Statins – The Cochrane Review

A recent Cochrane review of the use of cholesterol-lowering statin drugs in primary prevention has sparked some controversy.  The controversy is not so much over what the data says, but in what conclusions to draw from the data.

Statin drugs have been surrounded by controversy for a number of reasons. On the one hand they demonstrably lower cholesterol, and the evidence has shown that they also reduce the incidence of heart attacks and strokes. The data on whether or not they reduce mortality has been less clear, although this latest data actually supports that claim. However, statins have also been blockbuster drugs for pharmaceutical companies and this has spawned concerns (some might say paranoia) that drug companies are pushing billions of dollars worth of marginally effective drugs onto the public.

So are statins a savior or a scam? Life does not always provide nice clean answers to such simple dichotomies. The evidence clearly shows that statins work and are safe. However, pharmaceutical companies do like to present their data in the best light possible, and they need to be watched closely for this. The recent review does call them on some practices that might tend to exaggerate the utility of statins. Finally, the real question comes down to – where should we draw the line in terms of cost-benefit of a preventive measure like statins.

Let’s look as this recent review of the data to see what it actually shows.

First, for context, this Cochrane review looked specifically at statins for primary prevention – prevention of vascular events (mainly heart attacks, strokes, and overall mortality) in those who are at low risk for heart disease and who have not already had any vascular event. The evidence for statins for secondary prevention, after a heart attack, is more robust – decreasing risk of a second heart attack by about one-third. This makes sense, and is generally what we see. The higher the risk of disease the greater the potential benefit for any preventive measure, and the easier it is to measure this benefit in clinical trials.

Further, as the risk of the disease becomes smaller, the risk-benefit ratio and cost-benefit ratio of preventive measures goes down. At some point the side effects from the treatment become greater than the risk of the disease being prevented. Generally clinical trials divide risk into two broad categories – primary prevention and secondary prevention. However, in reality there is a spectrum of risk. A person without a history of a vascular event may still be at high risk if they have a lot of risk factors – hypertension, age, high cholesterol, diabetes, and smoking. And of course, since statins are cholesterol lowering agents, high cholesterol at baseline is a reasonable marker for the potential of benefit from statins.

Statins also have to be compared to other measures – like diet and exercise – for relative effectiveness and cost-effectiveness. No one doubts that it would be best if every patient had a healthy diet and weight and exercised regularly. Some argue that statins should be reserved for those who fail these lifestyle interventions, or who have genetically high cholesterol refractory to diet and exercise. The reality is that it is very difficult to get individual patients to change their behavior. In fact, a recent Cochrane review concluded:

Interventions using counselling and education aimed at behaviour change do not reduce total or CHD mortality or clinical events in general populations but may be effective in reducing mortality in high-risk hypertensive and diabetic populations. Risk factor declines were modest but owing to marked unexplained heterogeneity between trials, the pooled estimates are of dubious validity. Evidence suggests that health promotion interventions have limited use in general populations.

This is not very encouraging. Clearly we need to work on societal interventions and improving patient interventions to achieve a healthier lifestyle as a society. But also it is clear that lifestyle intervention is not a quick or easy fix, and so there will continue to be a role for medical intervention in vascular prevention.

Statins for Primary Prevention

When the Cochrane reviewers looked at the evidence for primary prevention they found that many trials included patients at high risk, or did not measure LDL levels. Essentially they felt that the data was contaminated in such a way as to exaggerate the benefit for primary prevention. Their review sought to correct those biases. They reviewed the data from 14 trials involving 34 272 patients. What they found was that total mortality had a relative risk reduction of 17%, risk of heart attacks was reduced by 28%, and strokes by 22%. In low risk patients the number needed to treat in order to prevent one death per year was 1000. The review also did not show any additional adverse events in those treated vs placebo groups.

The authors do not challenge the legitimacy of these results. The data is fairly robust – there is a reduction in risk of death and vascular events from statins in primary prevention. Study author, Dr. Shah Ebrahim, is quoted by Heartwire as saying:

“If you look at the hard end points of all deaths and coronary deaths, the effects are consistent with both benefit and with the play of chance. But importantly, the absolute benefits are really rather small—1000 people have to be treated for one year to prevent one death. It is probably a real effect, but it means a lot of people have to be treated to gain this small benefit. As we don’t know the harms, it seems wrong-minded to me to treat everyone with a statin. In these circumstances, lifestyle changes and stopping smoking would be far preferable.”

And that is where the controversy comes in. Other researchers think the authors are making conclusions that go beyond their own evidence. Heartwire also quoted Dr. Colin Baigent, a clinical researcher from Oxford, as saying:

“I object to the conclusions they have drawn from their review. They say there is not good evidence of benefit, but their own data show significant reductions in deaths and cardiac events. They didn’t show any increase in adverse events in their review, but they then say the benefit is not worth the risk. That doesn’t make sense.”

This does make for an interesting science-based medicine conversation. In this case the two sides largely agree on the data, but differ in terms of how to apply that data to the practice of medicine. This, I feel, can be a very constructive controversy. This is exactly the kind of question that should be agonized over by experts. While I think the Cochrane reviewers are displaying a negative bias against statins, they do provide balance to the pro-statin bias of pharmaceutical companies who sell statins. In the end, the data is out there and practitioners and patients will be better informed in making decisions about statin use. I am concerned about media reporting of this issue. It is easy to oversimplify the take-home message as “statins do not work” and I have already read commentaries quoting this study to support that position.

My read of this evidence is that there is solid evidence that statins have a real benefit for primary prevention. This benefit is small, which is exactly what I would predict for a preventive measure in a low-risk population. The data also show that statins are safe. The major risk is for the development of an inflammatory muscle disease, but that is very rare. For interventions that prevent death – that lower mortality – I think even small benefits are worthwhile. Further, having a heart attack or stroke, even if it is not a fatal event, has a very negative effect on quality of life. Taken together, one person per year out of several hundred taking statins for primary prevention will avoid a heart attack, stroke, or death. From a purely medical point of view, that sound pretty good to me.

What seems reasonable is to use statins for primary prevention in those who have some risk factors for vascular disease, in patients with genetically high cholesterol, and in those with high cholesterol or significant risk factors in whom lifestyle counseling has not yielded adequate results. Try diet and exercise first – and always in conjunction with medication, but statins are a reasonable choice in selected patients, even for primary prevention. We could use more studies to better delineate where to draw that line, but that will be difficult as any difference in outcome is likely to be slight and therefore massive trials will be needed to get statistically significant results.

Cost effectiveness is a tougher issue, because we then have to arbitrarily decide what a human life is worth in terms of medical expense. This issue has become more acute as health-care costs rise and everyone is looking for ways to cut back. What I have not seen is a calculation of the cost of statins for primary prevention vs the cost savings from reduced vascular events. Having a stroke or heart attack is expensive, and pays for a lot of prevention. The question is – exactly where is the line crossed in terms of the vascular risks of the population being treated.

The good news is that many statins are now becoming available as generics, with a marked reduction in cost. There is already a Spanish analysis showing that the availability of generics is making statin treatment more cost effective.


This recent Cochrane review of statin use for primary prevention supports the conclusion that statins are safe and effective in reducing vascular events and overall mortality even in primary prevention. The benefits are statistically small, which is expected for a preventive measure in a low risk population. It is still unclear where to draw the line in terms of which patients should receive statins, but these data will help practitioners and patients make individualized decisions about cholesterol management and vascular prophylaxis.

Because this is ultimately a judgment call, the results of this study can be spun to a variety of conclusions. The study authors chose to present an overall negative conclusion – that the effect size is too small to be worth it. While other experts, looking at the same data, have come to the opposite conclusion – that statins are worth it. It is important to emphasize that the debate is not about whether or not statins have a real effect – they do, but about the cost-benefit of statins as an intervention for primary prevention.

One could also argue that Cochrane reviewers, given that their purpose is to provide objective and thorough reviews of existing evidence for specific clinical questions, should take a more neutral approach to interpreting the data. This is not the first Cochrane review discussed on SBM that can be criticized for taking a decidedly biased approach to the evidence in their conclusions. This should prompt some soul-searching, in my opinion, on the pat of the Cochrane collaboration.

Posted in: Epidemiology

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27 thoughts on “Statins – The Cochrane Review

  1. says:

    Why are statins and diet/exercise presented as alternatives here? No sane doctor would tell a statin patient not to eat well and exercise.

  2. WilliamLawrenceUtridge says:

    Oh thank Dog for this. I’ve been waiting for some more reasonable analsis ever since the papers and intertubes started bleating about statins being worthless.

  3. Interesting about the interpretation. My own (spontaneous, uninformed) judgement as I read this post was that 1 in 1,000 lives saved per year in people who are not at any particular risk is actually really, really good evidence that they work. I haven’t been paying attention to media bleating, so I’m surprised to hear that people are using this data to say they don’t work.

    (Or — not surprised. It’s exactly the reaction to antidepressants. Because they don’t work better than placebo in people who aren’t very depressed, they are perceived as not working at all. Whatever.)

    My beloved’s parents both died of heart disease. His father had his first stroke in his early fifties and had to retire; he died of a heart attack in his early seventies. (Not obese, didn’t smoke, had no driver’s license so rode a bike.) His mother had TIAs and strokes starting in her mid-seventies, was disabled and moved to a nursing home, and died at 81. (Not obese, smoked cigars.)

    I want my beloved back on statins! Stat! His doctor had him taking them for a while then discontinued them — as far as I can tell, for no special reason other than his cholesteral wasn’t terribly high. My beloved is not obese, moderately active, and smokes up to a cigar a day. He’s not going to quit the cigars (both pleasurable and mood-stabilizing, which is a really significant important qol issue for him).

    He obviously does have risk factors, but say he doesn’t and the 1 in 1,000 nnt applies to him. That means that over the next 25 years his risk of dying of stroke drops by 2.5%. That is, a 1 in 40 chance of saving his life and a greater-than-that chance of delaying disability. That’s not nothing.

  4. mikerattlesnake says:

    “Why are statins and diet/exercise presented as alternatives here? No sane doctor would tell a statin patient not to eat well and exercise.”

    Interesting that that was your takeaway from this piece. Not only did Dr. Novella not present that dichotomy, he explicitly stated the opposite. Did you just skim the article?

  5. Harriet Hall says:

    Excellent post! Thanks, Steven. The slanted media coverage has been disappointing because this Cochrane review really didn’t change anything. The general consensus was already that statins help but that the NNT is relatively high and the benefit is greater as the CV risk increases.

    Another pro-statin consideration is that it has an anti-inflammatory effect that may benefit non-cardiac diseases. A lot of the anti-statin arguments are biased and seem to come from the “drugs aren’t natural” agenda. The International Network of Cholesterol Skeptics has demonized statins, wildly exaggerating the risk of side effects.

  6. Chris says:

    Some argue that statins should be reserved for those who fail these lifestyle interventions, or who have genetically high cholesterol refractory to diet and exercise.

    I fall into that category. I worked very hard and got my HDL levels up and my LDL levels down. Then the next year, while still avoiding yummy things and regular exercise, my levels went back up. Obviously my liver thought I was deficient.

    I take my statins, and still try to eat right and exercise (about to go climb a tree with a saw, woo hoo! Pruning time!).

  7. ConspicuousCarl says:

    My first thought, when it was implied that the statin tests were too focused towards high-risk patients, was “duh!”. Obviously the goal of medicine is to medicate the people who need it, not the people who don’t. And judging by the drastic increase in efficacy in the predetermined “high risk” group, there seems to be a fairly reasonable, if not perfect, way of determining who is more likely to have a heart attack without medication.

    It is possible for a low-risk patient to see a drug ad and think the impressive results might apply to them, but that’s why we have doctors to say “your risk of a heart attack in the next 10 years is just about zero, so you don’t need to take a drug advertised as reducing risk by 50%”… IF that is even the right decision among low-risk users. 1 in 1000 is a low numeric rate of return, but the prevented condition is kind of a big deal.

    Instead of thinking of 1:999 as a ratio, think of that many actual people. I imagine my junior-year high school class, which had about 800 students. If a doctor came along that year and said, “everyone take these pills, or else one of you is going to die this year”, I don’t think we would have been too quickly swayed towards the Cochrane standard that maybe it isn’t worth doing.

    It is also kind of ironic that the Cochrane people first decided that the existing data made the drugs look too good due to a bias towards testing in the most effective situations, and then they try to make their case by doing just the opposite.

    I was about to ask, “What is the point of showing how ineffective a drug is if intentionally applied in the least-effective way possible?” Ironically, in this case, the point seems to be that, even with intentionally-poor distribution, statins still protect 1 in 1000 people from death. DEATH!

  8. marilynmann says:

    Nice post and I agree with the overall points you are making. I’d like to make a small clarification on the benefit of statins in secondary prevention.

    First, while many people equate “secondary prevention” with “people who have had a heart attack,” the medical profession generally uses the term to include anyone with known coronary heart disease (this includes people who haven’t yet had a heart attack), and also people who have a “coronary risk equivalent.” Coronary risk equivalents include diabetes mellitus, symptomatic carotid artery disease, peripheral arterial disease, abdominal aortic aneurysm, and (sometimes) very high risk asymptomatic people, such as people with a 10-year risk of CHD that exceeds 20 percent. This differing use of the terms “primary prevention” and “secondary prevention” creates a lot of confusion, unfortunately. Once you exclude all the people with coronary risk equivalents, you are talking about a population whose 10-year risk is on average pretty low. So, yes, the NNT is high, because the event rate is low. You can’t prevent something that wasn’t destined to happen in the first place, and statins don’t prevent 100% of the events, only 25-30% of them, or slightly higher for intensive treatment (e.g., 80 mg. atorvastatin).

    You are correct that the benefits of statins for reducing cardiovascular events and total mortality in secondary prevention are well-established. However, I do not know of evidence supporting a 2/3 reduction in cardiovascular events in secondary prevention, and the study you linked to showed an adjusted hazard ratio for cardiovascular recurrence of 0.82. (I note also that this study is a cohort (i.e., observational) study.)

    For example, the landmark Scandinavian Simvastatin Survival Study (known as 4S) was a randomized controlled trial in patients with CHD (angina or previous heart attack) in which simvastatin (20 or 40 mg.) In 4S, which was published in The Lancet in 1994, the relative risk for major coronary events was 0.66. More recent trials that compared intensive vs. standard statin therapy have shown an additional risk reduction from intensive statin therapy, but not enough to reach your 2/3 figure. So I am curious as to your source for that figure.

    My personal opinion is that, in primary prevention, each person needs to look at their 10-year risk of CHD (there are online risk calculators you can use), the amount by which this can be lowered with a statin (generally 25-30 percent), and ask themselves if that amount of risk reduction is worth the expense, bother, and risk of side effects from taking a statin. It’s a personal decision. And yes, generic statins are quite inexpensive these days. Lipitor (atorvastatin) is going generic soon, and in the U.S. several statins are available in generic form.

    (The above paragraph does not apply to people with familial hypercholesterolemia (genetic high cholesterol), who are treated based on lifetime risk of CHD, which is very high.)

    I agree with you that serious adverse events from statins are rare, but nuisance side effects such as muscle pain are pretty common.

  9. tuck says:

    I’m confused… I thought that the rap against widespread statin use was that they didn’t show an increase in all-cause mortality for the average patient.

    Also, shouldn’t the bias always be against any treatment with what can be serious side effects?

    “This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up. ”

  10. marilyn – the article I linked to showed a decrease in heart attacks from 12.7 to 4.1 per 100 patient years. That’s a 2/3 reduction. But you are correct – data from clinical trials shows about 1/3 reduction, so I changed the text to reflect this.

    tuck – there doesn’t have to be any “bias”, rather a risk vs benefit approach is most appropriate. There are rare side effects to almost any intervention. But that has to be compared to the potential for benefit.

    Regarding your reference – different meta-analyses have come to different conclusions. What is ironic is that this meta-analysis shows a reduction in all-cause mortality. Also, it is reasonable to consider reduction in heart attacks and strokes in addition to mortality. Strokes still really suck, even if you don’t die.

  11. MikeLuciano says:

    According to the data, 1 out of every 1000 low-risk patients will benefit from statins, correct?

    Out of 1000 low-risk patients, then, how many will experience serious side effects (eg – inflammatory muscle disease)?



  12. Robin says:

    What type of cholesterol lowering diet is supported by data?

    I had elevated cholesterol in my 20s was told it was genetic. Even though my weight was in the high normal range I was counseled to lose weight and change my diet but given little advice about how to go about it.

    I began to eat mostly plant based foods (thanks, Michael Pollen) and slowly lost 40 pounds. My cholesterol is lower but it hovers around 200, because my HDL is high and my triglycerides are low I am not considered at risk enough to be on a statin. But I still can’t get that damn LDL down further!

    A lot of the nutrition research is conflicting, and though it’s been touched upon here (Harriet Hall’s article about the Bill Clinton diet) and elsewhere, it’s confusing. While it’s seems to be unanimous that “no one doubts that it would be best if every patient had a healthy diet”, I’m still unsure about what is proven best to eat.

  13. Harriet Hall says:

    Robin says “I’m still unsure about what is proven best to eat.”

    That’s the problem: it hasn’t been proven what is best to eat. I personally think Michael Pollan’s guess is as good as anyone’s.

    Also, most patients with high cholesterol are not able to get their numbers down into an acceptable level with diet alone.

  14. windriven says:


    “My cholesterol is lower but it hovers around 200, because my HDL is high and my triglycerides are low I am not considered at risk enough to be on a statin.”

    I would suggest that you discuss this again with your physician. If s/he is intransigent without giving you a reasonable explanation why you shouldn’t be on a statin you might seek a second opinion.

    FWIW, my physician dragged me kicking and screaming into statins with a total cholesterol that bounced around between 180 and 200. I don’t like to medicate unless there is a good reason. After discussing this with a number of physician friends I relented and went on prilosec.

  15. nybgrus says:

    @windriven: Prilosec is a proton pump inhibitor – not a statin. Perhaps you mistyped?

  16. pedshosp says:

    Thank you ConspicuousCarl! Despite the fact that I hate anything that reminds me of middle school, I love your idea of imagining your middle school classmates and find it very useful. This issue of when the risk of disease is enough to warrant testing or treatment comes up all the time, and is actually a focus of my research.

    I think the beauty of your idea is 1) it helps people think of individuals and 2) it helps them understand how big (or not so big) 1,000 actually is.


  17. Robin says:

    @ windriven, my doctor looks at the breakdown of HDL, LDL, and triglycerides and other risk factors (such as diabetes) rather than just total cholestorol. He says because my HDL is very good, my relatively young age and lack of other risk factors, it’s OK for the total cholesterol to be borderline. He monitors my LDL and says that if it goes up he’ll recommend a statin. (I could probably have one now, I just don’t want one.) His advice seems to be congruent to the American Heart Association guidelines so I’m pretty comfortable with it.

    I too do not like to medicate unless there is a good reason; especially since my dad ended up with rhabdomylosis from a statin. Probably as I get older I won’t have much a choice, though.

    Glad you got your cholesterol down!

    PS isn’t prilosec for acid reflux? ;)

  18. Anthro says:

    I had an experience similar to Chris in that after I lost 45 lbs, which normalized my blood sugar (I had crossed into diabetes land), My bp, cholesterol and triglycerides all normalized as well. I went off all meds to my delight! Within a year, however (with no weight gain) they started to go up. I now take a minimal dose of the same meds I took much higher doses of before the weight loss, including a generic statin and all numbers are very good.

    I felt utterly defeated, but perhaps this is inevitable for some physiological reason?

    For what its worth, I counted calories, measured all food, weighed regularly, and ate mostly plants with the exception of (small servings) of salmon. I didn’t eat out for six months and infrequently thereafter. I already exercised moderately, so just carried on with my LONG walks. I have maintained this for five years, with some minor fluctuations due to a love of chocolate that I sometimes fail to control. My idea is that the best way to avoid (or control) diabetes (and heart disease) is to eat like a diabetic is TOLD to eat by the nice dietician they send you to when you get the fatal blood sugar reading. She can work it out for meat or vegetarian, or even a foodie, like me!

    These endless arguments about what food groups to emphasize seem fruitless and few people who buy the books and follow them seem to succeed. Calories are calories, and you only need so many of them. If you get them all from doughnuts, you’re going to need drugs. If you get them from normal unprocessed food, you won’t, or at least not as much. The bottom line is that you have to learn to EAT LESS, whatever it may be.

  19. tuck says:

    “Strokes still really suck, even if you don’t die.”

    Been there, done that.

    Still don’t find the alleged science behind this compelling. 1 in a 1000 is well within any margin of error.

  20. gippgig says:

    As the risk of the disease becomes smaller, wouldn’t the risk-benefit ratio and cost-benefit ratio go up rather than down?

  21. Scott says:

    1 in a 1000 is well within any margin of error.

    Not true. A 1/1000 effect can most certainly be picked up given a large enough sample size. If you want to claim that this analysis was not sufficiently sensitive to pick up a 1/1000 effect, you’ll need to back that up with statistics.

  22. mark says:

    @ Steven Novella

    ‘The authors do not challenge the legitimacy of these results. The data is fairly robust – there is a reduction in risk of death and vascular events from statins in primary prevention.’

    In the discussion of the paper, the authors do challenge the legitimacy of the results. They highlight the problems they encountered with the studies in this analysis which include selective reporting of outcomes, failure to report adverse events, premature stopping of trials which may have exaggerated effect size, especially as some of the trials which did this were industry sponsored.

    They also had a hard time working out whether trials really were primary prevention and if participants really were free of pre-existing CVD. They selected an arbitrary cut off of <10% of patients with pre-existing CVD as one of the inclusion criteria, but inclusion of two other trials with pre-existing CVD of 14% and 18% attenuated the mortality results substantially. Another meta-analyses of patients without CVD from 4 large statin trials showed no reduction in mortality.

    It seemed to me that they were saying there were good reasons for doubting the validity of their results, which is why they should be interpreted very cautiously and should not be interpreted neutrally, as you suggest they should have done.

  23. mark says:

    Another reason for doubting the risk estimate for mortality is that in unselected populations, cardiovascular disease is the cause of about 40% of deaths. Many of those deaths are not thought to be prevented by statin use (eg pulmonary embolism). If say, half of CVD deaths are due to diseases that might be prevented by statins such as myocardial infarction or stroke, that means about 20% of total deaths could be potentially influenced by statin use. If statins reduce events by about 1/3 then the impact on total mortality would be expected to be in the order of 6% (1/3 of 20%), and very likely <10%. The observed risk reduction was much higher (2-3% the expected value), suggesting the results should be viewed with caution and are not likely generalizable to the unselected population.

    To explain the observed risk reduction, statins would have had to prevent almost every death from MI/stroke in the trials, or they prevent deaths from other diseases, or the trial participants were at much higher risk of CVD death than un-selected populations raising the issues the Cochrane authors discussed which led them to question the validity of the results.

  24. BillyJoe says:

    Conspicuous Carl,

    “I imagine my junior-year high school class, which had about 800 students.”

    On the other hand, I just think of myself. :)

    Well, actually, I do: I imagine sitting down in front of a pile of 365 tablets; and a bag of 1000 marbles. The choice then is: consume the pile of tablets at the rate of one every day for one year OR reach into the bag and avoid pulling out the single black marble because that would mean I die this year.

    I think I could live with that small risk of dying. But I would find the regimentation of taking a pill every day really off-putting.
    (It seems that makes me unusual around here.)

    On the other hand, I’ve never had my cholesterol measured so I don’t even have to play the game.

  25. Ali771 says:

    Here is a question:

    My Dad has been on statins for eight years. He eats well, exercises, doesn’t smoke. But due to his age (60’s) he was put on statins by his GP for primary prevention. A few years ago he began having some muscle pain, then it turned into severe muscle pain and weakness. A year ago he was sent to the hospital because his kidneys were shutting down. But, well, the doctors really didn’t know why. He now has wasting of his leg muscles and severe pain. He was diagnosed with CIPD. He can barely walk but makes it to physical therapy once a week.

    His doctor put him right back on statins, and didn’t believe his symptoms were side-effects.


    He takes fish oil and he eats a healthful diet. Wouldn’t it be wise to end the statins just in case he is one of the rare recipients of these serious possible side effects? No one (not one of the doctors) want to go there. I just don’t understand why not? I am on board with clinically researched preventitive medicine. But it is clearly getting harder for him to stand, walk, day by day. Could his doctors be blinded to the serious possible side effects of this drug in the case of my Dad?

  26. Barry2 says:

    What about this recent finding: “Statins may raise stroke risk in some: study”, According to Dr. Brandon Westover of Massachusetts General Hospital and Harvard Medical School and colleagues, “Our analysis indicates that in settings of high recurrent intracerebral hemorrhage risk, avoiding statin therapy may be preferred.”

  27. Jay Wortman MD says:

    It is entirely possible that the small benefit statins deliver is due to their anti-inflammatory properties. In the JUPITER study, for example, subjects with normal LDL but elevated CRP benefitted from statins. When Reaven first described metabolic syndrome as a collection of risk factors for CVD there was no mention of LDL. This is because the dyslipidemia with the greatest risk was a low HDL and an elevated TAG. Now we understand that sdLDL is associated with higher CVD risk, much more so than LDL as a whole. The whole focus on LDL is due to the fact that there is a very lucrative drug industry targeting this one thing. A very low-carbohydrate diet has been shown to raise HDL, lower TAG and change the LDL from sdLDL to light fluffy LDL. A range of inflammatory markers also drop significantly on this diet (see Volek et al in Lipids). People should not slavishly be put on statins based on one lab value. If someone has elevated LDL but high HDL and low TAG and CRP, one can assume that the quality of the LDL will be on the healthy end of the particle size spectrum. It would be foolish to prescribe a statin in a case such as this. For others, the first line therapy should involve carb restriction as this is highly effective in shifting a Pattern B lipid profile to Pattern A.

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