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Tags: cholesterol, Heart Disease, risks, side effects, statins, truth
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I’m curious to know your opinion of Dr. Andrew Weil http://www.drweil.com/
He’s a big advocate of Chinese medicine, amongst other things that seem in accordance with the things you write about, such as Omega-3′s, an anti-inflammatory diet. But he seems to have an almost opposite view of the food pyramid to you, placing grains much higher than meats, and having little time for fats except olive oil. I used to go to him first for insights into health matters, but as I’ve come over to the paleo idea I find it confusing that a guy who seems to be a decent skeptical voice for alternative medicine and for not reaching instinctively for the prescription pad seems to be at complete odds with things you’re advocating. -
I forgot to mention that in the context of statins, he disapproves of most drug statins, but advocates – and prescribes for his patients red yeast rice.
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I respect the contribution Dr. Weil has made. He has been a true pioneer of alternative medicine in the US, and was largely responsible for popularizing it.
However, I disagree with him on several issues – diet being the primary one. I’ve laid out my arguments here and have supported every claim I’ve made with peer-reviewed studies. Dr. Weil’s claim that saturated fat and cholesterol promote heart disease is not supported by the evidence.
I don’t know how current he is with the scientific literature at this point. But of course there are still plenty of people in the health world, such as Dr. Weil and Dean Ornish, who continue to believe in a low-fat diet in spite of the lack of evidence that it provides any benefit, and the considerable evidence that it can actually cause harm.
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The whole point is that total LDL cholesterol doesn’t matter as a marker. If small, dense LDL is high, that’s a risk factor. But the way to lower it isn’t statins or red yeast rice. It’s a low-carb, high fat diet. I explained this in my other presentation (see the previous post).
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When you described your cholesterol test it seemed that the relationship you had with your doctor was that you were not letting on about your own interpretation of the results. Or maybe I’m wrong. Do you ever interact with more widely known public figures in the medical field like Dr. Weil? Paleo is still not yet a phrase in the food world that has gained enough common currency, but I dare say a person like him has heard of it. Search “paleo” at his site and it returns zero results though.
It just seems to me that an otherwise skeptical “outsider” from conventional medicine who seems to have gotten so many things right over the years has this blind spot on the subject. But do you think there is a chance that you have a blind spot yourself? I’m only trying to provoke discussion, but I did have pause for thought when you posted your smoothie entry. It seemed to me at first that it was almost posted as a joke, a stunt. But thinking about it the conclusion I came to was that you are likely a person with a very fast metabolism and you can get away with swallowing that much in one go. A lot of people I think just would never be able to – especially more than two or three times a week – without gaining a lot of weight quickly.
I’ve only recently discovered the food/health sub-culture of “paleo” although I know it has been going for some time now. I just wish there was a wider discussion about all these issues as sometimes it feels like it’s a conversation amongst Herbalife reps or something. A person with a bigger platform like Weil for instance could help start that wider debate. -
Thank you Thank you, You are helping so many that suffer from the effects of Stains. I will be contributing to you because we need to support researchers like you.
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Your skepticism of Ornish might be a bit misplaced, no?
Ornish at the very leastonewell designed RCT under his belt with quite remarkable results, And you Chris? Your latest RCT?
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Ornish’s studies are notoriously sloppy. He doesn’t control for confounding factors. If you take someone who’s eating a standard American diet and living an unhealthy lifestyle, and then run a study where you put them on a low-fat diet, have them exercise, do yoga, and do meditation, and they improve, how can you possibly know what caused the improvement if you don’t have a control group? This is the issue with all of Ornish’s studies.
Show me well-controlled data supporting low-fat diets.
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I haven’t been to a conventional doctor in years. I ordered that test myself.
I’m not sure exactly how to respond, because I’m not clear what your point is. I can tell you that a high-fat, low carb diet doesn’t cause weight gain in many people. That’s why the Atkins diet became so popular. Sure, there are some people that would gain weight eating the smoothie I have for breakfast. But I never claimed everyone should eat the same amount of food with the same macronutrient ratios. My point was simply to demonstrate that fat doesn’t make you fat, and it doesn’t give you heart disease.
The paleo approach isn’t just another “diet trend”. It’s the way human beings ate for hundreds of thousands of years. The major shortcoming of most approaches to nutrition and wellness is that they ignore evolutionary reality.
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Chris,
Thank you Chris for all your endeavors, posts and public talks!
Many people do not want to surrender their ‘red pill’… despite the conclusions from RCTs (!!!) showing statins are highly and statistically associated with rhabdo, all-cause mortality, depression, suicide, violence, CANCER, lower antioxidant status, etc AND very little if ANY improvement in coronary risk.
Not even blogger cardiologists. Even Davis stopped his red pill, aka Crestor, in Feb 2010 — perhaps it worsened his baseline diabetic tendencies, as simvastatin and Crestor both have been shown to raise insulin resistance/HOMA, insulin levels and the incidence of fulminant diabetes..??
Without undertanding our evolutionary past, as you alluded, how will physicians treat chronic conditions like inflammation and gut dysbiosis, perhaps the root causes of all disease?
I’ve concluded they can’t. Ornish’s program is an EPIC FAIL imo. Yes somewhere on the bell curve 6-10% may improve — but the rest 80-90% will develop diabetes, metabolic syndrome and likely cancer later in life. You can read about it ALL over the internet — perhaps the best collective stories of n=10,000+ retrospective study (uncontrolled, unblinded!). Any hypocaloric diet temporarily works — but in the long run studies show they do not. I can show you several AHA step I or II low fat diets where the LDL particle size PLUMMETS to pattern ‘B’ — see Krauss et al. Ornish can walk/jog 5 miles daily and again for a minuscule percentage of cardiac individuals, this will take care of some inflammation but for the great majority meditation+5 miles a day won’t be enough.
-G
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@mart
As a pre diabetic, 23 years ago, at 250 lbs, I stopped eating grains, potatoes, and went low carb. I was in a National Weight registry for 10 years. They followed people who had lost more than 30 lbs and kept it off for 5 years. Now at age 69 my fasting glucose is 95, HDL 90, LDL 130 triglycerides 44 and my weight is 172 lbs. This was before I heard of low carb, Paleo, and other diets on the web. Dr Atkins was what got me started. My Dr., at the time disagreed with me about this diet. As my blood work improved from year to year, he finally said that I must have the genes to follow such a diet. I was probably OK eating this way, but he could not recommend it to his other patients. All of my Grandparents, & Dad died from diabetes. I know this is only one person showing great results from LC eating, but I think it saved me from a truly horrible future. I am glad I could trust what I saw, in spite of no support from the medical profession. Try it and see if it works. You may be surprised.
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Chris,
Fortunately I’ve known about the dangers of statins for a long time. I once told a doctor that I would never take statins because they would eventually kill me. I’m not sure if he liked that , but I won’t be going back to him.I’ve recently heard on local radio stations, local doctors telling patients not to forget to take there statins. I think what is happening is that patients may get a prescription for a statin and they either don’t take it or just reduce the dosage because it doesn’t make them feel okay. I suspect statin sales are being affected and so the pharmaceutical companies are enlisting the help of local doctors.
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Hi Chris,
Thanks for the excellent presentations.
I went to a bookstore today and browsed one of the large medical textbooks covering all major organ systems and related diseases. It’s scary. For instance, a chapter on “lipid dysregulation” doesn’t even mention small dense LDL, and statins were mentioned in every other paragraph as *the* treatment for problems with blood lipids. This in a textbook dated 2010. (The one redeeming feature I saw was that in the chapter on obesity, it recommended a reduction of carbs as a dietary intervention, however a lot of space was dedicated to talk about various drug- and surgical treatments.)
So, indeed, to get the message out is important. The next generation of doctors are getting as brainwashed as usual.
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brauh: good for you – although I have no idea what those numbers mean.
Chris: it’s not that I think that the Paleo diet is a fad, but the fact is that in today’s culture it will be regarded as such once it becomes more widely discussed. And at the moment, while there are no household names talking about it – like Dr. Weil (who if you didn’t know appears on “Oprah”) then there are few companies catering to it.
Imagine though a time when it has taken hold – like the organic movement has done – when grass-fed meat, dairy, eggs and all manner of foods are no longer the luxury priced items they are now. When large parts of the corn, wheat and soy fields around the country have reverted back to grassland and pasture farming is a viable, more profitable business than even the subsidized grain factories we have now.
Diet and health trends move a lot faster nowadays. My hope is that at some point soon the word Paleo will enter the common vernacular and as the discussion widens we can all find out a lot more about its possibilities and limitations. -
Yes, Christian, it’s scary. One thing that blows me away is that if you look in the index of those textbooks, there isn’t an entry for the word “health”. One of the biggest problems with allopathic medicine is that it has no definition of health. Doctors memorize the names of diseases and the drugs used to treat them. That’s not healthcare, it’s disease management.
The system is hopelessly broken and I am sometimes skeptical that it can even be changed at this point. There is too much money invested in it staying the same. The pharmaceutical industry is the second most profitable industry in the world, behind only the oil companies. The drug companies have a scary amount of influence and power, and our “healthcare” system is a direct result of those relationships.
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Just found this blog – thanks for this view on cholesterol Chris.
I’m currently having to keep a 2 week food diary under orders from my doctor, as my last blood test once again gave a high cholesterol reading. (And I’m not thast bothered either). It’ll be interesting to have the discussion around my diet and what changes he suggests.
This blog by Dr Briffa gives some good alternative information on the cholesterol obsession, and mentions C-Reactive protein as a different contributor to consider when discussing heart disease. Thanks, Alan -
Alan,
While I like Dr. Briffa’s blog and agree with him on many things, I don’t think the evidence supports CRP as a marker for heart disease. A large study involving 28,112 cases and 100,823 controls showed a lack of correlation between the effects on CHD complications of CRP genotypes and CRP levels. This is a pretty strong argument against a causal relationship between CRP and heart disease.
That said, I do believe heart disease is caused primarily by inflammation and oxidative damage. As I mentioned in my video presentation called “I Have High Cholesterol, and I Don’t Care”, the most important markers are small, dense LDL, triglycerides and HDL. If you can’t get small, dense LDL measured, you can just calculate the ratio of triglycerides to HDL. To do that, divide triglycerides by HDL. If the result is less than 3.8, it suggests you have mostly large, buoyant LDL. If it’s higher than 3.8, it suggests you have mostly small, dense LDL and you’re at risk.
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One more view point to add into the mix of diet, cholesterol and statins is that of Diana Schwarbein, MD. She wrote a very intriguing book, The Schwarzbein Principle, based on her work with diabetic patients- worth a look: http://tinyurl.com/26sf3xe
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I have Schwarzbein’s book and I like it. It’s a great contribution to the field.
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Second paragraph, second sentence: ” …, who don’t even have low cholesterol.” Didn’t you mean to write “high cholesterol”?
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Thanks Archie. I need a proofreader.
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Chris, in the same vein of proofreading, you wrote
“If you can’t get small, dense LDL measured, you can just calculate the ratio of triglycerides to HDL. To do that, divide triglycerides by HDL, then divide 1 by that number. If the result is less than 3.8, it suggests you have mostly large, buoyant LDL. If it’s higher than 3.8, it suggests you have mostly small, dense LDL and you’re at risk.”
This calculation is the same as HDL/triglycerides. But the higher the triglyceride number gets, the smaller this ratio becomes, whereas we’d expect a very high triglyceride value to be associated with increased risk.
Are you sure you don’t mean triglycerides/HDL instead?
As an example, after 1 month eating rather low carbs, my triglycerides lowered to 113 (from around 160, IIRC), and my HDL rose modestly to 43. These numbers give triglycerides/HDL = 2.63. If my triglyceride number were to rise to 164, that would put me over your threshold of 3.8. This would seem to make sense. The other way around would not.
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Yes, you’re right of course. I’ve been doing too much lately and things are slipping through the cracks. Need to take some time off!
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The article stated the “drug companies made $26 billion selling statins alone in 2008″ but later said “with sales like these”, which make me think the sales were $26B, not the profits. Which was it? As the owner of a business that had $20 million in sales last year, I can assure you there is a HUGE difference! (And no, I don’t take statins and never will, so I’m not a shill for drug companies.)
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Please provide the correct calculation and threshold for triglycerides and HDL. Is it 1/trigycerides/HDL should be < 3.8? My HDL is 101 and my triglycerides are 70, so that formula yields 1.4. Am I figuring that correctly?
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I believe the correct figure is $26 billion in sales.
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The correct calculation is to divide triglycerides by HDL. In your case, the number will be less than 1 (0.69) since your triglycerides are lower than your HDL. Your numbers are excellent, and very suggestive of a preponderance of large, buoyant LDL.
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Pingback from Are You Statinated? « Paleofriend on June 16, 2010 at 9:30 am
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Very nice presentation Chris. You are getting good in this. I’m considering writing a post with a link. Would you permit this? VBR Hans.
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Thanks for the feedback, Hans. Sure, feel free to link to it.
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Pingback from Links and Shout Outs | Musings of a Housewife on June 19, 2010 at 4:45 am
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i couldn’t help at notice that the statin trial summary pdf did not review the following studies:
1) 4S trial (scandinavian simvastatin survival study) – 4444 participants with angina or previous heart attack and baseline total cholesterol between 212 and 309. two groups, both with lifestyle modification and one placed on simvastatin, the other getting placebo.
Results of this study -after 5.4 years the simvastatin groups mortality was 8 percent vs the placebo mortality of 12 percent. Major coronary events in simvastatin group were 19 percent compared to placebo groups 28 percent.CHD deaths (42 percent reduction), revascularization procedures, and fatal plus nonfatal cerebrovascular events (2.7 versus 4.3 percent).
other benefits are noted such as a significant reduction of new or worsening angina.
also see 2) Lipid Trial, 3) TNT trial, 4) IDEAL trial, 5) BIP trial
In light of the significant clinical benefit demonstrated in these well designed studies this pdf can hardly be considered a summary of all relevant statin trials. -
The statin trial summary included the trials from 2008-2009 I mentioned in the presentation. Regarding the trials you mentioned:
In the treatment group of the 4S trial five percent, or 111 individuals, died from a heart attack; in the control group 8.5 percent, or 189 individuals, died, a difference, or a risk reduction of 3.5% That’s hardly a large reduction, especially when you consider the demonstrated side effects and risks of statins, as well as the number needed to treat in order to obtain that benefit.
To prevent these 3.5% of the patients or 78 individuals, from dying it was necessary to treat 2221 individuals for five years. You could also say that to prevent one death it was necessary to treat 25 individuals for five years. Or said in another way, if you have a heart attack the chance to avoid death from a new one in the next five years is 91.5%. If you take Zocor this chance increases to 95%. We’re talking about very, very small differences here.
I believe the LIPID trial demonstrated an absolute risk reduction of overall mortality of 3%. Again, we’re not talking about a huge number, especially when weighed against all of the negative results in 2008-2009 and the considerable side effects, risks and costs of statin therapy.
I don’t know why you would cite the IDEAL trial as a positive result. IDEAL Aggressively reduced LDL in patients who had already had a heart attack but did not reduce the percentage of deaths from heart disease, the occurrence of heart attacks or sudden heart stoppages in patients who had had to be resuscitated.
The TNT trial did reduce cardiovascular mortality, but there were no differences in overall mortality between the treatment and control groups and even an increase (my italics) in the number of deaths from noncardiovascular causes in the treatment group. If there were fewer deaths from CVD but no difference in overall mortality, that means statins increased the risk of death from other causes in the treatment group. “Disease substitution” is not an acceptable outcome. Total mortality is the most important endpoint and it wasn’t changed by statins in this study.
Nor do I know why you cited the BIP trial as positive. The difference between drug and placebo on the primary endpoint (fatal MI, nonfatal MI or sudden death) was not significant.
So of all the trials you directed me to, only two demonstrated any reduction in total mortality. Even then, the reduction is only valid for less than 5% of the population, and would require treating 25 patients for five years to prevent a single death. And we haven’t even started talking about the side effects that occur in up to 30% of patients that take statins, including potentially irreversible muscle damage, global transient amnesia, depression, impotence and more.
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touche’.
well, im going to take a much closer look at the literature and either send you my thanks or post a rebuttal. -
This post is organized as follows
1) A critique about two of the studies cited to support the claim that “…there is no justification for continuing to prescribe statins for any population subgroup, including secondary prevention men….” Found in the summary of statin research pdf
2) A comment on the TNT and 4s trials
3) A discussion on adverse events and statins
A I)The information on the ENHANCE trial in the pdf is inaccurate. This study compares 2 groups of people with familial hypercholesterolemia, one group treated with 80 mg simvastatin and placebo, the other with 80 mg simvastatin and 10 mg ezetimibe. Based on this design it is clear that any differences in outcomes can only be attributed to the ezetimibe.
And what about the results? According to the pdf link on this website the results were “Doubled the risk of heart disease. The lower the cholesterol, the higher the risk….” This is also incorrect, the primary outcome was mean change in carotid-artery intima-media thickness which is believed to be a reasonable surrogate for progression of atherosclerosis. Indeed, in the control group the change was 0.0058 +/- 0.0037 mm. the treatment group was 0.0111+/- 0.0038 mm. a difference of approximately double the thickness, however given the relatively large error in these measurements one must wonder how significant these results are. In fact, the authors of the article themselves mention on at least two separate occasions that these are statistically insignificant differences. Of course, even if these results were significant it wouldn’t reflect the effects of a statin anyways.
Interestingly enough, the authors go on to site 9 studies which apparently show that statins are effective in attenuating the primary outcome of this study in adult and pediatric patients with familial hypercholesterolemia. They can be found in the references of this article, numbers 11,79,26-32. I have not yet read these articles but I do plan to.
II)The information on the SEAS trial is misleading. The info provided includes the statement that there was “No significant difference in primary endpoints (aortic stenosis progression, CHD complications) 50% increase in new cases of cancer. ….” This is inaccurate.
First, the studies exclusion criteria excluded any patient with comorbid DM, coronary artery disease, cerebrovascular disease, or other conditions requiring lipid-lowering therapy. Thus this study’s results will not apply to the vast majority of statin users.
Ignoring that, a cardiovascular benefit was noted “Fewer patients had ischemic cardiovascular events in the simvastatin-exetimibe group… mainly because of the smaller number of patients who underwent coronary-artery bypasss grafting…” Interestingly, this benefit was seen in a patient population who had no indication for lipid lowering therapy.
Finally, the statement “…50% increase in new cases of cancer….” Is misleading as, while this may be true, this is almost certainly a coincidence. “Long-term statin therapy has not been associated with an increased risk of cancer. Analysis of data from 14 statin trials involving approximately 90,000 patients showed no evidence of an increased incidence of or death from cancer.41”….
In short:
1) Neither of these studies are reported accurately in the pdf file titled “summary of statin studies”
2) Neither of these studies support the statements present at the bottom of said pdf file.
3) I haven’t looked at the other studies yet, but I imagine that similar problems exsist with regard to the accuracy of info present on the pdf.
B I) 4S trial – 3.5 % or 4% improvement in 5 year mortality is significant. What is the 20 or 30 year mortality reduction? Is it additive? Synergistic? or some other association? What is the population effect on 10,000 individuals?
I believe the 4s trial also showed decreased progression of angina and incidence of new onset angina. These quality of life measures are significant
With regards to adverse events, while it is true a large number of people experience these adverse events, many things must be considered. How symptomatic? How reversible? Will progression continue if the drug is stopped?
For example, in the SEAS trial there was an increase number of significantly elevated liver enzymes in the treatment group, however “There were no differences in clinical, organ-related adverse events…” of any sort (except for the cancers which have been previously discussed.)
II) Finally. The TNT trial demonstrates a dose effect relationship. One group is given low dose, the other high dose statin. This resulted in an additional cardiovascular benefit on top of the low dose statin’s benefit. You do bring up a good point about overall mortality, however reading the paper in its entirety reveals the following:
1)the study was not powered to detect all cause mortality
2) the increased non-cardiovascular deaths in the high dose group were mostly cancer (mainly lung and gi) followed by respiratory diseases, infection, degenerative diseases, and metabolic abnormalities.
Again, statins have not been associated with these cancers, and you would have to pull a paper to convince me that statins cause any of these other diseases. So, I bring this study up to further show that statins improver mortality and morbidity in high risk populations and that there is a dose effect relationship.
C I)Adverse events – there are numerous studies detailing the frequency with which adverse events occur. Again, the heterogeneity in severity, reversibility, and overall clinical significance must be taken into account. Here is one such study (which I have skimmed but not fully read): Hippisley-Cox, Coupland. Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database BMJ 2010;340:c2197 (I think that’s the proper way to reference this article).
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George,
Thanks for your comment. Unfortunately, I won’t be able to respond in detail until after my State Board licensing exam in August. I’m studying like crazy and can only manage short responses to comments at this point.
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Thanks for all the lively and reassuring discussion of cholesterol measuring! Last year I was told I had high cholesterol but, using your formula on the Comments page, of triglycerides divided by HDL my measures work out at 1.12 triglycerides divided by 2.5 HDL. This puts the measure at under 1. So… is this ok? The British seem to be measure Triglycerides and HDL differently to the USA.
Thanks for the blog and the discussion – it has kept me balanced at times when the medical profession have sought to make me very alarmed. Really appreciate your comments and advice. -
I don’t think the ratio works with mmol/L, so I would convert your measurements into mg/dl. If we do this, your triglycerides would be 99 and your HDL would be 97. Then we divide 99 by 97 and get 1.02. You are still far below the 3.8 mark, which indicates an increased risk of heart disease. Nevertheless, you may want to consider brining your triglycerides down a bit (a low-carb, high saturated fat diet will do this).
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Well writtten and concise, I’ve referred to you from my blog as well. This post is greatly appreciated.
There is one minor editing issue I’d like to bring to your attention in your ‘Statin Trial Summary’ document. You probably intended to word the following sentence a tad differently:
“The hypothesis that statins reduce heart disease and death in secondary prevention men was tested with eight randomized clinical trials in 2008 and 2009.”
… perhaps something like:
“The hypothesis that statins reduce heart disease and death in secondary prevention _in_ men was tested with eight randomized clinical trials in 2008 and 2009.”
… or …
“Eight randominzed clinical trials tested the hypothesis that satins reduce heart disease and death when used for secondary prevention in the years 2008 and 2009.”
I follow your blog faithfully and think you’ve got great information. Please keep it coming and best of luck on your accupuncture boards.
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Thanks for catching that, Keith. And thanks for your feedback and encouragement!
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Pingback from Octagon Community Health − More on Statins on July 5, 2010 at 11:43 am
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Hey Chris,
I’m a physician, and am troubled by the influence that the pharmaceutical industry currently has in the field of medicine. I don’t have drug reps in my office. I’m not a huge fan of statins. So I read your post and watched your video with great interest. And then I saw the list of studies from 2008-2009 and looked them up in pubmed, and like george can’t find much there to support your case. As he points out, the very first one is a simvastatin vs. simva plus ezetimibe study. As I’m sure you know, this has nothing to say about the effectiveness of statin monotherapy, which is the topic of your post. And then the other studies are about examining the effects of statins on aortic stenosis, heart failure, etc., which also don’t relate to the primary issue as to whether statins prevent atherosclerotic disease and thus MI and stroke, which is their primary indication, and why they’re typically prescribed.
And as George pointed out, there are other well designed studies that do show benefits. And there’s an entire literature on statins for stroke prevention in patients with stroke and TIA that you’ve ignored – enough so that the Cochrane collaboration (who are notoriously stingy about approving anything, and only consider well designed RCTs) recommend statins for secondary stroke prevention.
I say all this not to argue that you’re wrong. (As I said, I’m not a big fan of statins. The available evidence to me indicates there’s a marginal benefit when it comes to stroke and MI prevention, but it’s certainly not clear if they’re worth the cost/risks). I say this rather to caution you against doing exactly what you’ve criticized big pharma for doing, which is cherry picking data to support your conclusions. In the end, you won’t end up changing anyone’s minds if it appears that this is what you’re doing. In fact, it will only make people further entrenched in their positions.
I think you’re doing a great thing with your blog, and think what you have to say in it is critically important. And I don’t want it to end up falling on deaf ears… So be rigorous! -
Hi Josh,
A few comments:
The purpose of the presentation was, among other things, to report on the statin studies performed in the last few years. As I’m sure you know, after the Merck/Vioxx scandal in 2005 new research regulations were put into effect that raised the bar for clinical trials. Researchers now have to comply with a more rigorous set of legal, ethical and procedural standards (described here). It is curious that all of the statin trials published since then have been negative. The only exception is JUPITER, but as I pointed out in the presentation it has serious methodological flaws that invalidate its results. Some researchers have suggested statin trials performed prior to the implementation of these new standards be reevaluated.
The trials I included were chosen based on when they were performed, not on their endpoint. That said, several of the studies I reported on did include MI (both fatal and non-fatal) as a primary or secondary endpoint. GISSI-HF measured total mortality (the most important endpoint for most people) and admissions to hospital for CVD events. In CORONA, the primary composite outcome was cardiac death, nonfatal infarction and nonfatal stroke. JUPITER included nonfatal and total MI and total stroke. In AURORA the combined primary end point was death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke. So I’m unclear on why you and George are having trouble seeing why these studies support my case. All of them except for SEAS and ENHANCE had hard clinical endpoints like MI and stroke.
I don’t deny that some studies show statins reduce nonfatal MI and stroke. In many of those studies, however, there was an increase in deaths from other causes so that total mortality either remained constant or even increased. Or they didn’t report on total mortality at all, which is suspicious and supports my earlier point about the importance of the more rigorous standards for data reporting introduced after the Vioxx scandal. And we haven’t even started talking about the risk vs. benefit analysis of statins for reducing these nonfatal events, and the fact that only secondary prevention middle-aged men have been shown to benefit (not women, not primary prevention men of any age, and not elderly over 65).
Since we now know that LDL isn’t a significant risk factor for CHD, the very premise of statin prescription is thrown into question. The trials summarized above clearly show that “lower isn’t better”, as many of them achieved dramatic reduction of LDL with no significant change in clinical endpoints. Statin supports have evolved a new theory of their mechanism of action in response to this evidence – the so-called pleiotropic effect. But the CORONA trial failed to show a clinical benefit from reducing CRP levels.
When all of this is taken together, I think it’s very hard to make a case for using statins in any population.
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By the way, Josh, you might enjoy reading the following articles/papers for more on this:
A balanced critique of the Jupiter study.
The original paper by De Lorgeril
A rebuttal to Dr. Ridker’s critique of De Lorgeril’s paper.
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@George
There’s 2 people that I know that, for one reason or another, stopped taking their cholesterol lowering statins drugs, and found their cholesterol had skyrocketed on their next blood test!
I have no idea whether it it’s there LDL or HDL that changed dramatically, but the point is, it seems statins do have an effect!
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There’s absolutely no controversy about whether statins lower cholesterol. They do – quite significantly. The question is whether they reduce heart disease, and even more importantly, whether they reduce the risk of death. That’s what my presentation and articles are about.
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Chris,
I don’t think that I have seen you mention it, but have you seen anything indicating that statins or other commonly prescribed drugs could transform LDL to small particle in the process of lowering LDL. Some discussion about that on http://heartscanblog.blogspot.com/ .
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Clarification: It’s not Dr Davis who is speculating about this effect of statins. The discussion is in the comments.
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Christian,
The literature is mixed on this, and the effect may even depend on which statin is taken:
http://www.nmcd-journal.com/article/S0939-4753(04)00009-2/abstract
http://www.ncbi.nlm.nih.gov/pubmed/18492534
http://www.ncbi.nlm.nih.gov/pubmed/18957124
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