statins provide a "statistically significant" reduction in heart disease, but that just means that the small risk reduction we see is not due to chance. Clinically, the risk reduction is meaningless. Plus, in most cases, statins don't improve oveall mortality. Low cholesterol has been associated with an increased cancer risk. If you don't die of a heart attack, you'll die of something else.

The fine print on Crestor ads say that it has NOT been shown to prevent heart attacks. If it doesn't prevent heart attacks, why take it???? I don't see how taking statins will prolong my life enough to bother with them and risk the side effects.

renegadediabetic:

Thank you for welcoming me. I'd like to respond to your comments:

- "statins provide only a small reduction in heart disease risk."

The relative risk reduction in statin trials tends to be ~30-35%. In other words, the people in the statin group have approximately one-third fewer CVD events than those who are in the placebo group. Admittedly, we would like to reduce events by more than one-third, which is why the days of statin mono-therapy are largely over - especially for high-risk patients. This is also why large-scale combination therapy trials such as AIM-HIGH are currently under way (expect the results in 3 years or so). In the meantime, wouldn't you rather join the group that has one-third fewer CVD events? If you could give your parents/spouse/kids one-third lower risk of a serious health problem, wouldn't you?

If you wear your seatbelt, then having an airbag doesn't reduce your risk of dying in a head-on collision by an additional one-third - and yet the insurance actuaries are willing to give you a discount for having the airbag, because they believe in the additional benefits conferred.

Note: AIM-HIGH is comparing simvastatin (Zocor) mono-therapy against the combination regimen of simvastatin plus extended release niacin (Niaspan - NOT the potentially dangerous and non-efficacious flush-free niacin formulations that are sold as supplements). Why is simvastatin/niacin being compared to a simvastatin mono-therapy group, rather than a placebo group? Because the data supporting the benefits of statins is so compelling that it is now considered medically unethical to withhold statin therapy from high-risk patients. You can't test a statin against a placebo anymore, unless all patients in the study have already met their lipid goals (and even then we should be checking lipoprotein particle levels as an additional goal). That should tell you something.

- statins only reduce risk "for middle aged men who have already had a heart attack."

Please provide a citation for this assertion! Patients who have already had a heart attack (or stroke, or CABG, etc.) are considered to be "Secondary Prevention." I'm sure your statements will come as a BIG SURPRISE to patients in studies such as West of Scotland (WOSCOPS) and AFCAPS/TexCAPS (both PRIMARY prevention populations) as well as folks in the Heart Protection Study. Event-reductions among the statin-treated folks in these studies were 31%, 38%, and 27%, respectively. And I can assure you that risk reduction was seen in patients other than "middle aged men." Are "middle aged men" who have had a cardiovascular event of some sort over-represented in statin trials compared to other segments of the population? Absolutely. But your statement that statins have ONLY been shown to benefit "middle aged men who have already had a heart attack" is very easily disproven by a cursory review of the medical literature.

- "I would still go back to the data and absolute risk reduction. Maybe statins provide a 'statistically significant' reduction in heart disease, but that just means that the small risk reduction we see is not do to chance."

I can make this same exact argument for other lipid/lipoprtein drugs such as niacin, fibrates, and bile-acid sequestrants - and of course statins have better data than these other drug classes. I can also make the same exact argument for anti-hypertensive drugs, diabetic drugs, depression drugs, any many other classes of drugs, so should we stop using pharmacotherapy to manage high blood pressure and diabetes and depression, too? Certainly exercise and diet (including low carb) play an important role in managing ALL of these conditions, but the logic you are applying to statins would seem to indicate that we should stop using pharmacotherapy for ALL of these conditions.

- "Clinically, the risk reduction is meaningless."

I can cite 20 years of prospective, randomized, double-blinded, peer-reviewed data published in a wide variety of medical and scientific journals, reviewed by many, many, many Expert Panels, and included in medical guidelines from around the globe, and yet you dismiss the outcomes data supporting statins as "meaningless?"

Ok, what's good for the goose is good for the gander, right? Show me ONE prospective, randomized, double-blinded, peer-reviewed and published outcomes trial supporting CVD risk reduction (or better yet "all-cause mortality" reduction) with low carb diets. You can't. The ONLY diet with outcomes data is the Mediterranean Diet. I still BELIEVE in low carb, just as I still BELIEVE in ezetimibe (Zetia). Both improve lipoproteins, and I believe that both will be supported by outcomes data in time. But for now, the most compelling body of data supports statins.

Also, EVERY expert panel of which I am aware (and there are many, both in the U.S. and abroad) consider statins to be THE first-line drug therapy for dyslipidemia (dyslipoproteinemia), and also recommend statin therapy regardless of cholesterol levels for people with diabetes and/or diagnosed CVD. Why would medical experts around the world all agree on this point if it wasn't extremely well-supported by many, many, many years of studies and analysis?

- "Plus, in most cases, statins don't improve overall mortality."

Again, I could argue the same point for many drug classes that treat other conditions, but the data supporting statins is actually BETTER than the data supporting most other drug classes, so why are statins treated as some sort of "whipping boy?"

And again, please provide a citation to support this assertion. All-cause mortality was reduced in WOSCOPS (pravastatin - 22%), 4S (simvastatin - 30%), and Heart Protection Study (simvastatin - I forget the exact reduction), as well as other statin trials. Of course there have also been reductions in all-cause mortality in studies of the Mediterranean Diet, Fish Oil, and Niacin, but why choose just ONE of these approaches to lower risk of morbidity and mortality? Why not embrace as many of them as apply to your particular situation? For many, many folks, a statin is an appropriate part of a comprehensive risk-reduction regimen. Statins are NOT a substitute for appropriate diet and exercise - but in study after study after study after study after study, the folks taking the statin lived longer and had less CVD events along the way. There's a mountain of data supporting my comments, and I have most of the studies on my bookshelf. Feel free to ask me questions (questions are good!).

- "Low cholesterol has been associated with an increased cancer risk."

The data on "increased cancer risk" is razor-thin compared to the fact that EVERY statin-treated population I am aware of has fared better than their placebo counterparts.

- "If you don't die of a heart attack, you'll die of something else."

Non sequitur. Why bother adhering to a low carb diet? You'll just die of "something else," right?

- "The fine print on Crestor ads say that it has NOT been shown to prevent heart attacks. If it doesn't prevent heart attacks, why take it???? I don't see how taking statins will prolong my life enough to bother with them and risk the side effects."

I'm citing landmark studies published in peer-reviewed medical journals and you're citing a 30-second TV ad. Here's the deal:

The Food & Drug Administration approves product "claims." In order for Astra-Zeneca to "claim" a particular benefit in their ads, a submission has to be made to the FDA, and it's a time-consuming, expensive process.

Statins have been in use for 20 years. Back when statins were new, it was common for Pharma Reps to argue against the "new statin on the block" by saying that there was "no outcomes data yet" for that particular drug. But as time went on, we realized that there was indeed benefit with lovastatin, pravastatin, fluvastatin, simvastatin, atorvastatin, and rosuvastatin (cerivastatin was pulled from the market, but there’s no reason to throw out an entire bushel due to one bad apple - but Baycol is a tangent discussion).

So ALL available statins have been shown to have outcomes benefit. This is called a "class effect." ALL drugs within the drug class have positive data supporting them. So why would I care very much if Crestor hasn't been "FDA-approved" to lower the risk of heart attacks? I wouldn't care about this point at all. Statins lower CVD event rates and all-cause mortality. Crestor is a potent statin that is supported both by "class effect" as well as SEVERAL good studies including data that show a reduction in both HEART ATTACK (myocardial infarction aka MI) and ALL-CAUSE MORTALITY. So why would I rule out Crestor simply because Astra-Zeneca hasn’t yet spent the money and time necessary to jump through a particular FDA “hoop” in order to have the FDA bless this particular claim?

- "I don't see how taking statins will prolong my life enough to bother with them and risk the side effects."

Then re-read my posts! ;-)

MOST of the "side effects" of statins are HARMLESS! Any real danger (i.e. rhabdo) is very, very rare (especially at low-to-moderate statin doses). If you use a statin with a fibrate, use fenofibrate, not gemfibrozil. A lot of expert panels (including the FDA) have done meta-analyses on the literature and weighed in on this issue.

I remember Dan Rather telling the Nation many years ago that "If you are takin a statin drug, you may want to stop!" or some line like that. If was one of Dan Rather's many examples of egregiously irresponsible journalism.

Admittedly, a small percentage of patients experience HARMLESS myalgias (muscle aches) with statin therapy, and there are some other side effects that can occur in a low percentage of patients. Just stop taking the pills, call your doctor, take a break for a few weeks, and let your doctor try another statin. If the second statin doesn't work, try a third. Try very low doses. Try taking the statin every other day, etc. And try fluvastatin or pravastatin before you give up all hope.

Now what I just wrote makes it sound like side effects are a HUGE problem with statin therapy. Not true. Over 95% of patients tolerate statins without a problem. And over 99% can tolerate a statin if you follow the routine I described above (based upon personal experience - not a published study, FWIW). A very small percentage of people cannot tolerate statins, and for these folks there are other options (but that's a seperate discussion).

Also, a lot of people worry about statins and their liver. Of course, when I ask folks how many people they know who died of cardiovascular causes (MI, stroke, etc.) the answer is invariably "a lot!" When I ask how many people they know who died of statin-induced liver failure, the answer is invariably "zero." If you want to gamble, the safer bet is to take the freakin' statin! ;-)

In closing, diet is important, and low carb diets do improve lipoproteins, and I do believe that Jimmy is doing a good thing by spreading this information. I just wish people wouldn't bash drug therapy. Diet and drugs are BOTH important.

Diet can REDUCE the need for drugs, but diet cannot ELIMINATE the need for drugs.

You shouldn't take a statin (or any other drug) while sitting in the Burger King drive-thru, because you can out-eat the benefit of the pills, and you shouldn't rely EXCLUSIVELY on diet for risk reduction - because to do so would be to deny the proven outcomes benefits of the pills.

Best Regards,

Marc

There is a lot of information to swallow here. Thanks everyone for taking the time. I think since my LDL-P is so high I probably will go on statins for at least a few months.

Therein is my question, Crestor says studies show it can lower my LDL-C by %40-50 over 6 weeks. What happens if I stop taking it after such a period? Does the LDL immediately shoot up again? What I'm really asking I guess is if Crestor can give me a boost out of the danger zone and then I can let diet/exercise take it from there.

Also when they talk in their Prescription Information http://www1.astrazeneca-us.com/pi/crestor.pdf (page 5) about these drops in LDL-C, would similar drops also be expected in the LDL-P number. From what I understand they are different ways of measuring the same thing?

You have to take statins for the rest of your life to keep the LDL artificially lowered. That along with the joint pain is why I choose NOT to take statins. Eat low-carb and your LDL particle size will become the large, fluffy protective kind. That's the bottom line.

(03-09-2009 03:53 PM)berserkertooth Wrote:  There is a lot of information to swallow here. Thanks everyone for taking the time. I think since my LDL-P is so high I probably will go on statins for at least a few months.

Therein is my question, Crestor says studies show it can lower my LDL-C by %40-50 over 6 weeks. What happens if I stop taking it after such a period? Does the LDL immediately shoot up again? What I'm really asking I guess is if Crestor can give me a boost out of the danger zone and then I can let diet/exercise take it from there.

Also when they talk in their Prescription Information http://www1.astrazeneca-us.com/pi/crestor.pdf (page 5) about these drops in LDL-C, would similar drops also be expected in the LDL-P number. From what I understand they are different ways of measuring the same thing?

Berserkertooth, before you take a statin, I encourage you to go to http://www.spacedoc.net and read what Dr. Duane Graveline has to say about them. His book, Lipitor, Thief of Memory is an account of how his health suffered from taking Lipitor, and I believe it is a must read before you make your decision.

Marc, two questions for you: 1. Are you taking a statin? and 2. If atherosclerosis is gradient driven, explain to me why the addition of iodine to a high fat diet stops plaque from forming? I've attached a paper describing this phenomenon for you.

Also a comment: It's incredible to me that you would call the side effects of statins harmless. These drugs have seriously harmed thousands of people. Before Baycol was pulled from the market, it killed some 60 people.

In my opinion, these drugs are dangerous and have very serious side effects. Many documented reports detail the severe side effects that otherwise healthy people have experienced after taking these drugs. The side effects include:

>Severe muscle cell damage leading to a fatal kidney condition called rhabdomyolysis. Complications of rhabdomyolysis include acute kidney failure, vascular blood clots, elevated blood potassium levels and cardiac arrest.

>Permanent and debilitating muscle pain and weakness.

>Neurological damage including global transient amnesia, memory loss, learning impairment and confusion.

>Congestive heart failure.

>Mood changes, including increased hostility, aggression and depression.

>Elevated liver enzymes, indicating liver damage.

>Statins also block the mevalonate metabolic pathway, which is involved not only in cholesterol, but in the production of important cell chemicals such as CoQ10. CoQ10 is the catalyst which drives cell energy production. A lack of CoQ10 can cause serious heart and skeletal muscle damage, and severely limit energy production for the body.

>Statins are linked to a condition known as Mitochondrial Myopathy, a condition in which cell mitochondria become damaged, accelerating the aging process, and resulting in permanent disabling weakness. This may be exacerbated by statin interference in the production of CoQ10 and L-Carnitine.

>Statins are also linked to a much greater risk of developing diabetes as a "side effect". Simvastatin (Zocor) in particular has been shown to interfere with cellular glucose signaling and insulin secretion, and reduce beneficial adiponectin levels.

>Statin side effects can be worse if they are ingested in conjunction with other substances using the same metabolic pathway in the body. Drugs such as cyclosporine, itraconazole, diltiazem and erythromycin, bile acid sequestrants (cholestyramine, colestipol), fibric acid derivatives (bezafibrate, fenofibrate, gemfibrozil), and other substances such as niacin and grapefruit juice are all contraindicated for use with statins.

>There are a host of other side effects, including pancreatitis, an increase in respiratory infections and pneumonia, peripheral neuropathy, skin rashes, sexual dysfunction, headaches, diarrhea, nausea, stomach pain and cramping, heartburn, constipation, and dizziness.

>In 1996, Newman and Tulley published a meticulous review of the links between cancer and statins in a paper titled The Carcinogenity of Lipid-Lowering Drugs in the Journal of American Medical Association. (JAMA 27 55:60, 1996).The CARE trial in particular, resulted in a much higher rate of breast cancer for the women in the treatment group.

I'm sorry, but I don't believe your hype about statins. Framingham and the MRFIT both show that people who have the highest cholesterol live the longest. And since LDL is part of cholesterol, teasing it out and blaming it for heart disease just doesn't make logical sense. And it doesn't fit all the facts. Read the Cholesterol Myths by Uffe Ravnskov if you want citations.

THANKS Ellen! I'm working on getting a podcast interview with Dr. Graveline about his book. Wish me luck!

I sure hope you get that interview, Jimmy.

(03-06-2009 12:45 PM)Jimmy Moore Wrote:  Mark, thanks for your input and welcome to my forum! However, I refuse to go on a statin drug because it has caused real harm to my body in the past. Sure, the drugs were Crestor and Lipitor and not this "low-dose" version, but I'm not interested in that. I disagree that people HAVE to take a statin to improve their lipids. I've discussed my own personal numbers with a noted low-carb researcher and practitioner at Duke University in Durham, NC named Dr. Eric Westman. While he noted the LDL-P is higher than normal, the small LDL-P being a minuscule 30 along with HDL over 50 and triglycerides under 100 said there is nothing to be alarmed about at all.


Jimmy - Forget particle "size." Please. If total LDL-P is high, then LDL-related risk is present.


Several other of the world's best health experts I have interviewed on my podcast show agreed with this analysis, including Dr. William Davis, Dr. Jim LaValle, Dr. John Salerno, and Dr. Mary C. Vernon, among many others. While there are plenty of medical professionals who would agree with your analysis of my situation as well as berserkertooth, like Dr. Dean Ornish and my upcoming podcast interview guest Dr. Michael Ozner, I don't think telling people they have to resort to taking a statin drug with their low-carb lifestyle is the answer. I'd be happy to talk to you today, so feel free to e-mail me at livinlowcarbman@charter.net so we can arrange a time to chat.


Jimmy - I will email you tonight and I hope to speak with you tomorrow.


THANK YOU again for your addition to the discussion and I look forward to speaking with you.

Check your email and we'll talk!

Best Regards,

Marc

(03-09-2009 03:53 PM)berserkertooth Wrote:  There is a lot of information to swallow here. Thanks everyone for taking the time. I think since my LDL-P is so high I probably will go on statins for at least a few months.

Therein is my question, Crestor says studies show it can lower my LDL-C by %40-50 over 6 weeks. What happens if I stop taking it after such a period? Does the LDL immediately shoot up again?


[Yes.]


What I'm really asking I guess is if Crestor can give me a boost out of the danger zone and then I can let diet/exercise take it from there.


[Diet and exercise are VERY IMPORTANT, and can reduce or possibly even (eventually) eliminate your need for a statin. That being said, many people who have multiple risk factors (i.e. diabetes, age, increased waist circumference, elevated fasting blood glucose, low HDL-C, high Triglycerides, Family History, Hypertension, etc.) will STILL benefit from statins even after beginning a diet and exercise regimen - and this therapy is often lifelong.]

Also when they talk in their Prescription Information http://www1.astrazeneca-us.com/pi/crestor.pdf (page 5) about these drops in LDL-C, would similar drops also be expected in the LDL-P number. From what I understand they are different ways of measuring the same thing?

[LDL-C is a surrogate marker for LDL-P. LDL-P is a direct measure, and is far more accurate. Reduction in LDL-C is related to reduction in LDL-P. That being said, statins tend to reduce LDL-C more than LDL-P. In other words, you may get a 50% reduction in LDL-C, but only a 30% reduction in LDL-P. This is common, and this is why so many Expert Panels have concluded that LDL-C is failing as a target of therapy, and why there is a need for particle number measurements such as apoB or LDL-P by NMR.]

Please let me know if you have any additional questions!

Best Regards,

Marc

(03-09-2009 05:07 PM)Jimmy Moore Wrote:  You have to take statins for the rest of your life to keep the LDL artificially lowered. That along with the joint pain is why I choose NOT to take statins. Eat low-carb and your LDL particle size will become the large, fluffy protective kind. That's the bottom line.

Jimmy, taking your points in order:

1. Yes, you MAY have to take statins for the rest of your life - although diet and exercise can potentially reduce the statin doses required, and in some cases lifestyle changes (i.e. diet) can eliminate the need for a statin. However, MOST high-risk patients will still benefit from lifelong low-to-moderate dose statin therapy (and many will need combination therapy). Some people can diet and exercise their way out of the need for statins - many cannot.

2. People who cannot tolerate a particular statin should discontinue therapy for about 6 weeks and then try again with a different statin. Some folks simply cannot tolerate statins at all, but bile acid sequestrants (i.e. WelChol), cholesterol absorption inhibitors (i.e. ezetimibe) and niacin (i.e. Niaspan) are all available if statins aren't tolerated. Granted, with an LDL-P approaching 1500, you might have to use two of the aforementioned products (in addition to your current diet and exercise) to get your LDL-P below 1000, but this is very doable!

3. You state: "Eat low-carb and your LDL particle size will become the large, fluffy protective kind. That's the bottom line."

Once again, please repeat after me: SIZE doesn't matter, SIZE doesn't matter, SIZE doesn't matter. I don't CARE what my WIFE says!

SIZE doesn't matter! IT IS LDL PARTICLE NUMBER NUMBER NUMBER THAT MATTERS! NUMBER! Not size! NUMBER NUMBER NUMBER!

People with Familial Hypercholesterolemia (FH disorder) have HUGE LDL particles - but they have a LOT OF THEM, and they have a LOT OF RISK! Having large LDL particles is not a "get-out-of-jail-free" card.

Jimmy - YES, low carb diets increase LDL particle size (and reduce LDL particle number), and that's why I'm a fan of what you're doing here, but please realize that it's particle NUMBER (apoB or LDL-P) that is important. The data on particle SIZE is slim (yes, a bunch of older studies concluded that size was important, but these conclusions are being re-examined as we speak).

NUMBER NUMBER NUMBER NUMBER NUMBER NUMBER NUMBER

Not SIZE!

Best Regards,

Marc

(03-06-2009 12:45 PM)Jimmy Moore Wrote:  Several other of the world's best health experts I have interviewed on my podcast show agreed with this analysis, including Dr. William Davis, Dr. Jim LaValle, Dr. John Salerno, and Dr. Mary C. Vernon, among many others.

Jimmy:

You mention Dr. Davis, the author of "Track Your Plaque." I have a lot of respect for Dr. Davis (although he still lends too much credence to LDL particle size - I think he's trying to "cover all the bases"). I'm not sure what Dr. Davis stated in his interview with you (I haven't had time to watch it, but will when I can), but in his book Dr. Davis suggests an LDL-P goal of <700. I would be pretty surprised to hear him state that he's ok with an LDL-P of >1400 (with the exception, perhaps, of a person with virtually no other risk factors). You might also want to check out:

"Age Strong Live Long" by Seth Baum, M.D. and "The HAPI Heart Diet" by Michael Varveris, M.D.

Best Regards,

Marc

Marc, you're still hung up on relative risk. The absolute risk reductions from statins are often on the order of 1%, according to the data I've seen. Using relative risk is just a way to hype the benefits. The Number Needed to Treat is rediculously high. You have to treat around 100 people with statins to prevent one heart attack. I don't see how that's worth the cost or potential side effects.

I really don't care what the "experts" say. I look at the actual data. Most of these "experts" have financial ties to the drug companies and will do all they can to hype the benefits and downplay the negatives. Furthermore, ENHANCE showed that Vytorin provided no additional benfit over Zocor alone, even though it lowered choesterol more. Plus the companies involed sat on that information for two years. I don't trust the "experts" or the drug companies. They are just trying to make money.

Ellen:

In response to your questions:

1. Yes, I am taking a statin. Gleefully. ;-)

2. My statement that atheroslcerosis is a gradient driven process is supported by 40+ years of studies published in peer-reviewed scientific, laboratory, and medical journals, medical and scientific textbooks, and numerous expert panels including The 30-person/10-country Report published in the "Journal of Internal Medicine" in 2006, The American Diabetes Association/American College of Cardiology Joint Consensus Statement on Lipoprotein Management published in "Diabetes Care" and "Journal of the American College of Cardiology" in April of 2008, and the American Association for Clinical Chemistry's Lipoproteins and Vascular Diseases Working Group on Best Practices in press now in the journal "Clinical Chemistry." I could go on.

In response, you send me one study that was conducted 76 years ago in a small number of rabbits. I appreciate you sending it, and I'll definitely read it, but I'll let the readers decide which one of us may have a better grasp on current scientific understandings pertaining to atherosclerosis. ;-)

You find it "incredible" that I would call the side effects of statins "harmless," but for some reason you fail to acknowledge that I qualified my statement by saying "MOST" (and even used all-caps in my original statement). MOST of the side effects of statins ARE harmless. The FDA has reviewed the data and weighed in on this issue, as has the National Lipid Association and other expert groups. I stand by my original statement.

I think you're actually understating the number of Baycol deaths. There were 60-some killed by the combination of gemfibrozil (Lopid) and cerivastatin (Baycol), but an additional 20 or so died from taking the .8mg dose of Baycol alone, so the total number was around 80-85 if I remember correctly (although I'm working purely from memory here). Lots of drugs get pulled from the market, so statins are not unique in this regard, and what's very important is that WE HAVEN'T SEEN SIMILAR PROBLEMS WITH OTHER STATINS.

With regard to your list of statin side effects, yes, side effects occur. Any time you put tens of millions of people on a drug, some of them ain't gonna tolderate it. So what? This same exact statement holds true for virtually every drug class. Why would you expect it to not hold true for statins? As I mentioned before, rhabdo is VERY RARE, and if you heed the simple advice of ceasing your statin and calling your doctor if you experience unexplained muscle aches, then the odds of getting into serious trouble are incredibly, incredibly low! And again, this sort of thing is not exclusive to statins. For example, cessation of beta-blocker therapy without gradually weaning yourself off of it can give you a very bad hair day.

The bottom line is that allergic reactions to antibiotics have killed a LOT more people than statins. Do you propose that we stop using antibiotics?

You reference metabolic pathways. The most common pathway for the metabolism of many drugs (including most statins) is the CYP-450 3A4 pathway. Some of the drugs that you list (such as cyclosporine and itraconazole) do indeed raise concerns, and statin therapy may need to be temporarily discontinued. This is not a big deal.

You also state that other drugs such as bile acid sequestrants, fenofibrate, and niacin are "contraindicated" for use with statins. This is completely untrue. The NCEP ATP III Addendum published in July of 2004 deemed fenofibrate to be generally safe to use in combination with statins, and a statin-fenofibrate combination drug is currently in development. TriLipix, the newest fenofibrate, is specifically approved by the FDA for use in combination with statins, and Advicor (a lovastatin/niacin combination drug) has been FDA-approved and on the market for many years, and Simcor (simvastatin/niacin) was recently launched. The ADA/ACC Expert panel I referenced above RECOMMENDS adding niacin to statins for people who need additional apoB/LDL-P reduction, and also discusses adding fenofibrates to statins.

You state that you don't believe my "hype" about statins. It isn't "my" hype, I've just read a large amount of the data (and please realize that I don't make any money from statin sales).

You state that Framingham and MRFIT both showed that people who had the highest cholesterol lived the longest. This is untrue. I've got the Framingham survival curves easily accessible, and I can probably dig out a some data on MRFIT (although I'm not sure where I put it).

You state that "since LDL is part of cholesterol, teasing it out and blaming it for heart disease just doesn't make logical sense." First, this statement shows a fundamental lack of appreciation for lipoprotein pathophysiology, but that's a whole separate post. Second, "LDL" is not cholesterol. LDL = Low Density Lipoprotein." LDL-C = the amount of cholesterol carried within Low Density Lipoproteins. LDL-P = the NUMBER of Low Density Lipoproteins (a close surrogate is apoB). If you'll re-read my posts on this thread, you'll see that I care far more about lipoprotein particles than I do about cholesterol.

Again, why are statins singled out as a whipping boy? The bias against statins is largely irrational, and is driven by a small number of people who really should know better - and by a large number of people who get caught up in some sort of quasi-religious fervor that causes them to willfully ignore and/or denigrate literal mountains of data that support statin use. A lot of well-intentioned but irresponsible and sometimes dangerous advice is the unfortunate result. People who are caught up in the fervor don't usually like talking to me, because they are generally unable to defend their bias against statins when I very rationally point out virtually ALL drug classes have potential side effects, and that the outcomes data supporting statins is actually better than the data supporting MOST other drug classes.

Best Regards,

Marc

Marc, you definitely know your arguments, and I am no match for bringing up data from federal sources and mainstream medicine, mostly because I believe the data provided by people who have a financial stake in the sale of statins or any other drug is inherently untrustworthy.

As for Framingham, the data you can pull out is, I'm sure the data that the Framingham researchers wanted to show because it supported their hypothesis. But it is a fact that in 1987, the Framingham researchers published a 30 year follow up report on the “all cause mortality rates” of the Framingham residents which showed that for every 1 mg/dl drop in cholesterol levels, there was a 14% increase in heart related death, and an 11% increase in overall mortality. In other words, declining levels of cholesterol increased the risk of death from all causes, not just CHD.

This newer information from the Framingham study, and indeed most study results which don’t support the cholesterol-heart disease link, have been largely ignored by the National Institutes of Health, the AHA, the National Heart, Lung and Blood Institute, the NCEP and the mainstream media. You won't find mention of this 30 year follow up paper on the Framingham website. And you certainly won't find it on the NCEP's website either. They would lose their funding if they told the truth.

We are going to have to agree to disagree, as I come from the viewpoint that even one death, or one permanent injury is too many, especially when it comes to the treatment of "high" cholesterol, a condition that was created by a committee of doctors and scientists who benefit from the sales of drugs to treat this condition. The guidelines offered by the NCEP are the least evidence based, and in fact the guidelines for most of the federal government's health advice is based on politics, not science.

For example, when a correspondent asked the National Heart, Lung and Blood Institute why there were no open meetings required for the development of the new cholesterol standards, and why the New Guidelines were not published in the Federal Register, he received the following reply:

". . . the guidelines for cholesterol management released on May 15, 2001 were developed by a panel of experts--the Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III [ATP III])--convened by the National Cholesterol Education Program, an educational program coordinated by the National Heart, Lung and Blood Institute. The ATP III panel is not an advisory committee to the NHLBI but rather a group of recognized experts providing their scientific judgment about cholesterol management to clinicians.

The "recognized experts" on this panel included Drs. Grundy, Hunninghake, McBride, Pasternak, Stone and Schwartz, all of whom have received consultant fees from the producers of statin drugs. See this page as evidence: http://www.nhlbi.nih.gov/guidelines/chol...tm#writers

People are being harmed, lives are being damaged, and people have died from taking statins.

The argument that "drugs have side effects, so what?" belittles the suffering that each of these individuals and their families have endured. Our outlooks on what is acceptable are fundamentally different, and I don't hope that my arguments would change your outlook, just as yours won't change mine.

I think this quote says it for me:
"The diet-heart hypothesis has been repeatedly shown to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century."--George Mann, ScD, MD, Former Co-Director, The Framingham Study

I would encourage anyone considering statin therapy to read these books and websites first, just so they have ALL the facts:

Health Policy on Blood Cholesterol -Time to Change Directions paper published in Circulation 1992 86:3:1026-1029 http://circ.ahajournals.org/cgi/reprint/86/3/1026
The Great Cholesterol Con by Anthony Colpo
Lipitor Thief of Memory by Dr. Duane Graveline.
The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease by Uffe Ravnskov.
The Great Cholesterol Con: The Truth About What Really Causes Heart Disease and How to Avoid It by Dr. Malcolm Kendrick.
THINCS: The International Network of Cholesterol Skeptics): http://www.thincs.org/
Spacedoc.net: http://www.spacedoc.net a website by Duane Graveline, M.D.
The Statin Effects Study website: https://www.statineffects.com/info/index.htm
Baycol Timeline of Events: http://findarticles.com/p/articles/mi_pw...rk02051931"