Sorry, I was not paying attention to the question...nevermind. Can't delete my message.

...are we treating lipid numbers or the arteriosclerosis?

You are treating atherosclerosis if you have plaque, and whether you have plaque or not, one of the fundamental concepts of TYP is that treating to the 60-60-60 target for lipids, will either prevent plaque growth or progression, or along with reduction of and/or elimination of things like Lp(a), VLDL, IDL, small dense LDL, etc., will induce either stablization of diagnosed plaque, or optimally regression (confirmed with serial CAC scoring either annually or less frequently).  So the answer is "Both."

Are the benefits of statins due to lower lipids or the anti-inflammation effect (and how inflammatory are the lipids themselves?). 

Both,  and yes.

Niacin could be called a supplement or a drug

In the doses prescribed by TYP (and every cardiologist or GP who prescribes it), nicontinic acid is taken in doses (>500 mg) that are considered pharmacuetical....It's a drug, no question about it.  Same thing with fish oil in the doses we are taking it (>3-10 gr p/day).   Ditto for argenine at large doses as a drug. Think "viagra" and the nitric oxide connection.
 
...prescription drugs tend to be better studied (with more financially induced biases) - but that does not mean statins are more (or less) effective than interventions that have no patent potential

I would not argue otherwise, but simply because an intervention has no patent potential (and thus appears to have little potential for commercial exploitation for development by large pharma) doesn't mean such interventions aren't using "drugs"....A great number of pharmacuetical companies do just fine producing "generic" drugs which have come off-patent and which have seemingly lost their potential for continued exploitation.

, , , We just can't know for sure right now.

All the more reason for many to use the interventional agent which has been studied, and whose effects are generally known.   I'm all for personal choice and the right to experiment with one's body, so in my book, do whatever you want and take whatever risks you want to take, whether known or unknown....But if an agent is known to have an effect that we're seeking and you can take it without sustaining any of the adverse effects some people seem to experience, why vilify those who can and do tolerate it and can derive benefit?  That's my point, and I believe that is what Dan F was saying as well.

The problem is that Statins are over hyped

By whom? How do you apply the "over-hyped" definition?  I lived for 53 years and NEVER took a statin.  My docs didn't simply tell me in 1998 when I first underwent coronary angiogram (after experiencing what appeared to be an MI, but which was confirmed as definitely NOT an MI) to "take a statin"....and yes, statins existed at the time.  My docs and the cardiologists who did the angiogram (and who found no blockages at all) didn't prescribe a statin but instead prescribed TLC (therapuetic lifestyle changes), albeit the "TLC" of the time was the AHA "fat-free" grain-loaded diet (which sadly is what the AHA still prescribes).   It wasn't until late 2006 when I was diagnosed with ACS, had an irregular ECG, and had undergone a heart scan (and CT coronary angiogram) which confirmed both coronary calcium (i.e., atheroslcerosis)--albeit at a rather low score of 26 all confined to the proximal LAD-- and a significant >75% blockage with a single focal lesion which was causing shortness of breath and angina, that any medical professional first even suggested a statin to me (Crestor at 10 mg, nothing higher ever).

In other words, I went more than half a century-- and more than 20 years after statins had become widespread-- before any doctor even thought to prescribe one to me.  My doctor (regular GP) had, however, prescribed niacin for me back in 1998 as a way to control lipids.   So which would you say was "over-hyped"...the non-statin, niacin approach a decade ago, or the statin, which was prescribed to me after I'd disregarded and blown off all of the eariier medical advice which involved non-statin treatment?    Are statins really "over-hyped" or is it truly a question of many patients who just don't really understand the seriousness of their situations until things are well-upon them?  

Frankly, I'm not buying into the "over-hyped" argument, not at all.  Many of my friends do not take statins, and they are mostly over-50's people like me.  Moderately active folks who lead somewhat sedentary lives during the day (e.g., lawyers, architects, doctors, other professionals who sit behind a desk or lead otherwise pressure-filled days, some with large monthly nuts they're chasing).    I frankly don't think they're "over-hyped" nor over-prescribed, at least not in my experience.  I read that they are, but I've just not experienced that.   I think the issue is really (a) a lack of motivation on the part of patients, and to a lesser extent docs, and real lack of education of patients about the very real risks of how heart disease develops and how to prevent it and (b) the effects of the foregoing once time and the disease catches up with us.  I don't disagree with Dr. Davis that many in the profession are quick to prescribe a drug where there may be other alternative ways to treat the same problem.  So if that's the sense you're using "over-hyped", well, ok.  But, that said, a statin is just a tool, so if it works, and one can tolerate it without adverse effects and derive the benefit quickly, what's wrong with that? 

Do we really know if statins are a tack hammer or a sledge hammer?

Yes, I think we pretty much know.  We know, for the most part what HMGA co-reductase enzyme, and its inhibition by the mechanisms of statins, does, how it works and what doses work, which are too strong (e.g., Baycol) and how LDL functions. It's certainly dose dependent as to whether it's going to function gently or excessively.  In some people, a dose of 10 mg of rosuvastatin is wonderful;  in others, they may experience myalgia, have a negative experience, or, in about 1 in a million it simply cannot be tolerated at all.   So again, yes, for the most part I think we know.

And lastly, when you refer to the recent Danish study which concluded that there was a causal (not merely an associative) connection between increased levels of Lp(a) and MI, who is the "they" who "talked down" the study?   Point me to one public statement made by any statin manufacturer....I don't think one was made.  

If you're referring to someone who "talked down" or attempted to downplay the significance of the study's findings, I'm betting you mean George Thanassoulis, M.D., and Christopher J. O'Donnell, M.D., M.P.H., of the National Heart, Lung and Blood Institute's Framingham Heart Study, Framingham, Mass.   Are they "Big Pharma" reps?   I have no idea, but all they really said in an editorial they wrote which accompanied the published study was that the issue of Lp(a) needs more study, preferably by a controlled clinical trial, to render the definitive word on the subject for clinicians. 

I'm certainly not an apologist, nor trying to say that there isn't an enormous profit-motive for the manufacturers of a drug to continue to market and sell their stuff, and the question is always going to be there in the minds of some that this profit motive has the potential to subvert the use of the knowledge about how to best utilize these tools.  Obviously there is a huge profit potential and the incentive for conflicts of interest to cloud judgment is ever-present, and it's particularly pernicious in the health, food and drug safety areas, because it often involves matters of life and death. 

That said though, as Dan F. notes, we're all adults.  I don't care if you want to stay high all day, if that's what you want to do.  Frankly it matters not to me, nor should it matter to you-- beyond a societal goal which has us all living in a productive, happy world, I suppose-- what any of us ingests in our bodies, so long as it's not causing harm to us and those around us. 

But if a tool can be beneficial, and can help me achieve the results I'm trying to get without doing harm, then it's the right tool for the job, no matter what label others might apply to it, and it doesn't, at least IMHO, deserve to be stigmatized or vilified simply because it's made by Merck, or any number of other "big pharma" companies. 

Anyway, that's just my feeling on the subject, my own opinion.  I don't expect everyone (or even anyone) to agree with me.  But I just think the "who is statin-free" question, while perhaps interesting if it was done in the context of a controlled clinical trial might be useful, presented as it was, is really counter-productive, and simply works to stigmatize the use by some of us of a tool that has worked very well to achieve the desired result. 

And by the way, we have hundreds of studies-- probably thousands actually-- which demonstrate in one way or another that reduction of circulating serum levels of LDL, which is the primary purpose of HMGA co-reductase enzyme inhibition is induced, reduces CAD and CVD events.   What we don't really know is how high one's HDL should be, because the functional value of high HDL (i.e., how high it should be) really isn't yet known.   So boosting HDL to high levels with intakes of perhaps larger amounts of dietary saturated fats than are traditionally recommended is a strategy that is only now being explored, and the long-term effects of the "Paleo" movement are just as understudied and unknown-- likely more so,  as anything medical science and commercial pharmacology has to offer.

That's all.  

PMID: 18237592

Interesting thread going on here, let's put it that way.  By way of disclosure, I am on a statin.  My pre-statin profile was:

LDL-C 168, HDL-C 60 (HDL-2 12, HDL-3 48), TG 54, Pattern B.

After taking 40 mg Lipitor:

LDL-C 60, HDL-C 67 (HDL-2 17, HDL-3 50), TG 44, Pattern B.

Adding 1000 mg Niacin:

LDL-C 51, HDL-C 88 (HDL-2 30, HDL-3 58), TG 40, Pattern A/B.

Increasing Niacin to 1500 mg:

LDL-C 51, HDL-C 90 (HDL-2 30, HDL-3 60), TG 35, Pattern A/B

Increasing Niacin to 2000 mg:

LDL-C 51, HDL-C 95 (HDL-2 35, HDL-3 60(, TG 41, Pattern A.

To recap, my LDL has gone down, my small LDL pattern has been rectified and my HDL has increased including a substantial increase in the HDL-2 fraction.

Recently I switched from Lipitor to Crestor (20 mg).  I am supposed to have blood work done in the next week.

Frankly, I find this discussion about statins vs. non-statins to be a bit tendentious.  JEG is, in my view, correct and what he said needs to be repeated.  Statins are a tool to obtain certain benefits.  The same is true for niacin, Vitamin D, fish oil, L-Arginine, etc. especially in the therapeutic doses we are taking.  The point of the 60/60/60 goal is that based upon Dr. Davis' clinical observations such a profile is the one that is most likely going to result in regression.  (Obviously, there are exceptions to every rule.)  As we know, high dose Crestor has been proven to cause regression.  If Crestor was a herbal solution available over-the-counter we would be flocking towards it as it would be seen as being beneficial in obtaining plaque regression.  Just because it is sold by Big Pharma does not mean it lacks value.  As I said, it is a tool to be used, depending upon the situation, as are the other agents recommended by TYP, to achieve regression. 

For me, I would not be able to achieve reductions in LDL that would put me in position to halt plaque progression or potentially reverse plaque growth absent this tool.  Given that I am not and have never been overweight, do not have high Lp(a), am relatively young, exercise regularly, have normal blood pressure both at rest and during exercise, and relatively high native HDL-C, I have no doubt that my increased LDL-C especially in the presence of a significant small LDL pattern was the cause of coronary plaque formations.

Having read enough studies that show causation between increased LDL and coronary artery disease I have no doubt that reducing LDL is helpful for me.  Is it the be-all and end-all?  Of course not.  If it were then no one who took a statin would have a coronary event.  But as far as I am concerned it is part of the solution and certainly not part of the problem.  Cherry-picking data to make a case against its use seems to me to be counter-productive.  I suspect that what G has stumbled upon is an association between statins and people with TGs below 180 mg/dL and not a causative link.  And yes, I think that having LDL-C levels in excess of 200 mg/dL in the face of ANY Agatston score is a clear indication that LDL needs to be reduced.  It may not be the sole reason for plaque formation but it certainly is a contributing factor.  Whether that is achieved through diet, statin agent or other therapies such as niacin or fibrates does not really matter (although I agree that eliminating dietary cholesterol is not the solution).  The goal is reduction in plaque growth and ultimately halting growth and promoting regression.  Whatever works to achieve that goal is fine.  If Bark can achieve that goal with LDL-C levels exceeding 200 mg/dL then that is truly great.  But if after doing another EBT Bark's plaque growth remains in excess of 20 percent annualized if it were me I would find a way to reduce LDL-C to the TYP guideline levels.

6/17/2009

Let me give my own opinion, and perspective in a simple way.  My take on all this about CVD, is  someone on Statin or no Statin. To me, whatever works for you, then go for it. The same with other prescription medicine or supplements. If this lowers your risk, then fine.
We are all in a journey.Whether you reached your goal by plane, car, boat or walking, then you accomlish your goals.

To me the real proof, on whatever plans, a person does, is whether a person is still alive in 5 years or less, or 20-30 years from now.

I have a personal story, to tell. My brother is a Physician, practicing in a country, with a limited resources(Health). No sophisticated lipid tests, or CT calcium score. All I know, is he had an MI, in his 40s, he did not even went to a hospital or consulted an MD. He ignored his symptoms. Could you believed this? He was not married then.
He had a coronary arteriogram, at a capital city, 500 miles from from where he lives.

I have seen, his coronary arteriogram and also I have it reviewed by a Cardiologist here in the US. He had 100% occlusion
of his RCA. and some other small branches. Also the Cardiologist noticed a small aneurysm in the left ventricle. He warned my about the potential, of a rupture. NO Cardiac intervention, i.e. Stents or Bypass.

Guess, what this man, lived another 30years. He got married, had children and grandchildren. His son is a nurse in North Carolina. He live to be 78 years old.

I am not familiar, as to what type of medicine or supplements he was taking,  statins or no statins.
This I know, after his cardiac event, he change his lifestyle and nutrition. Stopped smoking.
He eats fresh fish(still wriggling), when deliveredd to his house, plenty of vegetables. He eats this every day. He walks in a sunshine(vitamin D?), daily.

By the way he continued practicing medicine, for several decades more. If I am a betting person I would have not expected for him, to live another 30 years, after that CVD event. Obviously, I was completely wrong.

So for those with positive calcium score, I would do the best I can and all the advise from the TYP perspective. There is a lot of unknowns. Of course, this is anecdotal, one person. We should not despair. Only time will tell.

Thank you for your patience,
Kasing12

One possibility is that we do not have the right answer.  We could be entirely mistaken.  Another possiblitiy is that heart disease is not a one size fits all issue and that different approaches work better for different people.  HeartHawk, for instance, notes that his best years in terms of reducing plaque build-up was when he followed the Ornish diet along with antibiotics.  Yet we clearly do not believe that low-fat is the way to go.  That may be true on an overarching basis but for every rule there are always exceptions.  It is what makes us unique.

You have explained why there is a percentage "increase" in small LDL counts when taking a powerful statin but what you are not acknowledging is that on an absolute basis small LDL counts are dramatically reduced by statin agents.  As HeartHawk states, his total particle count rarely exceeds 600.  If 50% of that is small particles (say 300) is that worse or better than if his particle count was 1600 and 750 of these particles were small?

My sample of one shows that I went from having a significant small LDL pattern (squarely in the "B" range per VAP) to having a solidly "A" pattern after taking Lipitor 40 mg. combined with niacin at 1500 mg.  Unfortunately, I do not have the numerical breakdown of the particle types.  I also reduced total LDL-C from 168 to 51.  Now maybe this is the wrong approach - maybe LDL should be higher but made up exclusively of large particles.  But certainly, I have greatly reduced my small LDL pattern by combining the statin and niacin.  I should know more after the next EBT as to whether this approach works - if it doesn't I'll listen to my data and seek to make changes.  But based on what I have read (and JEG has listed some great excerpts regarding the benefits of statins beyond lowering LDL-C) including a statin in our program makes a lot of sense for someone with high LDL-C that is unlikely to be completely responsive to dietary strictures and supplements.