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New Cholesterol Guidelines

On November 15, the American College of Cardiology and the American Heart Association released an updated guideline for the use of statins to prevent and treat atherosclerotic cardiovascular disease (ASCVD). The full report is available online. It has already generated a lot of controversy. The news media have characterized it as a “huge departure” from previous practice and have trumpeted that it will lead doctors to prescribe statins to millions more people. As usual, the truth is much more nuanced. There are some problems with the guidelines, but on the whole they represent an improved, more rational approach to prescribing statins.

Statins have always been a source of controversy: people seem to either love them or hate them, and discussions about them generate a lot of emotion. The International Network of Cholesterol Skeptics denies that cholesterol has anything to do with cardiovascular disease. An article on HuffPo calls statins “an unsafe, unnecessary product that will now be recommended to healthy people to make them sicker.” Mercola says they can actually make heart disease worse and cause premature aging, and no one should take them unless they have the genetic defect of familial hypercholesterolemia. A website collects patient self-reports of adverse effects; but like the vaccine reports on VAERS, these are only anecdotal reports of correlation, not evidence for causation.

At one time the evidence only supported using statins for secondary prevention and for men. We now have better evidence showing that they are effective for both primary and secondary prevention in patients of both sexes and all ages, and that they are more effective for those with higher risk factors.

What are the new guidelines?

Under the previous guidelines, doctors aimed to keep LDL cholesterol below 160 mg/dL for low-risk patients, below 130mg/dL for people at moderate risk (10 year risk of cardiovascular event between 10 and 20%) and to reduce it to 100mg/dL for those with a history of cardiovascular disease or diabetes, or with a 10-year risk of greater than 20%. For high-risk patients, doctors often aimed for less than 70mg/dL.

An expert panel evaluated all the available published evidence. They found that there was no good evidence to support the current target levels for LDL cholesterol, so they recommended an approach that disregards target levels and is based only on risk level and intensity of statin therapy. In essence, they switched from treating lab tests to treating patients. They identified 4 groups of individuals for which an extensive body of RCT evidence demonstrated a reduction in ASCVD events with a good margin of safety from moderate- or high-intensity statin therapy:

  1. Individuals with clinical ASCVD
  2. Individuals with primary elevations of LDL–C ≥190 mg/dL.
  3. Individuals 40 to 75 years of age with diabetes and LDL–C 70 to 189 mg/dL without clinical ASCVD
  4. Individuals without clinical ASCVD or diabetes who are 40 to 75 years of age with LDL–C 70 to 189 mg/dL and have an estimated 10-year ASCVD risk of 7.5% or higher.

The guidelines are the same for women as for men.

They found no evidence to support adjusting treatment to achieve specific target levels of LDL-C. They found no evidence that using non-statin therapies for prevention would provide acceptable risk reduction compared to their potential for adverse events.

They provided a risk calculator to identify those with a risk of 7.5% or higher for having a cardiovascular event in the next 10 years. It quantifies risk based on age, sex, race, cholesterol, blood pressure, diabetes, and smoking. They pointed out that the data are inadequate to quantify risk for some racial, sex, and age groups, for instance those over the age of 75. The guidelines are not intended to be a cookbook, one-size-fits-all approach. Clinicians are expected to rule out secondary causes of hyperlipidemia, to take other individual patient factors into consideration, and to discuss risks/benefits and patient preferences before starting therapy. They stress that lifestyle modification (adhering to a heart healthy diet, regular exercise habits, avoidance of tobacco products, and maintenance of a healthy weight) is critically important for everyone, both before and during treatment.

For both primary (patients with clinical ASCVD) and secondary prevention, they recommend high-intensity statin treatment below age 75, and moderate intensity statin treatment for those over age 75. Table 5 in the report defines high, moderate, and low intensity statin dosages. High intensity includes atorvastatin (Lipitor) 40-80 mg and rosuvastatin (Crestor) 20 mg daily; these have been shown to lower LDL-C by 50% or more.

They provide guidelines for monitoring patients on statins:

  • Regular assessment of adherence to medication and lifestyle
  • Re-testing lipid levels at intervals as long as 12 months
  • Other safety measures as clinically indicated

They no longer recommend routine monitoring of liver function tests unless there are symptoms suggesting liver toxicity.

They provide safety recommendations, listing patient characteristics that might increase the risk of side effects and advising how to manage patients who report symptoms that might be side effects of the drugs.

For patients not in the 4 groups, other factors may be considered to inform decision-making: primary LDL–C ≥160 mg/dL or other evidence of genetic hyperlipidemias, family history of premature ASCVD with onset <55 years of age in a first degree male relative or <65 years of age in a first degree female relative, high-sensitivity C-reactive protein >2 mg/L, CAC score ≥300 Agatston units or ≥75 percentile for age, sex, and ethnicity, ankle-brachial index <0.9, or elevated lifetime risk of ASCVD. Additional factors may be identified in the future.

Criticism of the new guidelines

  1. The risk calculator was based on old data and it overestimates risk.
  2. Out of 46 recommendations, 20 were based only on expert opinion.
  3. Too many people will be put on statins.
  4. The American Academy of Family Physicians is not willing to endorse the new guidelines.
  5. Conflict of interest: six out of the 15 authors reported having recent or current ties to manufacturers of statin drugs.

These objections can be answered:

  1. Those who say the risk calculator overestimates risk are relying on studies that underestimate risk because they used research subjects who were much healthier than the average American (the Nurses’ Health Study, the Women’s Health Initiative, and the Physicians’ Health study). And the risk calculator is only a starting point; clinicians are expected to take other factors into account, and a risk over 7.5% doesn’t automatically engender a prescription.
  2. The major recommendations were based on high-quality evidence from RCTs; the ones based on expert opinion were about minor details.
  3. The new guidelines may put more patients on statins, but it will put more appropriate patients on statins and will make sure that those who are not appropriate will not be given statins. There are a lot more people at risk today because of changes in the population: the population is older, and there is more obesity, hypertension, and metabolic syndrome.
  4. The AAFP is only exercising its usual rigorous scientific caution. It tries to make independent decisions based on its own assessment of the evidence rather than slavishly following the recommendations of other groups. It has said it will not endorse the new recommendations until it has had time to thoroughly review the hundreds of pages of supporting evidence as well as evidence from other sources.
  5. There is no evidence that those with ties to drug companies influenced the findings of the panel. The majority of the panel had no conflicts of interest, and the panel leaders said no one with industry connections could vote on the recommendations.

Even those who criticize the new guidelines say they support the majority of the recommendations.

How Safe Are Statins?

Mercola cites an article that says 17% of patients stopped taking them because of side effects. But that study concluded “most patients who are rechallenged can tolerate statins long-term. This suggests that many of the statin-related events may have other causes, are tolerable, or may be specific to individual statins rather than the entire drug class.” It’s easy to find horror stories on the Internet from patients who are convinced statins have harmed them, but they don’t necessarily mean that the drugs were at fault in those cases. The way to find out, of course, is to do controlled studies. The evidence is mixed. The JUPITER study, with 17,802 subjects, reported a greater number of serious side effects in the placebo group than in the statin group (!), as well as fewer deaths from cancer; but only one difference was statistically significant: an increase in newly diagnosed diabetes in the statin group. The most common side effect is muscle pain, which is often mild and manageable. The most serious reported side effect is rhabdomyolysis, but it is rare: in the JUPITER trial there was only one nonfatal case reported in a 90-year-old patient after the study, and he also had febrile influenza, pneumonia, and trauma-induced myopathy. Increases in liver enzymes, digestive problems, rashes, and neurological side effects have also been reported, often in patients who are susceptible to those problems for other reasons. The neurological effects are memory loss and confusion, which can be reversed by stopping the medication; but on the other hand there is evidence that statins may actually improve brain function in patients with dementia or Alzheimer’s disease. There is a slight risk of increased blood glucose levels that prompted the FDA to include a warning on package labels. The risk of side effects is greater for women, those on multiple cholesterol-lowering meds, with a smaller body frame, aged 65 or older, diabetics, and people who overuse of alcohol.

All drugs with effects have side effects, and most cardiologists consider statins one of the best drugs we have ever had and consider them remarkably safe compared to most other drugs. The new guidelines include a section that objectively evaluates the evidence for risks. Those who object to Big Pharma and prefer natural alternatives may be reassured to learn that the first statin (lovastatin) was isolated from a fungus and can still be obtained from red yeast rice, although products sold in the US no longer contain the active ingredient since the FDA mandated its removal.

Conclusion

It is the overall management of risk factors, regardless of blood cholesterol levels attained, that is important for heart disease and associated mortality. The new guidelines are based on the best evidence we have today from RCTs; they simplify treatment by basing it on risk rather than chasing target levels, and they require fewer blood tests for monitoring. They are meant to be taken as recommendations, not as inflexible requirements; and they will undoubtedly evolve as more evidence comes in. Cardiologist Harlan Krumholz summarized the changes nicely: “The new message is don’t chase targets, know your risk, and — if you need drug therapy — use statins.”

Posted in: Pharmaceuticals

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352 thoughts on “New Cholesterol Guidelines

  1. Greg says:

    I have read that a better assessment for risk of CHD is measuring the ratio of total circulating triglycerides to HDL along with testing for levels of C-reactive proteins. A ratio of greater than 3:1 along with high levels of C-reactive protein indicates an at-risk individual. What are your thoughts on this?

    And my understanding of the role of cholesterol in ASCVD is that it accumulates / deposits, thereby narrowing the arteries, where there is damage to the arteries caused by inflammation. Is this correct? If so, it would seem the role of statins would be secondary to removing the underlying cause of inflammation and one might argue that statins may not be needed at all, if the inflammation was treated and ultimately removed.

    1. stanmrak says:

      You got that right, Greg. Cholesterol is not the culprit, but making it the boogey man sells a lot of statins.

    2. Harriet Hall says:

      The panel looked at triglycerides, ratios, and CRP and concluded that the evidence did not support using them for primary risk assessment, although they can be helpful as secondary aids to making decisions in cases where the calculated risk is borderline and the need for statins is not clear-cut.

      Inflammation is certainly implicated in atherosclerosis, but the degree of reduction of cardiac risk is correlated with the degree of cholesterol lowering. It has been argued that lowered cholesterol levels are only a marker for another, anti-inflammatory effect of statins. At this point, it doesn’t really matter: statins work, even though we don’t fully understand how they work. And it would be great if we had some other effective way to prevent, treat, or remove inflammation: we don’t.

      1. oderb says:

        funny thing but we do have something that seems to reduce inflammation as well as statins – Vitamin C . How about urging that more research be done to confirm the role of this cheap, safe and remarkable substance?

        http://www.ncbi.nlm.nih.gov/pubmed/18952164

      2. Pharmacist permanently harmed by lipitor says:

        “but the degree of reduction of cardiac risk is correlated with the degree of cholesterol lowering” this is a false assumption. Maybe increased dose of a statin will correlate, but the ENHANCE study shatters that myth completely.

        1. Harriet Hall says:

          Not really. The ENHANCE study was limited to patients with familial hypercholesterolemia, was designed to compare statins with and without the addition of Ezetimibe, and it didn’t look at cardiovascular events; it only looked at carotid intima-media thickness. The IMPROVE-IT trial will look at cardiovascular events, but it will not be completed until some time next year. ENHANCE did not show a reduction in the one specific risk factor it looked at, but they pointed out that other studies had shown a reduction in CV events on statins without any change in carotid thickness measurements. Other studies showed a reduction in the risk of a CV event that correlated with the degree of cholesterol lowering.

        2. windriven says:

          “but the ENHANCE study shatters that myth completely.”

          ?

          Did you read the study in a second language?

          The study certainly suggested that the linkage is complex and not directly proportional but you need to belly up to the bar with some stout citations if you’re going to claim that it “shatters that myth completely.” Moreover, no single study either shatters nor establishes anything with complete certainty.

      3. JP Sand says:

        Dr. Hall,

        In your foregoing comment you indicated that “inflammation is certainly implicated in atherosclerosis” and you noted that some believe the chief benefit of statin drugs is due to their anti-inflammatory effect rather than their cholesterol-lowering properties. You concluded that: “it would be great if we had some other effective way to prevent, treat, or remove inflammation: [but] we don’t”.

        QUESTION: How thoroughly have you researched the medical literature to determine the extent to which other, non-statin, methods may mitigate the inflammatory processes that are implicated in the development of atherosclerosis? Do you mean to say that, in your studied opinion, science-based medicine has found NO evidence of any other effective anti-inflammatory protocols whatsoever? Respectfully, perhaps a clarification is in order.

        1. Harriet Hall says:

          Other treatments have been shown to decrease inflammatory markers or to decrease inflammation in other diseases like rheumatoid arthritis, but I don’t know of any non-statin anti-inflammatory treatment that is known to reduce cardiovascular events. Statins clearly improve cardiovascular outcomes; we’re not sure how much of that is due to anti-inflammatory effects.

          1. Dr Robert Peers says:

            Inflammation may be reduced by a strict low-fat diet, which lowers vascular risk by about 15% [Cochrane Collaboration]. Fatty diet may cause inflammation by lowering the polyunsaturate content of mitochondrial membranes, which causes hydrogen peroxide release. H2O2 is known to promote the formation of inflammatory prostaglandins, and also to induce the expression of potent inflammatory transcription factors [NFkB and AP-1]. R C Moraes has shown that fat feeding causes mice to activate inflammation genes. Adding grains, nuts and legumes may greatly enhance the benefit of a low -fat diet: these foods provide the remarkable seed sugar myo-inositol, which has anti-anxiety, anti-inflammatory and anti-platelet effects [may be as good as aspirin]. Indeed, it inhibits both NFkB and AP-1!!. The forgotten Lyon Diet Heart Study, in 1994, using a low-fat high-legume Mediterranean diet in at-risk patients, reduced vascular risk by a whopping 72%–TWO TO THREE TIMES BETTER THAN STATINS!!! The first study–albeit only observational–to record major long term cardiac protection with whole grain diet was Prof Jerry Morris, London, 1977: “the benefit of a diet high in cereals cannot be explained”. Note that depression is perhaps the biggest risk factor for cardiac events: the underlying anxiety disorder [caused by fatty MATERNAL diet] is hard to link to cardiac risk, but adding fatty diet creates both depression [such a diet inflames the already stressed brain] and significant vascular risk–perhaps by adding an inflamed artery lining, and inflamed unstable plaques, to the pre-existing anxiety-related raised level of fibrinogen and platelet activation]. Grain inositol also lowers triglycerides, raises HDL “good cholesterol”, and even activates a range of anti-ageing genes, which provide further antioxidant and anti-inflammatory effects. Finally, inositol drives the synthesis of plasmalogen lipids–which increase the size of pro-atherogenic small dense LDL cholesterol particles. Needless to say, none of those folks put on statins will enjoy any of these benefits. Indeed, the anti-growth action of statins [via reduced isoprenoid synthesis] may lead to eventual muscle wasting and fatal falls–compare the anti-ageing effect of inositol, which activates the master energy gene PGC1alpha, causing enhanced stamina!!!

    3. Bryan says:

      Statins do much more than lower cholesterol: look up “pleiotropic effects of statins” for more information. Also, note that LDL cholesterol is both directly and indirectly involved in inflammation of the vessel wall, but drugs that just lower LDL perform much worse than statins.

    4. Jenni says:

      Big pharma and gov’t continue to push these “studies” forward and make such headlines with them ON PURPOSE. No study EVER has definitively shown that cholesterol from FATS cause MIs or CVAs…. cholesterol and triglycerides are manufactured in the liver when we overeat SUGARS. Cut out all the funding for grain producers, stop encouraging people to eat up to 10 servings of carbs per day, and many of us in health care will be out of jobs…. SERIOUSLY! I have many patients eating this way; they are getting “cleaner” and healthier than they’ve been in years; most are reducing or eliminating meds….

      1. Andrey Pavlov says:

        No study EVER has definitively shown that cholesterol from FATS cause MIs or CVAs

        This is correct. Because cholesterol does not come from fats. Cholesterol is a heterocyclic binary ring structure whereas fats are chains of carbohydrates, typically alkanes or alkenes with some actually being alkynes as well. Triglycerides are these chains stuck together 3 at a time with a glycerol group.

        cholesterol and triglycerides are manufactured in the liver when we overeat SUGARS

        Actually they are produced at all times regardless of diet. Sugars alone, however, do not particularly cause an increase in the average level of cholesterol.

        I have many patients eating this way; they are getting “cleaner” and healthier than they’ve been in years; most are reducing or eliminating meds….

        Now, for my own sanity, please tell me you aren’t an actual MD but some sort of naturopath or homeopath or other sort of quack.

      2. weing says:

        @Jenni,

        I’m sure your local cardiologist will remain busy and wealthy thanks to you.

  2. epmd says:

    The big change seems to have come from the Cholesterol Treatment Trialists (CTT) study published in The Lancet last year. The issue with this study is the denominator – they looked at the effect on cardiovascular risk per unit LDL reduction. The risk of using this denominator is that there’s no way to calculate an NNT for statins – they potentially excluded those that are on a statin with minimal LDL reduction, but included those on a statin that may have lowered their LDL thru other means.

  3. windriven says:

    I downloaded the calculator and somewhat to my surprise I’m a good candidate for a statin with a 10 year ASCVD risk of 13.5%. Definitely a topic for discussion with my internist at my January visit.

    I played with some of the numbers in the calculator and systolic BP seems to have a great impact. But my BP varies widely throughout the day. I took it just now at 5:50am and it is 115. At the end of a stressful day I’ve measured it as high as 149(!). After a glass of wine in the evening it is generally in the low 120s.

    My point is that selection of values can be somewhat arbitrary and yet put one on either side of a given line.

    Calculator lives here:
    http://my.americanheart.org/professional/StatementsGuidelines/PreventionGuidelines/Prevention-Guidelines_UCM_457698_SubHomePage.jsp

    1. stanmrak says:

      This is not really a ‘calculator,’ it’s a ‘marketing tool.’ It’s primary purpose is to sell more drugs, not assess true risk. I know, I know – the numbers come from “the government”. ha ha. I’ve been in marketing all my life – this is one way that it works.

      1. windriven says:

        You know stan, most complex organisms develop different apertures for ingestion and excretion. Not so, you.

        Do you have anything substantial to offer or just your usual diarrhetic paroxysm of fantasy, ignorance and hate? This is, of course, a rhetorical question as we can all extrapolate the answer from your history in these pages.

        1. stanmrak says:

          Most people would be grateful if someone told them they’re being duped. This someone is a career marketing professional who knows how these things work. When they make up these numbers, potential sales are one of the primary factors they use. Thinking otherwise is just naive. Once they ran out of sick people to market these drugs to, they branch out to expand their market to include the healthy ones. It’s just good business.

          1. Harriet Hall says:

            There were no marketers on the panel, and the members who had ties to drug companies were not allowed to vote.

            1. Sawyer says:

              I don’t know how these panel assessments work behind the scenes, but I suspect some sort of argument could be made that those with conflicts of interest can still skew the perceptions of other members, even without a final vote. It doesn’t have to be blatant marketing or over the top pseudoscience, just a subtle push towards desired treatment changes. Not really sure how to prevent this though. You absolutely want some people on the panel that know the drugs forwards and backwards, and those people are always going to have some connections with industry.

              Of course any hope of a careful, respectful conversation about these issues is now lost thanks to Stanmrak’s tirade of gibberish. Thanks a bunch Stan!

              1. Self Skeptic says:

                Yes, I agree that it is a tricky issue. I think there’s a problem, in that the most conflicted experts are regarded as the most successful ones; extensive and lucrative industry connections seem to be admired, rather than shamed, in much of medical culture.

                These top-tier academics get pretty good salaries; not as much as a business-savvy doctor who does lots of procedures can make, but certainly a good living. I think it looks bad for medicine, that these academics see fit to supplement their adequate salaries with “consultancy” fees, and that their colleagues mostly don’t find this disturbing enough to temper their respect for such “thought leaders.” as they’re called in the drug business.

                Pharma grant support for their research is a more complex problem. It seems justified, in one perspective; who is supposed to pay to do studies on drugs? But some (many?) university departments seem willing to overlook quite a bit of questionable behavior (depending on what one regards as questionable, of course) to hire a successful fundraiser. This could be an interesting topic of discussion.

            2. stanmrak says:

              It’s been reported that anyone with conflicts did not actually vote on the final draft, so some news outlets reported that there were NO conflicts of interest involved in the making of the guidelines. However, members of this panel actually have ties to more than 50 different drug companies.

              Whether they voted on the final draft or not, they were still instrumental in creating the guidelines in the first place. There’s more than one way to push through your agenda while appearing independent.

              http://articles.mercola.com/sites/articles/archive/2013/11/27/statins-cholesterol-treatment-guidelines.aspx?e_cid=20131127Z1A_DNL_art_1&utm_source=dnl&utm_medium=email&utm_content=art1&utm_campaign=20131127Z1A&et_cid=DM34111&et_rid=350490514

              1. WilliamLawrenceUtridge says:

                Aw, look at you pretending Mercola is a real news source!

              2. Self Skeptic says:

                Yes, it’s always a mistake to cite Mercola. Dr. Hall cited him in her blog post, twice, to try to discredit critics of the new guidelines, by associating the criticism with a disreputable source. She could have cited respectible experts making those criticisms instead, but that would not have served the rhetorical function.

                This reminds me of the comment, that if the village idiot says the sky is blue, on a sunny day, we may have to agree with him.

              3. Harriet Hall says:

                “Dr. Hall cited him in her blog post, twice, to try to discredit critics of the new guidelines, by associating the criticism with a disreputable source. ”
                I mentioned Mercola only as one of several examples of the controversy in the media. Responsible experts do not make those criticisms because they do not resort to misrepresentation and cherry-picking.

          2. weing says:

            Most of the meds are now generic. You must be a shill for the cardiac surgeons and cardiologists. If more people end up with CAD because they don’t follow this advice, they stand to make a bundle and can put deposits on a second house in the Hamptons.

          3. windriven says:

            Most people would be grateful if someone demonstrated they were being duped. As hard as this may be for you to fathom, the word of stanmrak, the great and wise, isn’t quite enough.

            What really irritates me is that you spray vague assertions without ever laying out an argument. That ‘float like a butterfly, sting like a moth’ drivel might work elsewhere but it won’t buy you many disciples here.

            Strip away all of your nonsense and what you are really alleging is large scale, wide spread scientific fraud. That is an outrageous accusation and it demands pretty substantial proof. So where is it?
            Hint: your fevered imagination doesn’t quite clear the bar.

              1. Harriet Hall says:

                Citing Mercola on this blog automatically loses the argument. Find a reliable source.

      2. WilliamLawrenceUtridge says:

        Stan, it’s funny that you think knowledge of marketing can substitute for knowledge of science.

        Then again, you are in marketing.

    2. Harriet Hall says:

      There is evidence suggesting that variable blood pressure is a risk factor for stroke. Mine used to vary wildly: one time my systolic was measured at 170 in the clinic, and when I got home and re-checked it a few hours later, it was 96/48! On blood pressure medications, it is now staying consistently below 120/80.

      1. windriven says:

        My internist has been gently nudging me toward an ACE inhibitor but I’ve been reluctant. I was not aware of the link between labile pressure and stroke. Time for me to rethink this. Thanks.

    3. stanmrak says:

      Here’s one doctor’s experience with this calculator:

      At what age would a perfectly healthy man (with ‘optimal’ risk factors) have to take a statin for the rest of his life, according to this calculator?

      Using the ‘optimal’ figures for cholesterol and blood pressure on the risk calculator.

      THE PERFECTLY HEALTHY MAN
      Male
      Age 63
      Race: white
      Total cholesterol 170mg/dl
      HDL cholesterol 50md/dl
      Systolic blood pressure 110mmHg
      Non-smoker
      No treatment for high blood pressure
      Non diabetic

      CV risk over the next 10 years = 7.5%

      So, there you are. You can do absolutely everything ‘right’ be as healthy as healthy can be – according to the AHA and ACC. Yet, by the age of sixty three you need to take a statin – for the rest of your life.

      Is there any doubt that this is a marketing tool – not a helpful guide for the public?

      http://drmalcolmkendrick.org/2013/11/18/you-need-a-statin-now-what-was-the-question/

      1. Harriet Hall says:

        Malcolm Kendrick puts a spin on this because he is a cholesterol denier. Here’s a different spin: Age is one of the biggest risk factors for CVD. If you agree that everyone with a risk over 7.5% can reduce that risk by taking a statin, it doesn’t matter which factors cause the risk, even if it’s only age.

      2. weing says:

        If you take a thousand of those perfectly healthy men, 75 of them will have had an MI within 10 years. Do you feel lucky?

        1. oderb says:

          Why is there no discussion of the NNT’s?

          The most authoritative source for estimating NNT’s is thennt.com

          They estimate that 4 out of 100 people with heart disease will avoid an event by taking a statin for 5 years, and two out of 100 without heart disease. That’s a whole lot more helpful than simply saying one has a 7.5% risk.

          See http://www.thennt.com/nnt/statins-for-heart-disease-prevention-without-prior-heart-disease/

          1. Harriet Hall says:

            As I pointed out, those NNTs are reported by a single ER doctor. I’m skeptical that they are “the most authoritative” source.

            1. oderb says:

              Whether of not that site (which has contributions from a number of doctors) is the most authoritative or not, do you materially disagree with the stated NNT values? And don’t you believe that patients would be better served in most cases if are they informed of the NNT’s and NNH’s when a prescription – or indeed any intervention – is recommended, assuming of course that adequate data exists.

              1. weing says:

                @oderb,

                The referenced JACC paper with the guidelines discusses NNTs and NNHs also.

          2. weing says:

            “The most authoritative source for estimating NNT’s is thennt.com”

            Says who? When I checked warfarinfor afib, there was no stratification according to CHADS2 scores. No HAS-BLED score. I think it would be great to have a data-bank we could reference. At present, this ain’t it.

  4. Stuart says:

    One issue I’m struggling with is patients already on a statin at a (prior goal) LDL target, but who achieved that with a lower dose or lower potency statin than is being recommneded. The guidelines would suggest I take a patient who is “well controlled” on $3 a month pravastatin 40mg and now have to change them to, for example, $200 a month Crestor

    1. windriven says:

      @Stuart

      “The guidelines would suggest I take a patient who is “well controlled” on $3 a month pravastatin 40mg and now have to change them to, for example, $200 a month Crestor”

      I don’t get that at all. From what specifically do you infer this? These are general guidelines to be used to inform the physicians clinical judgment.

      1. Stuart says:

        The guidelines say a person with known vascular disease should be on a “High intensity statin” such as lipitor 40-80mg daily or Crestor 20-40 mg daily. Hence my difficulty with a patient who is “well controlled” but not on a “high intensity” regimen

  5. This is great information on cholesterol. I’m a person with high blood pressure myself, so I have to watch out what I eat – sodium and everything.

    Thanks for sharing.

    1. interested party says:

      Maybe you should start doing more reading of research papers. Salt is just not a big thing and never has been. Another myth perpetrated by bad “science”.

  6. stanmrak says:

    Just yesterday, David Gorski posted an article on the triumph of marketing over science. If you were to teach a course on that topic, the cholesterol theory of heart disease and the use of statin drugs to lower cholesterol would be the best example you will ever find — it’s a hoax that’s endured for over 40 years. Cholesterol “science” isn’t science at all – it’s marketing. The “science” was fraudulent from the start. The marketing was a magnificent success; most people still believe it today, hence our obsession with low-fat foods.

    1. windriven says:

      Again stan, do you have some evidence or is this just more of your predictable stream of consciousness stupidity?

      I wonder why neither you nor any of your co-delusionals ever take me up on my challenge: name the top ten medical conditions that your favorite brand of woo has conquered – or all the various woos put together. We’ll compare and contrast with my top ten that medical science has conquered.

      Are you up to the challenge? Or are your stones as puny as your intellect?

      1. stanmrak says:

        Woo has nothing to do with this. It’s about the triumph of marketing statin drugs over the science.

        1. MadisonMD says:

          Woo has nothing to do with this. It’s about the triumph of marketing statin drugs over the science.

          Sez the self-proclaimed lifetime and knowledgeable marketer of woo.

        2. WilliamLawrenceUtridge says:

          You keep saying “marketing over science” but you never say which science that the marketing is winning over. You never engage with the actual evidence, you just assert that it’s flawed and then stop. How is the evidence flawed? What studies specifically are invalid? What is your justification for a blanket condemnation of all studies? It’s not like Big Pharma is all-powerful; drugs are pulled from the market when studies reveal unappreciated flaws – and such studies do occur, rather regularly. Drugs make it all the way through phase III clinical trials and then are not licensed. The consistent failure of potential drugs to be licensed is one of the reasons why drug development is so expensive.

          So tell us, Stan, draw upon your incredible scientific knowledge to engage with the primary sources to show why they are flawed. Show us why you think statins are ineffective in the prevention of heart attacks, using pubmed and whatnot.

          Or is it that you can’t? Is it just that you’ll accept Joe Mercola’s assertions without evidence simply because he panders to a streak of paranoia found in credulous “natural is better” types? Why are you so willing to accept anything Mercola says uncritically on his website while completely distrusting real scientists and researchers in the notoriously argumentative peer-reviewed press?

      2. Flower says:

        Re Stan’s doubting of the whole cholesterol ‘science’, here’s an excerpt from a Sep 2009 WHO report entitled Fats and Fatty Acid Requirements for Adults.

        On page 191 it states 1 that ”the available evidence from cohort and randomised controlled trials is unsatisfactory and unreliable to make judgement about and substantiate the effects of dietary fat on risk of CHD- and that “the data on the association between total fat intake and saturated fat intake and body weight remain inconclusive”.

        http://www.karger.com/Journal/Issue/250361 / http://www.karger.com/Article/Pdf/229002

        1. WilliamLawrenceUtridge says:

          Oh look, selective quotation. Actual section:

          Differences between populations in the amount and type of fat consumed explain much of the variation in the incidence of cardiovascular diseases

          Now comes your quote…and the following sentences:

          The available evidence from cohort and randomised controlled trials is unsatisfactory and unreliable to make judgement about and substantiate the effects of dietary fat on risk of CHD. The null results of the observational studies of dietary lipids and CHD do not negate the importance of the underlying associations, but reflect the combined effects of limitations of dietary assessment methods, inadequate numbers of participants studied and the prolonged follow-up of individuals. Furthermore, the evidence from cohort studies of dietary intake of fats and CHD is mostly unreliable (with few exceptions) because most studies have ignored the effects of measurement errors and regression dilution bias. Few studies attempted to measure the within-person variability or reproducibility of the categorization of dietary fat when assessing these associations. Hence, the null results are very likely to result from regression dilution bias and confounding of 1 nutrient by another.

          And there’s more. which basically comes down to – your selective quotation of a single statement without any of the qualifications and analysis is deceptive. Unsurprisingly.

    2. WilliamLawrenceUtridge says:

      Stan, what’s the basis for the comment that it’s all marketing, not science? I can’t tell, since you never actually engage with the science, you just claim it’s all fraud and that somehow you’re smarter than all the doctors and researchers because you can see this. But since you never say anything specific, there’s no way to test your assertion.

      What, are we just supposed to trust you, despite your ongoing denialism of science, your continued claims that “IT’S ALL A CONSPIRACY” and your factual errors when you do say something that can be checked? Honestly, why do you believe you are right and the experts are wrong? Because you’re in marketing? How does marketing prepare you to understand the complicated science of cholesterol biochemistry and cardiology?

      Rhetorical, it doesn’t.

  7. Rob Cordes, DO says:

    So much media attention to the statin recommendations and very little to the life style recommendations. It seems more attention and action needs to be given to the reasons people need statins.
    BTW did the physicians recommending DASH and Mediterranean diet disclose any ties to the produce industry ?

    I was surprised that the risk calculator did not include trigylcerides or exercise capacity.

    Dr Hall aren’t those who have increase incidence of Type 2 DM on statins already at risk for Type 2 DM?

    1. Harriet Hall says:

      Yes, the media ignored the part of the guidelines that stressed lifestyle modifications for everyone. The evidence did not show that triglycerides or exercise capacity were useful for calculating risk, but they both can contribute to the clinical judgment that doctors should use when deciding whether to apply the guidelines to individual patients.
      And yes, higher risk factors for DM put patients at higher risk of developing DM on statins: http://www.medscape.com/viewarticle/781684

  8. goodnightirene says:

    As someone whose father had a heart attack at 40, whose grandmother died of heart attack at 50 and whose father’s six siblings have all had bypass or other major heart disease-related surgery, I have taken statins since age 50, following stent placement. All of my doctors have paid close attention to my family history, as well as to other factors (and differences from my family, mostly that they all smoked and I don’t).

    At the time of my stent I was 49, had not experienced menopause, did not smoke, was a vegetarian (though not a vegan), rode my bike about 15 miles a day and was also a runner and lifted weights regularly. I have had high bp since age 40 as well–controlled. I was not at my present (almost ideal) weight in spite of lifestyle–that didn’t occur until I came down with Type II and learned the value of not only eating well, but counting the wretched calories. Now I take only a minimal dose of bp meds and statin and have normal blood sugar.

    Damn those greedy doctors for “marketing” to me to take statins! Damn them for being present each week at the clinic when I weighed in to cheer me on, even though they had other patients to see. Damn them for making sure they kept up on valid studies and applied actual science to help keep me here to watch my six grandchildren becoming adults. Damn them for listening when I had muscle aches and getting me free samples so I could try other, more expensive statins, and writing me rx’s so I could get them from Canada. Damn them for trying to get my numbers in an acceptable range even though I did not lose the weight when I should have. Double-damn them for seeing me when I had no insurance or insurance that provided very meager reimbursement.
    Greedy bastards one and all!

    I am relieved to know that the new guidelines (not dictates) require less monitoring. For many years I had quarterly blood work, which was tiresome. It’s now only annual, thank goodness, as I’ve been very stable since the weight loss in spite of a lower level of exercise, and the inevitable ravages of aging.

    I only wish I could forward a copy of this post to the 90% or so of negative comments that appeared in the NY Times following the publication of an article on the same topic. I did my best to refute the onslaught (as did a few docs), but once again, the task is immense and the misinformation proliferates.

    1. windriven says:

      @irene

      “As someone whose father had a heart attack at 40, whose grandmother died of heart attack at 50 and whose father’s six siblings have all had bypass or other major heart disease-related surgery, I have taken statins since age 50, following stent placement. ”

      Genetics is a honey badger too. Sucks. Great that you’ve managed it so adeptly.

    2. stanmrak says:

      Doctors are only the pawns. Many of them don’t realize they’re being deviously “marketed to” or they don’t think they are susceptible to marketing tricks. If they want to see ‘science,’ the rep will supply them with a stack of research papers as tall as they want, all positive. More female college cheerleaders become sales reps for the drug industry than any other demographic group. i’m not making this up. That tells you something, doesn’t it?

      1. davdoodles says:

        “More female college cheerleaders become sales reps for the drug industry than any other demographic group. i’m not making this up. That tells you something, doesn’t it?”

        That drug companies like to hire fit, attractive, perky people to sell their products?

        How positively Machiavellian!
        .

        1. windriven says:

          I guess stan would allow only beer-bellied guys wearing wife-beaters be pharmaceutical salespeople. And no research papers. OK, research papers, but only negative ones.

          Somewhere ol’ stan claimed to be in marketing. But I’m think he isn’t or if he is he isn’t particularly good at it. He doesn’t seem to understand it all that well.

          First, sales and marketing are different animals. Drug reps are salespeople. They need to be well-groomed, well-spoken and able to endure lots of rejection. They make lots of calls, don’t see nearly as many prescribers as they call, and get many fewer still positive affirmations.

          Marketing tries to “shape the battlefield” to use one of the inevitable military analogies, and provides the sales force with a features and benefits analysis, competitive info, studies, brochures, and all the rest.

          Do marketing people and sales reps try to push their products? Uh, yeah. Do they occasionally deform the truth to achieve their goals. Uh, yeah. Are the physicians they try to influence guileless rubes ready to change their practice at the sight of a pretty leg? I don’t think so.

          1. Pharmacist permanently harmed by lipitor says:

            But add bagels and donuts and free samples to those killer smiles and those numbers start to move.

            1. windriven says:

              Oh, you’re right, pharmacist! Of course a cardiologist earning upwards of a quarter million dollars a year will change her practice for a bagel with a schmear. I can’t believe I didn’t think of that myself.

      2. CHotel says:

        “More female college cheerleaders become sales reps for the drug industry than any other demographic group. i’m not making this up.”

        Speaking as a Pharmacist, (a) Citation needed, and (b) I’ve maybe seen one drug rep ever that I might think was a cheerleader in her past? Maybe they don’t send the model employees into the rural circuit.

      3. WilliamLawrenceUtridge says:

        It tells me that you don’t understand the concept of “meta-analysis” and the ongoing reactions of the research and medical community to the pernicious influence of drug companies. Up to date. Consensus statements.

        You give to much agency to drug companies, and not enough to doctors and the medical community at large, which is working to oppose the efforts of drug companies. You ignore the large body of research and guidelines that are building to address these issues.

        And above all, you pretend that because there are problems with the research and marketing of drugs, that invalidates the entire enterprise and all research ever conducted. You substitute for science your own opinions, uninformed, unscientific and based on dogma rather than evidence. Why is that better? Why is your gut instinct and background in marketing adequate to proclaim all science to be pointless and flawed?

  9. Dave says:

    The british medical journal had a recent article on cholesterol and saturated fat which sparked a lively and intelligent discussion. Those interested can access this by getting onto http://www.bmj.com and looking for the “most read” box. Much more enlightening than Stanmrak’s diatribes. I believe he is a marketing guy, as he says, because it colors his entire worldview – everything is to sell something. Perhaps Stanmrak can explain why atromid never became a popular drug. It was studied as a cholesterol lowering agent, which it does admirably, and prevents some cardiac events in association with this. Sounds like a great setup to market a drug. (The answer is that the WHO study published in 1984 showed an increase in all-cause mortality with this agent. Note that the current recommendations say nothing about ezetemibe. Why is that, Stan, if this is all a scam to sell drugs?).
    I know many cardiologists who feel that statins work by methods other than by lowering cholesterol – plaque stabilization, endothelial function modification etc. so maybe their effectiveness is not all tied to the cholesterol effect, as Dr Hall alluded to. I don’t know a single cardiologist who does not take a statin, though maybe their worldview is also colored by what they do.

    Great post, goodnightirene. Thanks for relating it.

    1. stanmrak says:

      Everyone here is selling something, even if it’s just an opinion. You don’t have to be a marketing expert to realize this.

      1. Harriet Hall says:

        And you are selling something. We are selling science and reason; I’m not sure what you’re selling.

      2. mouethatroared says:

        In my world, selling something means an exchange of money takes place. No one is paying me for my opinion (although, if you’d like to, let me know and I’ll set it up in pay pal. :)) I suppose one could say that people give their opinion in exchange for intangible rewards such as connection to other people or the enjoyment that takes place in problem solving. But, that leave us with suggesting that the monkey who is grooming his family member is “selling something” and the person who takes a bit of their lunch hour to walk dogs at the animal shelter is “selling something” and a person who builds and flys model airplanes is “selling something”. That undermines the meaning of “selling” and leave us with an exceptionally cynical and one dimensional view of life.

        1. windriven says:

          mouse, stan means selling in a broader sense and this is perhaps the only thing that stan and I agree on. Everyone, in a broad sense, engages in ‘selling’ all the time.

          “Hey mouse, let’s go to see the Barber of Seville tonight. Boris Hvorostovsky*is singing Figaro…” is, in the sense stan means, an effort to sell you on accompanying me to the opera.

          *To the best of my knowledge Hvorostovsky has never sung Barber, only the Largo. But we can hope.

          1. mousethatroared says:

            Hey windriven – I missed your response and just came across it now. I did get that Stan was representing that view point. I’m just not fond of relying on the use of vague language to support a bias and cynical viewpoint.

            I know I am not one to talk, since I often have to substitute the not quite right word because the right word is playing hide and seek in my brain, but clarity of language leads to clarity of thought and all that…

            1. windriven says:

              Understood and agreed. And yours is not the only brain that plays odd tricks. In my response I mentioned Boris Hvorostovsky. Who the heck is that? The baritone is Dmitri Hvorostovsky. No idea where Boris came from. Must be moose and squirrel.

      3. WilliamLawrenceUtridge says:

        I love how Stan keeps proclaiming himself a “marketing expert” as if that did anything but discredit his ability to properly summarize the scientific evidence. I mean when was the last time someone said “trust me, I’m in marketing”, and it made you do anything but laugh in their face? Basically you’re saying “I’m in the profession that is defined by deception, but in this case I’m totally right about facts”!

  10. davidrlogan says:

    Would someone please explain what a “7.5% chance” of an event in 10 years means? I really tried to look in the paper (didn’t look hard enough, obviously) and couldn’t figure it out, exactly. Does it mean that if you lived 100 times over 10 years, 7.5% of those counterfactuals would have an event? And whatever it does mean, how is it calculated?

    I realize this sounds monumentally stupid/trollish but I am sincere. I think from there I can get a better idea what things are about…

    1. Harriet Hall says:

      It means out of every 100 people, 7.5 will have an event in the next 10 years. (Actually 75 out of 1000, since you can’t have half a person.) It is calculated from the statistics showing the actual number of events in other people who have the same risk factors.

      1. Harriet Hall says:

        I see where the confusion comes from. It’s not really “your” risk, but the group’s risk. Because that’s the best we can do.

      2. davidrlogan says:

        Thanks Dr. Hall!

  11. Max says:

    “There is no evidence that those with ties to drug companies influenced the findings of the panel.”
    Then what were they doing on the panel? Would the panel have been better off without them?

    “The new guidelines… will make sure that those who are not appropriate will not be given statins.”
    When you tell some group not to take a drug after telling them to take the drug, isn’t it an admission that taking the drug did more harm than good for that group?

    1. windriven says:

      “Then what were they doing on the panel?”

      Experts in most fields do a lot of work … because they’re experts. They may consult with drug companies. They may consult with governments. They may have research support from a foundation whose chairman’s uncle-in-law was once a member of the John Birch Society. So freaking what? The guilt by association thing cascades into whack-o-land pretty quickly, no?

      ” isn’t it an admission that taking the drug did more harm than good for that group?”

      No. At least not necessarily. It can also mean that they no longer fit in a category where the drug does much good.

      1. Max says:

        If they didn’t influence the findings of the panel, then what were they doing on the panel?

        “It can also mean that they no longer fit in a category where the drug does much good.”

        Their condition didn’t change; the guidelines changed. If they’re better off without the drug than with the drug, then by definition the drug did more harm than good. At the very least it was a waste of money. I wonder how many people will be harmed by the new guidelines.

        1. windriven says:

          “If they’re better off without the drug than with the drug, then by definition the drug did more harm than good. ”

          That is a non sequitur.

          You seem to see this as a binary step function. Sorry, biology doesn’t work that way.

          It may well have been a waste of money. And recognizing that the tiny benefit for some populations did not justify the expense, those populations could be removed from the recommendation.

          But wait. How does that square with your concerns about the panelists with ties to the pharma industry? Would their secret agenda be to expand the prescription base?

    2. Harriet Hall says:

      It isn’t an admission that the drug did any harm at all. It’s an acknowledgement of the fortunate fact that science progresses as more and better evidence accumulates.

      1. Max says:

        You tell them to take a drug, and then you tell them that they would’ve been better off without taking the drug. How is that not an admission that the drug did more harm than good?
        You just can’t admit that guidelines can harm people.

        1. Harriet Hall says:

          You are essentially quibbling about the semantics rather than the reality. That individual patient was not harmed. We prescribed a statin based on the best available evidence that benefit outweighed risk for him, and now we are no longer recommending it because better evidence says, not that the harms are any greater than we thought, but that the benefits are less than we thought. Do you admit that guidelines can help people? I most certainly DO “admit that guidelines can harm people.” That’s why we change guidelines when the evidence changes. It’s all about the risk/benefit ratio. But I want to stress that guidelines are far more likely to help people than to harm: the old guidelines were demonstrably saving lives, and far more people were being helped than were being hurt.

          1. Max says:

            I’d like to know the probability that a guideline does more harm than good before deciding to follow it. Has anyone calculated it for previous guidelines?

            1. Harriet Hall says:

              Obviously, we have no evidence that current guidelines do more harm than good, or they would never have been written. Do you mean you want to know the risk/benefit ratio for guidelines in general? Just how do you imagine anyone could go about calculating that? And if you decide not to follow the guidelines, how will you know what to do instead, and how can you judge that your alternative is more effective and safer?

              1. Max says:

                For starters, examine past guidelines, and see how many people were told to stop taking some drug or getting some screening.

              2. Harriet Hall says:

                That would not be evidence of harm, only of improved science.

              3. Vicki says:

                There’s also a real difference between “I didn’t need this, I guess I and/or my insurance company and/or the government [if you live in someplace with socialized medicine] wasted some money” and “I would have been better off not doing this.”

                But in the real world, the best I can do here and now (currently September 2013) is act on the knowledge we have. Maybe if I had a much more detailed family medical history I would make different choices, but I don’t have that information. (I don’t even know what my father died of.) “Don’t take any drug, it might turn out later that it would be a bad idea” is essentially betting that current medicine is always wrong. “Don’t take anything that hasn’t been in use for at least ten years, in case of side effects that only turn up in large, long-term population studies” is betting that you have no underlying condition that won’t harm you in the next ten years.

                You can’t just postpone the decision: you either take a statin, or a low-dose aspirin, or an antidepressant, or you don’t. You can’t climb in the box with Schrodinger’s cat, wait ten years, and then wave your hand to have done whatever science in 2023 thinks would have been best.

                So, in the real world, I am no longer taking calcium supplements, but I don’t blame the people who recommended them. (I do blame people who still urge everyone to take calcium, or vitamin A, or vitamin C–but if they aren’t marketers, they’re more likely to be a random relative, friend, or co-worker without medical training who doesn’t make a point of keeping up on the literature.)

              4. Pharmacist permanently harmed by lipitor says:

                “Obviously, we have no evidence that current guidelines do more harm than good, or they would never have been written” That was a whopper!

              5. Harriet Hall says:

                Not a whopper. The guidelines were based on the best available evidence indicating that they would do more good than harm. The new guidelines are not based on any evidence that the earlier guidelines were harming patients, but rather on better evidence about who would benefit. Both sets of guidelines looked at benefit/risk ratios.

    3. weing says:

      “When you tell some group not to take a drug after telling them to take the drug, isn’t it an admission that taking the drug did more harm than good for that group?”

      Not sure what you mean by this. If someone is experiencing adverse side effects of the drug, I have them to stop it, they cannot benefit from the drug. If they are taking a drug and not experiencing side effects and now we find that it is not helping them, then stop it. The risk of harm is always there and the benefit is not present. Why would you continue it?

      1. Harriet Hall says:

        That’s not evidence; that’s Mercola. He also says “statins have nothing to do with reducing your heart disease risk.”

        1. stanmrak says:

          If you bothered to read the article, it’s really the New York Times making the assertions.

          1. Harriet Hall says:

            Mercola uses assertions from the NY Times as part of his one-sided screed against statins. People can speculate all they want, but there is no actual evidence that the panel’s recommendations were anything other than the results of an objective analysis of the published data. When did the NY Times ever say “statins have nothing to do with reducing your heart disease risk.”?

  12. I find the beliefs of Winddriven and Stanmrak very refreshing. Two opposition points who think they are both correct. Windriven is on the side of my profession in this debate. Since the ACA is driven by “thought experts” like Dr. Nissen you need to be careful what you think is “fundamentally supported”. Evidence based medicine is only good if your initial premise of target is good. That point is debatable with respect to statins. And when you become aware of this, then you must realize if you target is off your literature, upon which you rely is worthless in cause and effect relationships. I have found much of what I learned in med school and residency did not match my clinical observations. Physics follows an axiom biology needs to adopt. “It doesn’t matter how beautiful your theory is, it doesn’t matter how smart you are. If it doesn’t agree with experiment, it’s wrong.” The Nobel Laureate, Richard Feynman had several other good quotes about this conundrum medicine faces with respect to heart disease and causation.
    1.“There is no authority who decides what is a good idea.”
    2. “Scientific knowledge is a body of statements of varying degrees of certainty — some most unsure, some nearly sure, none absolutely certain.”
    3. “I think it’s much more interesting to live not knowing than to have answers which might be wrong.” (sadly I think we are)
    4. “If you thought that science was certain – well, that is just an error on your part.” (windriven)
    5. And my favorite for cardiologist and lipidologists, “Science is the belief in the ignorance of experts.” (take a look at how right the major ACA expert has been in the link below)
    I’d suggest we all be a bit more skeptical of the dogma of the day. Statins have very little benefit for the great majority of people. Do they have a role, maybe, in specific cases. This implies if we think like Feynman instead of reading a literature replete with conclusions based upon a faulty premise that we ask better questions when it is clear heart disease is still killing more humans than any other disease. I think the answer lies in in Feynman world of the molecular mechanisms of light, food, and circadian biology and not in statins.
    http://drmalcolmkendrick.org/2013/11/25/a-farewell-to-statins-part-one/

    1. Harriet Hall says:

      It is true that the majority of people taking statins will not have any personal benefit, because the benefit is a statistical one. It is nevertheless true that statins save lives: it’s just that we don’t know which lives, so we have to treat the group based on the statistical risks. We treat everyone with high blood pressure, but not everyone with high blood pressure is going to have a stroke without treatment. We are constantly asking “better questions” about heart disease; but until those questions are answered, we have a drug that is proven to help, and it would be foolish to reject it in favor of the ravings of the International Network of Cholesterol Skeptics. The link you provided is from a member of THINCS. They are not thinking clearly. See http://www.sciencebasedmedicine.org/the-international-network-of-cholesterol-skeptics/

    2. windriven says:

      Threading is still hit and miss. I won’t waste space by repeating my response in 15 below.

      In that post I asked, a bit facetiously, if you were going stan on us. Having reread your comment I realize that you are. First you buzz around with lots of high-toned musings about science – though not many of them apropos to the subject at hand. Then you sleaze around casting aspersions but never actually stake out your ground.

      So, doctor, I call bullshit.

      If you were a scientist and not a poseur, you would state your objection with specificity, lay out the argument supporting your objection, and back it up with meaningful citations. Instead, you curl your nose and pretend to be offended by flatulence.

      1. interested party says:

        Windriven,
        What are you talking about? Where is your postion? Where is your science? I haven’t seen anything intelligent in any of your comments. There is no science in correlations. And that is all you have, and also of course EXPERTS. And Harriet has the audacity to quote a 2008 blog on the THINC group, a group of very well qualified medical practioners who have no financial interest in panning cholesterol theories or Statins, in which she describes them as a bunch renegades. This is not a site about science , it is just lofty words and intimidation by the groupies surrounding Harriet.

        Did you even check the reference blog of Dr. Kendrick? Did you read some of the comments? This is very relevant stuff. Your stuff is bullshit.

        1. Harriet Hall says:

          I explained the flaws in reasoning and the omission of data by the THINCS people at http://www.sciencebasedmedicine.org/the-international-network-of-cholesterol-skeptics/

          If you think there is no science in correlations, what kind of studies would convince you?

          1. Interested party says:

            @Dr. Hall.
            I guess I was not impressed by your blog on THINCS. It was mosly opinion. We all read the same reports – we just see different results based on the data. This is fine, and it is reasonable to disagee, but to characterize the group as scientists who “are not thinking clearly” is a bit special.

            You ask what kind of studies would convince me? Just the ordinary kind of RCT’s with a control group and a placebo group, the kind that have been done over and over again around the world with very mixed resutls. Can you site at least one study which reported a clear result in favor of statins, one that is not confounded by multiple interventions, without bias (this is difficult given that statins will reduce Cholesterol so it is easy to see which group is which), and which showed a significant decrease (significant for me means more than just statistical significance. Signifcant to me means a risk reduction that is glaringly attractive in terms of decision making, for or against) in absolute risk of all cause mortality. I understand that we are looking for correlations that could point us in the right direction regarding the formualtion of a heart disease model, but that is far from justifiying the use correlations as causes to attack the “badness” of LDL-C or any other lipoprotein. Hypothesising a model for CHD and testing it through rigorously designed RCT’s is science. At this point it appears we don’ have a testable hypothesis for CHD, so no such RCT’s are in the works to my knowledge. Maybe we are doing the best that we can, but prescibing statins for primary care is far from “our best” based on the meager evidence that exists.

            @Weing
            You say that I only accept science in correlations in the context of statins and side effect claims. I think that i have been very clear in my position regarding correlations. As an exampe of the wild world of correlations, check out this report in the media regarding a report on a study of NUT CONSUMPTION based on data analysis from the Nurses Health Study and entitled “Large study links nut consumption to reduced death rate” found at the this link.
            http://www.eurekalert.org/pub_releases/2013-11/dci-lsl111513.php
            The media report says”BOSTON— In the largest study of its kind, people who ate a daily handful of nuts were 20 percent less likely to die from any cause over a 30-year period than were those who didn’t consume nuts, say scientists from Dana-Farber Cancer Institute, Brigham and Women’s Hospital, and the Harvard School of Public Health.” And a bit further, it states “”The most obvious benefit was a reduction of 29 percent in deaths from heart disease – the major killer of people in America,” said Charles S. Fuchs, MD, MPH, director of the Gastrointestinal Cancer Center at Dana-Farber, who is the senior author of the report. “But we also saw a significant reduction – 11 percent – in the risk of dying from cancer,” ……
            If you go to the orginal report you will easily be able to figure out the absolute risks. I did this in about five minutes without a calculator just to get the rough numbers. I arrived at less than 0.80% mortality if you did not eat nuts, and less than 0.64% if you did. Here in a good example of a correllation at work. These results show, at best, a correlation between populations who ate nuts and those who did not. No causation can be determined here. Yet the media report says that your risk of dying of heart disease is 29% lower if eat a handful of nuts 7 or more time per week. What do you think the average reader will interpret from this media report?
            First of all, the was no evidence of causation, there was no scientific model of heart disease whose accuracy would be advanced by this information, and the reported risks are very misleading. Why do you suppose such action goes on? Why do the medical professionals involved in such “research” support such action with their comments? That is one reason I don’t like associative studies. The researchers too often make totally misleading statements and these get translated to the media and the truth gets distorted. Is this part of what you call science?

            @Windriven
            I am sorry but again your response discourse did not add anything new to my understanding of why you support these guidelines. You repeat the stuff about experts, 40 years of history, bla bla bla. There is no justification of accusing anyone who disagrees with your positon as being a “denier” . We are just trying to do the same as you but our objectives are different. We also cite scholarly studies which bring contradictory evidence to statemenst which are made in this blog., but for some reason such studies are either rejected by you or ignored. Your writing style is very condescending and not at all helpful in furthering your cause.

            1. weing says:

              So, what you are saying is you don’t like nuts? That’s fine. I’ve been eating a handful a day for the past 19 years now. Medicine is hard. I tend to give more weight to studies where one of the factors can be manipulated. As in the nut case you cited, there was a dose effect noted.

              1. interested party says:

                What a dumb reply. I love nuts and eat tons. I just don’t believe for a second that eating nuts will help be live longer to any significant degree. Maybe I will change my mind when newer research shows some causation, but until then I will just enjoy eating nuts without any illusion that they are contributing to my longevity.

            2. Harriet Hall says:

              ” I was not impressed by your blog on THINCS. It was mosly opinion”

              In my opinion, it was much more than opinion. :-)
              I cited contrary studies and showed that THINCS only cited studies that agreed with their thesis, ignoring all the evidence that disagreed with them. I think that is substantiated by the fact that the consensus of non-activist scientists, after reviewing ALL the evidence, disagrees with THINCS.

              1. interested party says:

                @Harriet Hall
                So you believe in numbers, the bigger the consensus on your side, the more likely you are right. Such logic makes me think of the history of the discovery of Halobacteria after the consensus was that ulcers were caused by too much acid in the stomach, etc. You of course know the story. Such things happen. Sometimes the little group struggling to break the conventional wisdom is right. If your side had overwhelming evidence that Statins worked, I would say hurrah. But the evidence is almost non-existent, and certainly far from proving anything. Just a correlation. I find it sad that groups like Thincs are considered misguided renegades.

              2. Sawyer says:

                @Interested

                Is there a secret flowchart you guys are consulting for how to talk about medical research? It seems like the mere mention of expertise elicits the inevitable comment about either heliobacter pylori, prion diseases, or Semmelweis. I can understand why you think these analogies are relevant, but when they are brought up five times a week it really starts to get stale.

                Just imagine how absurd it would look if you saw this type of argument in a journal paper. “Here is some low-quality evidence that shows a new species of hominid, but we should treat it like high quality evidence because other scientists don’t accept it and I’m like Semmelweis.” Evidence is what trumps experts, not vague analogies.

            3. windriven says:

              @ip

              “And that is all you have, and also of course EXPERTS.”

              Yes, the expert opinion of cardiologists and internists and others who work with these patients every day.

              But of course the great ‘interested party’ has … what besides a half-baked understanding of the science of statins? You piss and moan about statin therapy and I’ll be damned if I understand what your actual root objection is.

        2. weing says:

          I think he only accepts science in correlations in the context of statins and side effect claims.

        3. windriven says:

          interested, the science linking cholesterol and CVD has been around for 40 years. Yes, there are deniers. There are deniers about evolution, about global warming, about nearly every subject whether controversial or not.

          Dr. Hall reported the latest recommendations on statin use. It is not her opinion. It is not based on some lonely voice in Scotland raging against the wind. It is the consensus position of experts in the field.

          This is not the be all and end all regarding statins. it is just the best information available reviewed in the larger context of cardiovascular disease etiology that we have TODAY.

          Dr. Jack spews lots of opinion but his and Kendrick’s are fairly lonely voices. Moreover, good ole Jack never lays his cards face up on the table to give us his version of reality and how that can be translated into useful clinical advice. Instead he sits in the back of the room and shoots spitballs at the teacher. That is simply chicken-s**t.

          You see, interested, this isn’t a sophomore class bull session. This is an effort to assembleone of the tools that practicing physicians will use to inform their clinical judgment when treating living human beings.

          Medicine isn’t House. It isn’t Gray’s Anatomy. There are rarely any perfect answers. There is the best judgment of highly trained and deeply experienced experts in their field based on a thorough reading of the available science. Or there are the ravings and pot shots of GPs in Scotland and an, ummm, unique individual who allegedly tried to infect himself with MRSA, then sit in an ice bath to soak it away. I am comfortable with the ACC. You are welcome to sit on the Group W bench. The choice is yours.

          Toodles.

  13. Josh says:

    Almost all statins are generic now. They are dirt cheap. So with the exception of Crestor, there really is no money in it for “Big Pharma”.

  14. windriven says:

    “If you thought that science was certain – well, that is just an error on your part.” (windriven)

    I wonder what I’ve said that would have you associate me with the notion that science is ever certain?

    And for what it is worth, I am a physicist, though certainly not in Feyman’s league.

    “Statins have very little benefit for the great majority of people.”

    By ‘the great majority of people’ do you mean the general population (who could disagree?), the population for which statins have been prescribed, the population at risk for CVD, or some other population? And do you have citations to offer here for whatever that population is or are you going stan on us?

  15. Tdwimo, MD says:

    It is a bogus thing to mimic NATURE for just money, greed and power. For every
    drug deviced by industry there are many natural body-friendly substances that
    do much better job CURING diseases without dangerous secondary effects and
    chipper than drugs that only muffle symptoms and erode our physiology and pockets. LDL (the tarjet) is not the culprit in CV disease, it is Lp(a) which is untoucha-
    ble by statins. Arterial plaque is mostly made up of Lp(a) and can be lowered to non
    atherogenic levels by high doses of Vit C, L-Lysine, L-Proline, R-Lipoic acid (Linus Pau-
    ling, M. Rath 1992). Vit C is THE NATURAL STATIN.

    1. Harriet Hall says:

      “For every drug deviced by industry there are many natural body-friendly substances that
      do much better job CURING diseases without dangerous secondary effects and
      chipper than drugs that only muffle symptoms and erode our physiology and pockets.”

      Every drug? Really? “Many of them” for every drug? Please list the “many” natural substances that do a much better job than insulin for diabetes, than DMARDs for RA, than HAART for AIDS, than triple antibiotic therapy for ulcers, than vaccines for polio, than anticonvulsants for epilepsy. Vitamin C and what others can cure cardiovascular disease? How do you define cure: total removal of arterial plaque? What percent reduction in cardiovascular events can be achieved by lowering Lp(a) with what dose of vitamin C? References, please!

      1. mouethatroared says:

        Well, death is natural and it cures ALL illnesses. But, silly humans, we are always looking for an easy out.

        1. windriven says:

          Thanks mouse! Started my day with a chuckle.

    2. WilliamLawrenceUtridge says:

      I’m really curious why there would exist in nature a 1:1 cure for each human disease or morbidity. What on earth would drive the evolution of plants and/or animals to be so specific in their biochemical outputs? I mean sure, there are some plants that produce chemicals that have effects on the human body, but these tend to be messy, with a lot of side effects (because human cellular receptors are themselves duplicated and redundant throughout the body) and are primarily designed as poisons for insects and herbivores to protect against being eaten.

      Also, Tdwimo, where is your evidence that vitamin C, lysine, proline and lipoic acid are equivalent to statins? Where did Pauling get his evidence from, where are the primary studies in humans? And why a date of 1992, if these compounds are so successful at lowering Lp(a) and reducing the risk of atherosclerosis, why aren’t these strategies appearing in the recommendations written by the panel? It can’t be because of the low cost or some other “Big Pharma can’t profit” reason, since the panel spent an extensive amount of text on the essentially free option of lifestyle modifications.

      Yours,

      A critical thinker

  16. Tdwimo, MD says:

    Sirs: My comments are purely scientific and truthful. Thank you

    1. windriven says:

      Sir, you are purely and truthfully full of bat guano. Answer Dr. Hall’s questions, please. And be sure to include citations. And stop pretending to be a physician, something that you are clearly not.

    2. MTDoc says:

      You really don’t sound like any MD I have knowingly associated with in the past half century. Perhaps you meant ND?

    3. WilliamLawrenceUtridge says:

      Here’s a hint Tdwimo – thinking, and saying your comments are scientific and truthful doesn’t make them scientific and truthful. Scientific research could find out if they were truthful, but science only reveals what already is, it has no power to change what already is into whatever notion you fancy. Your version of science bears more resemblance to childish wishful thinking and magic.

  17. RobLL says:

    Several weeks after having an Internist double my statin dose because my triglycerides were high I suffered a serious case of peripheral neuropathy and general muscle weakness. Both Int. and neurologist absolutely refused to consider that statins might be a cause. From what I have seen about statin side effects and the number needed to treat to benefit one person a patient is justified in not taking them unless there is a presence of current heart disease or family history.

    1. windriven says:

      @RobLL

      “Both Int. and neurologist absolutely refused to consider that statins might be a cause. ”

      I would say you are either lying or in desperate need of a new internist and neurologist. Myopathies are a well known ADR of statins. Could it be that they evaluated statins as the cause and ruled that out? Could it be that you are trying to sell your position with a carefully shaped personal anecdote?

      And this is just silly: “You seem to be an unduly enthusiastic cheerleader.”

      Dr. Hall reported on new recommendations. She has reported on statins before as well as on a variety of other interventions. Her position is invariably cautious and reasoned.

  18. RobLL says:

    ps – pretty sober doctors have suggested that any drug or procedure for which the NNT is great than 5 or 6 need be considered with a jaundiced eye. You seem to be an unduly enthusiastic cheerleader.

    1. Harriet Hall says:

      How many people buy fire insurance for their house and how many have house fires? How many people have to get vaccines to save one life? There can be no arbitrary cut-off for NNT. NNT needs to be considered in conjunction with NNH, and individuals will differ in their attitudes about risk. You might find this table of NNTs of interest: http://www.medicine.ox.ac.uk/bandolier/band50/b50-8.html It lists the NNT for primary prevention with statins as 35. Assuming that’s accurate (I don’t) would mean that 34 people will take it as unnecessary insurance, but one life will be saved. I consider that pretty good odds, and maybe you would too if you thought you might be that 1 person in 35.

      1. agitato says:

        Dr. Hall,
        Is the site called: thennt.com at all reliable? It takes a pretty dim view of statins.

        http://www.thennt.com/nnt/statins-for-heart-disease-prevention-without-prior-heart-disease/

        Could someone tell me how to make a link look like a link? ie turn blue? Or better….how to replace a link with a blue word?

        1. Harriet Hall says:

          I was not familiar with thennt.com. I noticed that the assessments are by single authors who are mostly ER docs. I looked at a few of their reviews about subjects I was familiar with, and I thought they were over-simplified and ignored important nuances. My first impression is not very favorable. I’d be interested in hearing what others think about it. I would put more trust in the consensus recommendations of groups of experts in each field who have reviewed all the evidence. I wish the new cholesterol recommendations had provided NNT and NNH numbers.

          1. weing says:

            “I wish the new cholesterol recommendations had provided NNT and NNH numbers.”

            That would be ideal, not only for statins, but diet and exercise too.

        2. windriven says:

          @agitato

          “Could someone tell me how to make a link look like a link?”

          This should work but of course you need to leave off the beginning and ending quotes.

          A Woo Free Zone

          1. windriven says:

            Crud. I can make it work but am not clever enough to print it and not have it hyperlink. This link shows you how

      2. interested party says:

        I think that comparing NNT numbers for a drug to some equivalent to NNT for car insurance or the like is misleading. The side effects of buying insurance are known in advance. The protection if an event occurs is known in advance. The case with drugs is not so clear. Yes we know that statistically some % of us will crash our cars or have a heart attack, but at least car insurance makes us whole. Drugs? Well, sorry, I guess they didn’t work for you, even though you paid your “dues” for all those years.

        1. weing says:

          Think of it as a lottery. You have an LDL of 100 you get a lottery ticket for the jackpot, i.e. heart attack. LDL of 200, you have 10 lottery tickets. Take a statin, you only get 5 instead of 10. Doesn’t mean you will win the jackpot but your chances are better with the number of tickets you hold. It also doesn’t mean you can’t win with only 1 ticket. Life is uncertain, isn’t it?

          1. Interested party says:

            @ weing
            i think that you missed my point. In a lottery, the downside is not winning and losing the investment. No big deal and a very known possible outcome. With statins, the outcome is not well known at all. You might die from taking statins or you may suffer very undesirable health effects. I think that we patients would like a little more certainty when taking drugs than just the statistical ones. Our lives are at stake. Too many studies have shown either meager benefits or no benefits. And some studies have shown possible very high mortality risk if TC is reduced below 106 mg/dl when compared width mortality risk at TC levels of 200 to 219. This should not be viewed as would a lottery.

            1. Interested party says:

              Sorry, I meant to write 160 mg/dl , not 106.

            2. weing says:

              @interested,
              “i think that you missed my point.”

              No I did not miss your point. You missed mine though. Sorry.

              “very high mortality risk if TC is reduced below 106 mg/dl when compared width mortality risk at TC levels of 200 to 219.”

              Associative studies? Reduced by statins or disease? Citations?

              1. interested party says:

                @weing
                Here is the link – see table 6.
                https://www.jstage.jst.go.jp/article/circj/66/12/66_12_1087/_pdf

              2. weing says:

                Right. If cholesterol drops because of statin, it’s a good sign and prevents coronary events. If it drops because of a cancer, and it will drop significantly in that case, then it’s not a good sign. They will die of the cancer. Tell me something we don’t know. It’s what causes the drop is what’s important.

  19. weing says:

    “pretty sober doctors have suggested that any drug or procedure for which the NNT is great than 5 or 6 need be considered with a jaundiced eye.”

    I think this is something that society as well as the individual have to decide. What is the benefit? If I need to treat 5 people like you with a medication for a year to prevent a stuffy nose in one of you, it would be too much from my point of view. If I took 50 of you and treated for a year and prevented 1 death, that would be worthwhile, in my opinion. But the decision is still up to you. I can’t make that for you. Are you feeling lucky? Next you need to consider the NNH. Then you also have to consider the cost of the med.

  20. eddie says:

    Thankyou Stan, its nice to hear from someone who can see behind the curtain. If what I have read is correct, the lipid theory was questioned from the start, and marketing played the largest role in its success, with tactics such as pushing the bogus seven counties study etc.

    1. Harriet Hall says:

      Even if the lipid theory is entirely wrong, that wouldn’t change the guidelines, since elevated blood cholesterol would still be a significant surrogate marker for risk, and since statins have been shown effective at saving lives.

  21. Flower says:

    A study published in the journal Atherosclerosis found that statin use is associated with a 52% increased prevalence and extent of coronary artery plaques.
    http://www.ncbi.nlm.nih.gov/pubmed/22981406

    Another study in the journal Diabetes Care, found that coronary artery calcification “was significantly higher in more frequent statin users than in less frequent users,” among patients with type 2 diabetes and advanced atherosclerosis.
    http://www.ncbi.nlm.nih.gov/pubmed/22875226

    Statin drugs can induce autoimmune myopathies such as dermatomyositis, polymyositis, and immune-mediated necrotizing myopathies
    http://www.ncbi.nlm.nih.gov/pubmed/21654717

    Furthermore,

    - Statin drugs deplete the heart muscle of coenzyme Q10, a fundamental cofactor for mitochondrial energy production (the heart muscle cells have one of the highest mitochondrial densities (approximately 5,000 mitochondria per muscle cell, versus 50 for skeletal muscle), and therefore are most susceptible to statin-induced coenzyme Q10 depletion, and subsequent mitochondrial dysfunction.

    - Statins increase the risk of type 2 diabetes, a condition whose hallmark pathology is high blood sugar-induced endothelial dysfunction, which is the beginning stage of cardiovascular disease, as it leads to damage in the arteries, only after which cholesterol-containing plaques form.

    - Statin drugs are muscle-damaging (myotoxic) and nerve-damaging (neurotoxic). The heart is a highly innervated muscle (densely packed with nerves), indicating that statin drugs are uniquely toxic to heart tissue.

    - Statin use is associated associated with an increased prevalence of microalbuminuria, a well-known marker of vascular dysfunction, affecting both cardiovascular and kidney disease risk.

    The public is wising up and is increasingly challenging doctors about the need for long-term drug taking, thanks to publicly broadcast programs even the MSM is now bringing to their attention.

    e.g. A recent 2-part ABC “Catalyst” series on the cholesterol myth and statin drugs:
    Part 1 http://www.abc.net.au/catalyst/heartofthematter/
    Part 2 http://www.abc.net.au/catalyst/stories/3881441.htm

    1. Sawyer says:

      I’d be willing to bet every single side effect you provided was discussed in detail when coming up with these guidelines, and probably by people that have a much better grasp of those side effects than you or I. The evaluation of risk vs. benefit requires a tremendous amount of research experience and knowledge of statistics, neither of which are demonstrated when you throw up cherry-picked critiques of statins.

      And once again, I would have been somewhat receptive to your point of view if you didn’t wander into “cholesterol skeptic” territory. Too late now.

      1. john umiastowski says:

        Sawyer, you must be an eternal and naive optimist. Did you even bother to check out those “ABC network ” Catalyst series mentioned by Flower or even the book by Dr. Ben Goldacre? Check him out on Ted Talks. Let me know if you think he is a quack?

        Get real! Do you really believe that those who question the evidence which support statin use are idiots? They are all really caring medical practioners who looked at the evidence and just don’t buy it. They truly want to prevent harm to patients, and there is lots of potential harm available.

        What happened to the research report from June 2010, link here below,
        http://archinte.jamanetwork.com/article.aspx?articleid=416105
        which found …
        “Conclusion: 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.”

        Has this work been discredited now, 3 years later?

        1. WilliamLawrenceUtridge says:

          John, this is known. Statins have different risk:benefit profiles for primary prevention than they do for secondary prevention. The recommendations are not “statins for everyone!” That’s rather what the post is about. It’s a complicated issue.

          I’ve read Dr. Goldacre’s book. I’ve even corresponded with him. What did you think of his idea to randomize patients into similar classes of drugs in real-world conditions? You could apply it to statins, I think it’s a great idea.

          But merely because Big Pharma are bastards doesn’t mean all of the data is invalid.

    2. WilliamLawrenceUtridge says:

      Hi Flower. Still scientifically ignorant I see.

      Your first two links are correlational studies. Rather than proving that statins cause calcifications, all they show is that statins and calcifications appear together. So do people with calcifications get put on statins, or do statins cause calcifications? The studies you present can’t answer that question, there was no randomization.

      Also, yes, statins have side effects. This is not news. If you have a better way than statins to prevent heart attacks in those with poor lipid profiles, please provide it. Sometimes exercise and diet will help, but even better is to have a good set of genes. Please get right on that!

  22. Rob Cordes, D.O. says:

    I fail to see the influence of pharma companies in a guideline that states:

    “2.1. Lifestyle as the Foundation for ASCVD Risk Reduction Efforts
    It must be emphasized that lifestyle modification (i.e., adhering to a heart healthy diet, regular exercise
    habits, avoidance of tobacco products, and maintenance of a healthy weight) remains a critical component
    of health promotion and ASCVD risk reduction, both prior to and in concert with the use of cholesterol lowering drug therapies.
    Healthy diet or lifestyle modifications were recommended as background therapy for the RCTs of cholesterol-lowering drug therapy. See the 2013 Lifestyle Management Work Group
    Guideline (10) for lifestyle recommendations for healthy adults. “

    1. Flower says:

      Unfortunately, such lifestyle advice rarely centres around what’s really important: The avoidance of processed foods, incl trans-fats and, especially sugar (fructose) which drive up cholesterol (and TGs) – see: http://jn.nutrition.org/content/early/2013/07/02/jn.113.175323.abstract

      1. WilliamLawrenceUtridge says:

        Does your definition of a “heart healthy diet” include processed foods, trans fats and triglyceride-promoting foods? Because nobody else’s did.

        Say, how do you reconcile the need to avoid fructose with the recommendations to consume large amounts of fruits? Did you know that “fructose” means “fruit sugar”? I did.

        Talk about tilting at windmills.

  23. Dave says:

    I looked at the first study you reported and it raised questions about the mechanism of action of statins more than anything else. Other reviewers can elaborate further. A quote from the article:

    “Monitoring atheroma progression using serial intravascular ultrasound (IVUS) has been used to characterize the natural history of atherosclerosis and the effect of anti-atherosclerotic therapies. Serial IVUS studies have demonstrated that reduction in LDL cholesterol levels by statins may slow the rate of atherosclerotic disease progression [4] and [5] and may induce very small amounts of coronary atherosclerosis regression if “goal” LDL cholesterol levels are achieved [16]. Collectively, these studies show a strong linear relationship between the degree of LDL cholesterol lowering and change in atheroma volume [16]. Further, limited studies specifically examining coronary plaques by composition have demonstrated a slowing of non-calcified plaque progression in a manner that is out of proportion to the slowing of the overall atherosclerotic process.”

    I think there is a lot of debate in the medical community about how statins work. Please reference the BMJ article I pointed out earlier for a debate in a major medical journal about cholesterol as a cause versus association of coronary disease. The mortality data for secondary prevention I think speaks for itself, and mortality is a pretty hard endpoint. Any drug has problems, that’s why the “number needed to harm” is looked at and why, for example, atromid is never used for type 2 hyperlipidemia – it hurts more people than it helps. Probucol elevates HDL levels which should make it good to prevent heart attacks. Unfortunately, it doesn’t, which is why you never hear about it anymore.

    As far as number needed to treat, that’s a questionable call. For a disease which kills several hundred thousand pople a year, an NNT of 50 can produce big dividends. Unfortunately, preventive medicine, other than doing what your mother told you to do when you were 4 about eating your fruits and vegetables, not smoking, wearing seatbelts, getting off your butt and exercising and looking when you cross a street, involves treating a lot of people to prevent some outcomes. It’s a lot of work for the gain. If I give this drug to 50 people for one year, one will be helped, but I don’t know which one.

    So much of what we do is like this and I think this is not well understood by the public. Example: I give anticoagulants to patients with atrial fib to prevent strokes. What anticoagulant depends on a risk assessment using a score. If a patient has a CHADS 2 score of three, his chance of a stroke without anticoagulation in the next year is about 6 %. His risk from the anticoagulant recommended for this score is about 1% for a major bleed. Most patients choose to take the anticoagulant. In terms of destroying a person’s quality of life, strokes are way up there.

    1. Flower says:

      You’d think that the scientists publishing their studies in the journal Atherosclerosis would know what they’re talking about….

      1. WilliamLawrenceUtridge says:

        You mean the studies that are correlational and thus do not determine causality?

        Why do you think that a single study proves or disproves an entire body of research?

  24. goodnightirene says:

    Now you regulars will see what I mean about the comments at the NY Times article on the same subject.

    People seem to easily believe anything they hear or read about “evil drugs” and equally as easily reject basic science. They clearly do not understand how science works or how it differs from “in my experience”. Nor do they care one bit that heart disease and related deaths have plummeted since statins became widely used. They care only for conspiracies they “discover” on the interwebs.

    I cannot wait until they all die of heart attacks or strokes. I realize this is why I could never be a proper health care professional, but there you have it. I do not have the patience anymore of someone such as Dr. Hall, who does her best to explain the facts over and over. Are these minds closed by ignorance, or just incapable of taking in a complex thought (stupid)?

    1. weing says:

      Look on the bright side. Cardiac surgeons and cardiologists will have job security for a long time.

    2. windriven says:

      “Are these minds closed by ignorance, or just incapable of taking in a complex thought (stupid)?”

      Most likely on my opinion is that they’ve signed on to an ideology that says medicine is all about money. As with religious zealots facts and rational arguments are no match for dogma. Mercola said it, they believe it, that settles it. Depressing, no?

    3. Pharmacist permanently harmed by lipitor says:

      Just how bad is your statin cognitive Damage? Can’t wait for them to Die? Your cortisol levels must be through the roof. Stress kills.

  25. Josh says:

    I love the people that say drugs (synthetic chemicals) are bad and then recommend vitamin c (ascorbic acid or calcium ascorbate) pills. I do not think these people know how they are made. They are synthesized using the Reichstein Process. http://en.wikipedia.org/wiki/Reichstein_process
    This “natural product” is in no way natural. It is made by chemical and pharmaceutical companies. So spare me the B*******t about your “natural remedies”

  26. A frustrated doc says:

    I am going to try one last time.

    Please watch the following short video URL (entitled ‘Cavities and coronaries: our choice’):

    http://nutritionfacts.org/video/cavities-and-coronaries-our-choice/

    This website – SBM – purports to be scientific but I have found that many of the readers and even the commentators bury their heads in the sand when it comes to lifestyle modification – ie a plant-based diet.

    At least our political leaders are beginning to follow this dietary choice (Bill Clinton, Al Gore, Chelsea Clinton). Doctors as a group tend to be ultraconservative and the last to change their dogma – hence the popularity of bloodletting and other false palliatives over centuries.

    This is my last post on this website. Thanks.

    1. Self Skeptic says:

      @Windriven said, in response to another poster’s comment on undue pharmaceutical influence in the medical literature:
      “…what you are really alleging is large scale, wide spread scientific fraud. That is an outrageous accusation and it demands pretty substantial proof. So where is it?”

      The following books, from highly respected medical publishing experts, provide detailed information on why the medical literature can’t be taken at face value, as “the best information current science can provide.” They also address how RTCs, systematic reviews, meta-analyses, and clinical guidelines produced by panels of experts, are compromised by this well-documented problem:

      Former NEJM editor Kassirer, “On the Take”.
      Former NEJM editor Angell, “The Truth About the Drug Companies”
      Popular skeptic author Ben Goldacre, MD “Bad Pharma.”

      There is also a new book I have on Kindle, but haven’t read yet.
      I apologize for having to cite a book with such an inflammatory title; but coming from the director of the Nordic Cochrane Center, and with forewords by Richard Smith of BMJ and Drummond Rennie of JAMA, I think it merits our attention:

      Cochrane leader Peter Gotzsche, MD “Deadly Medicines and Organised Crime: How Big Pharma Has Corrupted Medicine.”

      I am just as interested in intellectual bias, as in marketing bias, but it’s a lot easier to follow the money. I think examining marketing-driven bias is the best way to make the general case that peer review is not keeping seriously biased studies, posing as science, out of medical journals, even the most prestigious ones. This holds true, even when the direction of bias should be obvious, as in commercially-funded studies. It’s more difficult when the COIs are non-financial, as when a true-believer in some medical hypothesis becomes a dominant influence, through political skill.

      Once we acknowledge how often form or prestige trumps substance, in the medical literature, we can appreciate the need to apply skeptical investigation, to all expert recommendations, rather than merely accepting them at face value.

      1. windriven says:

        @Selfie-

        Let’s not move the pieces. My comment that you refer to was in response to the inimitable stanmrak:

        “This is not really a ‘calculator,’ it’s a ‘marketing tool.’ It’s primary purpose is to sell more drugs, not assess true risk. I know, I know – the numbers come from “the government”. ha ha. I’ve been in marketing all my life – this is one way that it works.”

        If you, stan, and the supposed doctor Jack cannot differentiate between the quite real and disturbing prostitution of the scientific literature by drug companies and the bald allegation that the American College of Cardiology is in the pay of Big Pharma to stimulate sales of a f*****g family of drugs (Crestor excepted) that is long off patent and notably inexpensive, then you really need to wrap the tinfoil a little tighter.

        Then you go on to cite books that detail the evils of pharma marketing as if this is some kind of news flash. IT HAS NOT A BLOODY THING TO DO WITH stan’s outrageous allegation.

    2. Dave says:

      Most doctors I know favor a plant based diet. I don’t know any who think it’s unhealthy.

      1. interested party says:

        @Dave
        Well there are several out there. The best i have seen is Denise Minger. Just google the name and read her bio. She was an ardent vegeterian for about 10 years until her hair started to fall out. But I would rather have you read it yourself.

    3. windriven says:

      @frustrated

      “This is my last post on this website”

      Bye-d-bye. I don’t think anyone here believes a healthy diet isn’t a good thing. Of course I don’t know what kind of diet you’re flogging. Might be a reasonable Mediterranean-type diet, might be one of the less mainstream diets, might be bat-crap crazy. Given your approach, I for one am not busting a gut to find out.

  27. Self Skeptic says:

    A discussion of these guidelines, with more specific information and citations, occurred in the comments section of this thread:
    http://www.sciencebasedmedicine.org/irritated-by-the-skeptical-inquirer-again/
    Dr. Hall participated, briefly.

    1. windriven says:

      Selfie-

      “A discussion of these guidelines, with more specific information and citations, occurred in the comments section of this thread:
      http://www.sciencebasedmedicine.org/irritated-by-the-skeptical-inquirer-again/
      Dr. Hall participated, briefly.”

      I for one am interested in following along. But linking to the comments section of a blog post with 110 comments is ridiculous. If you want to direct attention to something, copy and quote or at a minimum cite the comment number. Few of us have the time to sort through 110 comments trying to figure out what the heck you are trying to say.

  28. Self Skeptic says:

    BTW, threading may be malfunctioning. My comment beginning with “@Windriven said…”, above, was supposed to be a free-standing comment, not a reply to @a frustrated doc, whose recommendation I haven’t investigated; so I have no opinion on it.

  29. Jack Kruse says:

    Self skeptic most of those are excellent counter points to the windrivwen but I dont believe he is interested in why heart disease is not solved by statins. We have to be careful about dogma because it blinds us and makes ourselves the easiest to fool. There are many doctors who do nto recommend plant based diets because they understand endocrinology and evolutionary based medicine. You can not have a perfectly functioning brain or thyroid eating like a rabbit. The extensive work of Stephen Cunnane, Michael Crawford and Remko Kuipers hammers that current biologic myth away. We must all become aware of what we dont know. That is where the truth often lies. Statins do not improve lifespan and do not cure heart disease therefore this makes them fair game to be examined. The data on both sides needs to be weighed. I have weighed them myself and I do nto believe the AHA ACA or Dr. Nissen beliefs are the beliefs we should apply to the masses.

    1. Harriet Hall says:

      “Statins do not improve lifespan ”
      We have clear evidence that they do.

      1. windriven says:

        I don’t think that Dr. Jack is much interested in evidence. He has never offered any himself. Innuendo is more his style.

        1. Jack Kruse says:

          Extraordinary claims require extraordinary evidence. Statins and their supporters have made those claims. Dr. Nissen the leader of the pack……..and the evidence is just not there. And no the evidence is not good that they save lives. That is a belief some have, based upon very circumstantial evidence, much of what is tainted by shoddy research.
          http://www.bmj.com/content/347/bmj.f6900?ijkey=TpaKlRN20axHgvv&keytype=ref

          1. Sawyer says:

            How many times do we have to explain this? What’s required to change the minds of most regular readers here is a careful, nuanced, scientifically supported critique of the new statin guidelines. NOT an over the top editorial. NOT a link to a crank site. NOT vague complaints about marketing or corruption. All that you’ve shown us is that BMJ has pretty weak criteria for publishing an opinion piece.

            The irony is that originally I would have had no problem accepting good arguments against the new recommendations, but all you’ve done is pushed me closer to Dr. Hall’s interpretation.

            1. Self Skeptic says:

              Sawyer said, “What’s required to change the minds of most regular readers here is a careful, nuanced, scientifically supported critique of the new statin guidelines…
              NOT vague complaints about marketing or corruption…”

              {Note to newbies: I’m a scientist, and I don’t use CAM.}

              Sawyer, even though your post wasn’t directed at me, I’ll articulate my thoughts on this matter.

              I don’t think regular readers here have the patience, or the flexibility, for such careful critiques. The bias toward believing in allexpert guidelines (which admittedly makes the practice of medicine faster, simpler, and legally safer) is so strong, that even mainstream critiques are automatically discounted. To a scientist in a more rigorous field, this bias looks like a self-protective belief system, rather than a commitment to science and reason.

              I offered details as to why I suspect that side effects of statins are not being adequately appreciated, in addition to the possible overestimation of benefits in lower-risk population groups.
              See the long thread following comment #24, which thread turned into a discussion on the statin guidelines. Comment #24 itself was by the unpopular FastBuckArtist, so ignore that comment, to prevent bias) here:
              http://www.sciencebasedmedicine.org/irritated-by-the-skeptical-inquirer-again/

              I cited a few respectable books that provide the background needed, to understand how the common drug company practice of stacking the medical literature in favor of their drugs, is compromising medicine’s science base. I’ll cite them again, as you didn’t seem to note them the first time around. There’s nothing “vague” about them:

              Quoting my own post above:

              “The following books, from highly respected medical publishing experts, provide detailed information on why the medical literature, unfortunately, can’t be taken at face value, as “the best information current science can provide.” They also address how RTCs, systematic reviews, and clinical guidelines produced by panels of experts, are compromised by this problem:

              “Former NEJM editor Kassirer, “On the Take”.
              Former NEJM editor Angell, “The Truth About the Drug Companies”
              Popular skeptic author Ben Goldacre, MD “Bad Pharma.”

              “There is also a new entry I have on Kindle, but haven’t read yet.
              I apologize for having to cite a book with such an inflammatory title; but coming from the director of the Nordic Cochrane Center, and with forewords by Richard Smith of BMJ and Drummond Rennie of JAMA, I think it merits our attention:

              “Cochrane leader Peter Gotzsche, MD “Deadly Medicines and Organised Crime: How Big Pharma Has Corrupted Medicine.”
              [end quote]

              People interested in science-based medicine, (in the literal sense, rather than the selective anti-CAM sense) should have assimilated this evidence long ago. It almost looks as if people here simply can’t take it in, and give it proper weight, in their judgments of what is likely to be true in medicine, and what has been affected by marketing hype disguised as science (which has been unwittingly absorbed into both experts’ and practitioners’ knowledge base as if it were proven fact).

              It’s bad news, but ignoring it won’t make it go away. Until the regular readers (and bloggers) here understand the full implications of this, they’ll be operating in a bubble of unwarranted faith in authority.

              Okay, I’m off to celebrate. I wish you all a very happy Thanksgiving!

              1. windriven says:

                “I don’t think regular readers here have the patience, or the flexibility, for such careful critiques.”

                On what possible grounds do you make this claim? I have no idea what the composition of the readership here is and neither do you. But I can tell you that a large fraction of the commenters appear to be quite well educated and many claim to be scientists themselves.

                Moreover, as an educational resource it is important that even casual readers come to understand that medicine isn’t House or Gray’s Anatomy. Pushing back the frontiers of knowledge is a careful, meticulous process often moving two steps forward and one step back. But look what this process has accomplished in the last hundred years!
                To a scientist in a more rigorous field, this bias looks like a self-protective belief system, rather than a commitment to science and reason.

                “To a scientist in a more rigorous field, this bias looks like a self-protective belief system, rather than a commitment to science and reason.”

                This betrays your disrespect for the ethics of medical science. When new modalities are used they have direct and often profound effects on people’s lives. A hundred and fifty years ago what passed for medicine sometimes treated waning libido with the transplantation of goat testicles into men … with often fatal results. Yes, medicine is much more cautious than physics or chemistry where an experiment gone bad just means a bad day at the office.

                Finally, you roll out the same bunch of books that we all know about. This is old news – not just yesterday’s news but really old news. That is why there is always the demand for “careful, nuanced, scientifically supported arguments.”

                You and stan and Dr. Jack seem to have a comic book appreciation of scientific research: Snidely Whiplash in the executive suite directing a battalion of MD, PhDs falsifying data while the rest of the medical and scientific establishment sits like rubes on the porch of the general store saying, ‘well gollee.’ The manipulation by the drug companies is at once more subtle and more troubling as it inevitably slows medical progress as the chaff is sorted from the wheat.

                Which brings us (mercifully) back to statins and the end of this comment. Perhaps you believe that all of the data (except, of course the data supporting your view) is falsified. Forty-odd years of carefully managed deception culminating in the current pay-off of the American College of Cardiology so that Pfizer or somebody can sell more 10 cent pills. If so I think you should read Jesse Ventura’s new book blowing the lid off the Kennedy assassination cover-up and The Protocols of the Elder’s of Zion so that you can get a deeper understanding of the Jew and his manipulation of … everything.

              2. Harriet Hall says:

                @SelfSkeptic: Do you imagine that all the experts in their fields are unaware of Big Pharma influence and don’t take it into account? If you think all the research is falsified, where does that leave you? Do you just reject all pharmaceuticals, or do you have some better approach?

              3. vadaisy says:

                I don’t think regular readers here have the patience, or the flexibility, for such careful critiques.

                To a scientist in a more rigorous field, this bias looks like a self-protective belief system, rather than a commitment to science and reason.

                It almost looks as if people here simply can’t take it in, and give it proper weight, in their judgments of what is likely to be true in medicine, and what has been affected by marketing hype disguised as science (which has been unwittingly absorbed into both experts’ and practitioners’ knowledge base as if it were proven fact).

                Until the regular readers (and bloggers) here understand the full implications of this, they’ll be operating in a bubble of unwarranted faith in authority. Okay, I’m off to celebrate.

                Oh, no! Don’t go. How will we be able to think for ourselves if you take a few days off? Exactly what type of science do you practice that is more sciencey than a physicist, or more medically astute and experienced than an infectious disease physician with over a quarter of a century (sorry, Dr. Crislip) of direct patient and research experience? Goodness! You must must know everything. Oh, so impressive. We bow to your wisdom.

            2. Self Skeptic says:

              Harriet Hall says:
              November 28, 2013 at 12:30 pm
              @SelfSkeptic: Do you imagine that all the experts in their fields are unaware of Big Pharma influence and don’t take it into account? If you think all the research is falsified, where does that leave you? Do you just reject all pharmaceuticals, or do you have some better approach?

              Dr. Hall,
              I’m going to assume that these aren’t rhetorical questions, and try to answer them. I’ll break it up into a few separate posts, to keep it from getting too long. You obviously think I’m making extraordinary claims, so I’ll have to explain at length, why I think we should apply critical thinking to claims of expert consensus such as guidelines, rather than accepting them uncritically, as you recommend.

              @Andres’ post summarizing the various clinical trials was a great, short but information-packed summary, of one way to look at the statin issue. It’s not the way I tend to think, but I like it, when it’s applicable. And I think it is, here. I’ll try to learn from him, in my future writing about guidelines like these, that are based on a small collection of RCTs. This seems like an effective way of communicating with busy MDs.

              Dr. Hall said:
              “Do you just reject all pharmaceuticals, or do you have some better approach?”

              That’s a two-part question. The first is simple, the second is complex.

              I take levothyroxine. I’m not anti-drug. I’m just careful about which drugs I choose to take, because of my awareness of marketing. The value of treating hypothyroidism is undisputed, though the details of exactly how, in patients who don’t respond well, using the conventional recommendations, can be debated. The conventional treatment has been adequate, in my case.

              The thyroid guidelines, which changed in 2010, are another interesting case to study. In this case, my judgment is that the experts who wrote the AACE-sponsored guidelines were right, when they lowered the threshhold for treatment from a TSH level of 5.0 to 3.0. There was no large public outcry like we’re seeing with statins, about this, even though it increased the number of treated patients considerably. But that’s another topic that requires detailed examination, before it can be discussed intelligently.

              See following posts for some thoughts about “a better approach.”

              1. Harriet Hall says:

                “rather than accepting them uncritically, as you recommend”

                I don’t recommend doing anything uncritically. I recommend using good judgment before rejecting the consensus of experts in favor of something that may very well be worse.

                “my judgment is that the experts who wrote the AACE-sponsored guidelines were right”

                What hubris! Who are you to judge which experts are right about which guidelines?

                “I take levothyroxine.”

                You are inconsistent. How do you know the research on prescription thyroxine wasn’t biased? Maybe the drug companies distorted the evidence so they could sell their product and put the producers of natural desiccated thyroid extract out of business. Ah, yes, you know because your judgment is infallible and is better than that of the experts! And just possibly because you need to believe their product will help you.

            3. Self Skeptic says:

              Dr. Hall said, “If you think all the research is falsified, where does that leave you?”

              I don’t think it is all falsified. Some of it is scrupulously reported and appropriately, modestly interpreted. Some of it is falsified; some makes unwarranted generalizations based on too limited evidence; some is in the category of “placeholder fiction;” some is repetition of received wisdom dressed up to look like science using questionable numbers, graphs, and statistics; some is a product of “least publishable unit” calculation by struggling academics; some is the elaboration of a political skillful academic’s pet hypothesis that has caught on; etc.

              Peer review isn’t working well enough, in keeping quality high. One could argue that this quality-control problem is coming to crisis point, considering the burden of the medical profession/industry on the US economy (approaching 20% of GDP), coupled with the fact that so much of the medical literature is easily searchable and readable on the internet, where its flaws can be seen and exposed by those not biased toward ignoring them.

              Where all this leaves me, is willing to do some detailed digging into the primary and secondary literature of a field, to evaluate whether it has any gaping holes, or obvious fictions, that have affected it. I also leaves me indignant that I have to sort this out for myself, and concerned about patients and primary care doctors, whose skill sets don’t prepare them for doing this kind of investigation. Even with the skills, no one person has the time to evaluate every field relevant to primary care, to this depth. One could call this the GP’s Dilemma. I’m a professional researcher in a medically relevant field, which gives me a head start. I know some skeptical doctors, and some smart patients in unrelated professions, who have learned to do it well, and we can all share our acquired knowledge. But obviously, most people don’t have the tools to investigate a disease field. They can witness what happens to them or their families or patients, but not deconstruct faulty science that has gone mainstream.

              1. Andrey Pavlov says:

                The difference, SS, is that while we recognize the issues we don’t have the audacity and hubris to think we can somehow sift through it to come up with a better answer. You are not fundamentally wrong in some of your assessments of the medical literature which is why I am a member of the AllTrials campaign from Ben Goldacre. We here work to demonstrate false studies are being false.

                But the mistake you make is that you can somehow transcend the built in limitations to the literature – limitations we all know and work within – when nobody else can. Your only other possible statement could be that you think the expert groups – groups with unequivocally more expertise in analyzing these sorts of things and vastly more experiential context than you – simply can’t do their job as well as you can. And that is downright ridiculous hubris.

            4. Self Skeptic says:

              Continuing my answers to Dr. Hall’s three original questions to me:

              Dr. Hall said,
              …or do you have some better approach?

              I think all cases of medical controversy have to be assessed independently. Each has its own history and cast of characters, which needs to be appreciated. There is no litmus paper one can dip in, and get an instant answer. I might take a stab at suggesting a first step, since you asked; see my final post in this series. (You do recall that I’m a scientist, I hope. I’ve been successful in discovery, and am regarded as an expert myself, in my field. So it doesn’t seem unreasonable, on the face of it, for a senior scientist to offer suggestions to a senior doctor, at a site called Science-Based Medicine.)

              My reason for participating at this site is to understand why the medical community isn’t detecting and debunking misleading papers, particularly those published by prestigious experts. Peer review is not succeeding, either pre- or post-publication. (Why not? It’s obviously some kind of systemic, cultural problem.

              Perhaps it’s a combination of the excessive deference that Des Spence described in the BMJ, and a willing suspension of critical thinking, just to impose some order on the cacophony of information we have. When you include individual patient differences, it must be truly overwhelming, especially for GPs. That is a real problem, with no easy answer. But what kind of simplifying technique to use, is open to debate. The retreat into simple obedience to authority is a time honored approach in medicine, which you are clearly advocating. But it’s an affront to us practicing scientists, to advocate mere obedience while pretending you’re committed to science, which requires investigation and independent thinking. The name of this authoritarian site is rather insulting, to people who are actually engaged in science.

              Fortunately, most sub-fields of medicine do seem to have a little cadre of skeptical doctors, challenging the status quo with probing questions, and publishing their critiques in journals, or online, or both. Some are right, and some are wrong; all these arguments have to be critically evaluated. I don’t automatically believe anyone, even if I respect him or her. For instance, I think David Healy has raised some good points about psychiatry and big pharma…but I know too many people helped by SSRIs to view them as dimly as he does. Similarly,I have some differences of opinion and emphasis, with Peter Gotzsche, Jerome Groopman, Atul Gawande, Ben Goldacre, etc, although I respect and admire them. If I agreed with any of them completely, someone should snap their fingers in front of my eyes, and tell me to wake up. Hypnosis is dangerous.

              Next up: thoughts about how to evaluate critiques offered by dissenters.

              1. Harriet Hall says:

                The medical community IS constantly challenging papers. I agree that the peer review system is not working as well as it should, but faulty studies are eventually identified and rejected, or supplanted by better quality studies with different conclusions. As an example, the Seralini GMO corn study was critiqued by two SBM editors along with many others, and it is now being retracted.

                We are not “retreating into simple obedience to authority.” We are, however, respecting the conclusions of whole groups of experts who are working together, agree with each other, and know more about the subject than we do. I’m sorry if you can’t see the difference.

          2. weing says:

            That BMJ reference is a book review. From the author of the book:

            “My book is not about the well-known benefits of drugs such as our great successes with treating infections, heart diseases, some cancers, and hormone deficiencies like type 1 diabetes.”

          3. windriven says:

            This is it, Jack? A book review? Man, you sure know how to deliver a high-powered argument.

            Everyone here knows that Pharma twists science to its purposes. It is is as if you were standing on a street corner bellowing that politicians lie. Well no kidding. Shall we nominate you for a Nobel?

            If you had the integrity to read a bit in these pages before wading in to clear the eyes of the blind you would know how critically new research is received here. But this isn’t new research, Jack. Statins have been studied for decades. The benefits to at risk populations is now well beyond dispute.

            Pharma spin is one thing. Scientific fraud is another. It happens. But it is rare. People who spend a lifetime building their credentials don’t often risk them for a few pieces of silver.

            We’ve pointed out that the fevered belief that Big Pharma manipulated the ACC to promote statin use doesn’t make even a lick of sense as statins are now trivially inexpensive.

            And still, doctor Jack, you are happy to emit a miasma of innuendo, never bothering to state a position and argue it. Do you lack the intellectual tools or do you already know that your argument is specious? Pretty pathetic either way, don’t you think?

            1. Interested party says:

              Windriven, you sure are vitriolic. I personally found what jack and Self Skeptic has to say was wise and well referenced.

              Have you ever read a research report and tried to follow it through to determine whether the conclusions reported were consistent with the results? Did you ever see clinical report that included only the results that were favorable to their cause and ignored results that would have cast doubt on the conclusions? What about reports that clearly simply misrepresented the data or ignored data that should have been inlcuded? All of this stuff happens, and it is not hubris to be skeptical. It is wise. Recently I came across Dr. John Ionannidis

              http://publications.mcgill.ca/reporter/2013/10/john-ioannidis-on-flawed-research-separating-the-wheat-from-the-chaff/

              who says that about 50% of the published research reports and flawed and many are junk.

              You would be wise to be skeptical.

              1. Harriet Hall says:

                Ioannidis recommended caution; he didn’t recommend distrusting all research, and he gave some guidelines to help readers determine which studies are more likely to have correct results. We never rely on a single study, but when evidence from many studies is coherent in supporting a hypothesis, we can be reassured that we’re on the right track. Skepticism is indeed wise; but denialism is foolish. Despite all its flaws, SCIENCE WORKS.

              2. weing says:

                @Interested party,

                “Recently I came across Dr. John Ionannidis”

                Type in “Ioannidis”in the search box on the right near the top of this website. I don’t mean to intimidate you, but you spelled his name wrong.

              3. windriven says:

                @interested

                My vitriol is saved for the vapid and the inane: trolls, delusionals, wooly thinkers and the like. They litter these pages with idiocy and do not advance the conversation a centimeter.

                Neither Jack nor Selfie has articulated a carefully thought out alternate position and supported that position with quality citations. Saying what one doesn’t like or doesn’t think is true is not enough.

                The link between cholesterol and CVD is clear and has been for some time. We can have reasoned debates about which populations are most likely to benefit from statin therapy, we can have reasoned debates about statin ADRs and their relative frequency in given populations, we can even have wonderful and illuminating conversations about whether cholesterol is a primary cause or simply a marker for elevated risk.

                But comments that amount to nothing more than (Mr. Mackey voice:) “statins are, ummm, bad” doesn’t cut it with me. ABC news reports and newspaper editorials as sources of medical information don’t cut it either.

                Ioannidis is a well revered figure here as Dr. Hall and weing suggest. But my reading of Ioannidis does’t suggest that studies I agree with are good and studies that I don’t agree with are bad.

                Jack or Selfie or you or me can always cherry pick a study or two that will ‘prove’ that the moon is made of well-aged Stilton cheese. That is why consensus reports by well respected panels of experts who are conversant with the broad scope of research in a given area are so important. It doesn’t mean that their consensus opinion is perfect. It means that it is the best that the state-of-the-art can offer at the moment. And it sure as heck doesn’t mean that Jack or Selfie or Antonio has a better one.

                Scientific ignorami who appear here to set the world straight because they don’t like the consensus or they don’t like BigPharma or they don’t like ‘allopathic’ medicine, who cherry pick, who spread fog and darkness instead of offering reasoned arguments are a plague.

                Vitriolic? Maybe. But I offer no apologies.

      2. john umiastowski says:

        Harriet, would you please provide some source that substatiates your statement that Statins prolong life? I have done a lot of searching on the web and have not found a single reliable report that would support your statement.

        Also, in a earlier comment, you stated that high cholesterol levels are a marker for heart disease risk. Could you please provide a source for that? I have not found any reliable study that supports your statement.

        1. Harriet Hall says:

          See my 4:54 comment for substantiation that statins prolong life.

          High cholesterol levels are clearly correlated with heart disease risk for those under 75. We have known this since the first reports from the Framingham study started to come in.
          See http://jama.jamanetwork.com/article.aspx?articleid=365739
          The association of cholesterol and CVD risk is less certain over the age of 75. Some studies have even shown an inverse correlation, but that could be related to recent decreases in cholesterol due to illness and poor nutrition. Some studies have shown a clear benefit of statins in the elderly http://www.ncbi.nlm.nih.gov/pubmed/18174034?ordinalpos=13&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
          That was for secondary prevention and had a NNT of 28.

          Available data are insufficient to quantify risks for those over 75. That’s why the new guidelines did not make recommendations for primary prevention in that age group and stressed that decisions in the elderly should be individualized.

          1. John umiastowski says:

            Harriet, the Framingham report you referenced is a prospective study, mining of data collected from questionnaires filled out by test subjects every 2 or 4 years. Such a study will only show ASSOCIATIONS or correlations, and not causality. So, yes, there may be an association between cholesterol levels and heart disease, but so what? Maybe heart disease is caused by too much insulin in the circulation for too long caused by too much sugar or carbohydrate in the diet. Maybe LDL cholesterol is part of nature’s repair mechanism to combat coronary damage. Where is the evidence that suggests that cholesterol in the blood should be reduced? Scientific research should include the forming of an hypothesis and then testing the validity of that hypothesis. Framingham does not do this, so the associations that are discovered are not very helpful. In fact, such research is about as helpful as measuring the level of crime in a city and correlating this level with the size of the police force. I guess there might be a strong correlation, but what does that prove? It certainly doesn’t prove that high crime rates are caused by a large number of police. Where is the attempt at understanding the true cause of heart disease? I have seen several theories attempt to model the chemistry behind heart disease but to my knowledge no research to test such models has been done. Therefore, I have to conclude that there is NO evidence that reducing cholesterol through drug treatment or even through diet is a noble and worthwhile objective and no amount of association studies will ever change that. Furthermore, given the severe and debilitating side effects (muscle weakness and memory deterioration) of statins, and the truly nearly insignificant level of mortality improvements evident in a lot of trials (it should take only one such trial to debunk a hypothesis), I just can’t understand why any medical practitioner would prescribe such drugs to his or her patients.
            It is interesting that in the last paragraph of the abstract of this Framingham based report there is the following:
            “Under age 50 years these data suggest that having a very low cholesterol level improves longevity. After age 50 years the association of mortality with cholesterol values is confounded by people whose cholesterol levels are falling—perhaps due to diseases predisposing to death.”
            To those who believe in the cholesterol theory of heart disease, why would falling cholesterol levels after age 50 be a confounding factor? Isn’t the objective to lower LDL levels? So it seems that after age 50, a falling level is something that doesn’t seem to fit with the trend. I wonder why that would be?

            Regarding the statin report, I was unable to obtain the full text to see which research reports were included in the meta-analysis. However, I was able to review a report from 2002 entitled “Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial.
            http://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&Cmd=ShowDetailView&TermToSearch=12457784&ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

            Perhaps this was one of the studies included in the meta-analysis which you referenced in your reply.

            The abstract of this above referenced study suggests that the results were really positive. However, in digging into the actual data, we find that there were 2913 patients in the placebo group. A total of 306 died during their 3 years of not taking a statin, or 10.5% died. In the treatment group there were 2891 patients and 298 died, that’s 10.3%. This is hardly stellar performance and begs the question “why did the abstract fail to highlight this fact”

            So forgive me for being sceptical, but after reading books like “BAD PHARMA” by Ben Goldacre, I really don’t accept drug testing studies or even nutritional studies at face value. In the case of Nutitional research studies, I have seen many cases where the intent to mislead or downplay non-supportive results was present.

            If you have the full text of the meta-analysis, or if you can direct me to a source where I could download it for free, I would really love to read it.

            1. interested party says:

              Windriven, you say
              “we can even have wonderful and illuminating conversations about whether cholesterol is a primary cause or simply a marker for elevated risk.”
              Does it make all the difference if cholesterol is just a marker? Should you be killing the messenger? It seems to me that that is what statins do.

              1. interested party says:

                Sorry, I meant to say “Does it not make all the difference…..

              2. Andrey Pavlov says:

                It would, if all we relied upon was the presupposition of causality. The reality though is that we have evidence that not only does increased cholesterol correlate with increased cardiovascular events, but decreased cholesterol correlates with decreased cardiovascular events. We also have data that statins themselves lead to decreased cardiovascular events so even if cholesterol had nothing to do with it at all, statins would still have a demonstrated mortality benefit even if the mechanism was not known. And in fact, there is such a benefit since we find that there is mortality benefit from statins that is independent from and cannot fully be explained by their cholesterol lowering effects in stroke patients – regardless of whether they are hemorrhagic or ischemic – which is posited to come from some general anti-inflammatory effect of statins (either directly or indirectly by lowering the LDL burden which decreases the total level of atheromatous plaques which are themselves foci of inflammation, as separately evidenced by the generally increase CRP levels in people with atherosclerotic disease).

                In other words, a perfect causation we do not have, but numerous lines of correlation combined with what evidence of causation we do have (a much more detailed molecular understanding of atheroma formation, maturation, and rupture) establish quite well that cholesterol does indeed lead to increased atherosclerotic disease which in turns leads to cardiovascular events. Statins directly and indirectly mitigate this risk.

                Of course, it isn’t that LDL in and of itself causes all these problems, it is the complex interactions of LDL with apolipoproteins and the vessel walls plus the immune system which combined lead to adverse cardiovascular outcomes. Which is precisely why it is not a perfect correlation between cholesterol and CVS disease/events and why the new guidelines make even more sense than the previous ones.

              3. windriven says:

                Killing the messenger? How?

                That there is a relationship between cholesterol and CVD is clear but the relationship is not yet well understood. Statins reduce cholesterol and reduce CVD in some populations. It will be interesting to tease out the biology of what is actually going on. In the meantime we go with what we have … cautiously.

                I’m not clear where you are trying to go with the “Does it not make all the difference…..” theme. It makes a difference. It doesn’t make all the difference.

                Let’s say – and I’m just making this up now – that plaques are a response to inflammatory processes in arterial structures. Statins reduce cholesterol. They also seem to mediate inflammatory processes – at least some of them. It will be very illuminating to understand the details and will undoubtedly lead to better therapies. In the meantime, statins help, so…..

                Medicine understands quite a lot about quite a few things but everything about almost nothing. That does not mean that medicine is useless or that working with what is known today should be shelved until we know what we will know tomorrow. It is the very, very, very best that we can do to help our fellow beings… today. And it is a hell of a lot more than we knew yesterday.

                It is important to be skeptical but there is are huge differences between skepticism and cynicism, skepticism and denialism and epistemology lies at the heart. That is why a thorough understanding of the scientific method and of the measures of uncertainty that attend it are essential. That is also why I get cranky when commenters present with potshots or ill-formed arguments. It is probably a character defect but I can’t seem to master it. Andrey and WLU are much more patient. I envy them their equanimity.

            2. weing says:

              “I just can’t understand why any medical practitioner would prescribe such drugs to his or her patients.”

              That is a failing on your part. Maybe you need to go through medical school and training to find out why. It’s interesting that you knock down association studies when it comes to cholesterol playing role in causing heart disease but you have no problem accepting associations of side effects with statins as the cause of the side effects.

            3. Harriet Hall says:

              I only mentioned Framingham because it was the first of many studies showing a correlation. I have also supplied a list of other better, more recent citations. It’s not just that there is a correlation between LDL and CV events: there is a reduction of risk when patients are taking statins and when their LDL level goes down. The panel was aware of all the studies and of the kind of concerns you bring up; they took all those things into consideration when making the new recommendations.

              “To those who believe in the cholesterol theory of heart disease, why would falling cholesterol levels after age 50 be a confounding factor? Isn’t the objective to lower LDL levels? So it seems that after age 50, a falling level is something that doesn’t seem to fit with the trend. I wonder why that would be?”

              Older people are more likely to have cancer or other severe chronic illness, and can be relatively malnourished, and blood cholesterol levels drop in consequence. In their case, the lower cholesterol is a marker for chronic illness. Their other medical problems increase their risk of death more than the lower LDL decreases it. Again, as the recommendations state, it is important to look at all the available information about the patient that might tend to raise or lower CV risk and/or the risk/benefit ratio for statins before deciding to prescribe it. The recommendations are not a cookbook, and they do not make any recommendations for older patients.

      3. Pharmacist permanently harmed by lipitor says:

        I have been looking for that evidence for several years, where did you find It? I keep finding the opposite.

    2. WilliamLawrenceUtridge says:

      The clearest way to attack dogma is with evidence. That’s what the panel reviewed. What did they miss?

      Stephen Cunnane is a proponent of the aquatic ape hypothesis, and that fish is absolutely necessary for human flourishing. This is despite the existence of developmentally normal humans who live far from any water and eat virtually no fish. The aquatic ape hypothesis is a biologic myth.

      If statins do not improve lifespan, why did the panel reach that conclusion?

      1. Andrés says:

        WLU said:

        Stephen Cunnane is a proponent of the aquatic ape hypothesis, and that fish is absolutely necessary for human flourishing. This is despite the existence of developmentally normal humans who live far from any water and eat virtually no fish. The aquatic ape hypothesis is a biologic myth.

        I have only read a short piece by Cunnane but I got the impression that the hypothesis is more about kickstarting our brain evolution through seafood and seaweed than mantaining it once we were capable of hunting and eating our prays’ brains.

        Certainly it is not a myth when it has supporting evidence such as our wrinkly fingers to grasp wet objects.

        1. windriven says:

          “Certainly it is not a myth when it has supporting evidence such as our wrinkly fingers to grasp wet objects.”

          Supporting evidence??? That is a leap over the Grand Canyon on a unicycle.

          You can find a comprehensive takedown here of the whole aquatic ape nonsense.

        2. Andrés says:

          windriven said:

          Supporting evidence??? That is a leap over the Grand Canyon on a unicycle.

          You haven’t read the link to the wrinkly fingers experiment, have you? It points to a 2013 paper. I don’t know how you hope that a 1997 debunking critique paper (I have read it: no falsifying data apart of narrowing the possible time window of when it happened) was going to deal with newer evidence.

        3. Sawyer says:

          It is generally not a good idea to bump old discussions unless there’s new research that is relevant to the topic. It’s really not a good idea to bump old discussions by claiming that the aquatic ape theory is good science.

          Too bad. You probably had a few people here that were marginally interested in your viewpoints on vitamin supplements until they see this post.

        4. windriven says:

          @Andres

          I certainly did read the wrinkly fingers link. I would be the first to agree that it reports an interesting finding. But suggesting that it demonstrates or supports the aquatic ape idea is,as I said, a monumental leap.

        5. Andrés says:

          @windriven: I don’t think of the aquatic ape hypothesis in terms of demonstration but in falsification à la Popper so I don’t think about demonstrating the hypothesis but in falsifying it. All the arguments against the aquatic ape hypothesis in the paper pointed out by you is concerned about parsimonious explanation of human evolution. Parsimonious terrestrial evolution is almost* falsified by our wrinkly fingers characteristic.

          * Since we share that characteristic with macaques it is important to pinpoint if it has been convergent evolution or simply we share a common ancestor with such a characteristic. I don’t know if chimpanzee (or any other ape) has been check for wrinkly fingers when wet.

          1. windriven says:

            @Andres

            It struck me when reading ‘wrinkly fingers’ that the wrinkling could be a consequence of a totally unrelated adaptation. For instance humans have thin, highly enervated skin on their fingers. Is wrinkling when wet a consequence of this? I don’t know.

            Also, it appears that humans, macaques and chimpanzees evolved from a common ancestor – yet chimpanzees do not, as I understand it, share the wrinkly fingers characteristic. Of course that does not mean that other and different evolutionary pressures on pan troglodytes didn’t erase the wrinkly fingers trait but …

            In any event, it was an interesting piece. Thanks for linking it.

            1. Andrés says:

              You’re welcome.

  30. Dave says:

    I should ne more clear. By plant based I mean a diet containing a wide variety of vegetables and fruit, I do not mean excluding meat totally. I believe evidence suggests the Mediterranean diet is beneficial for heart disease. There are so many confounding factors when one looks at diets that it’s hard to make iron-clad statements.

    1. Self Skeptic says:

      Yes, I agree. Mediterranean seems good (and most tasty, IMO). I’m hypothyroid, and I’ve been told to not eat a few things, like soy and flax, to excess. And then of course there are all the individual allergies and genetic intolerances, like lactose, peanuts, shellfish, wheat…

      People who are thriving on sugar and other junk food tend to think concerns about diet are silly. But once someone intelligent gets sick, and stays that way, usually they will tinker with their diets almost obsessively, at least for a while, in an effort to feel better. That seems like common sense, to me.

      I doubt there is a one-size-fits-all diet, especially for a heterogeneous group like Americans.

        1. windriven says:

          Thanks weing! I feel better about the 18 jillion calories I’m going to ingest over the next couple of hours.

          1. Self Skeptic says:

            :) Good one, Weing. If not for Windriven’s comment I wouldn’t have gotten it, I’m afraid.

            Time to go eat some more leftovers. I just restocked whipped cream (“light”, of course) to enhance the pumpkin pudding (no crust, much healthier). Turkey korma…well, I have no excuse.

        2. agitato says:

          Weing: The first study abstract states that 65% of the 902 patients were over 65 but it doesn’t state what percentage over 65 each category was. Could it be that many of the obese patients were simply younger and that (not obesity) led to a better outcome? But surely, if I’ve thought of that, a statistician would have too.

          The second one speaks of a multivariate analysis which may have included age but it isn’t stated.

          I just don’t want to believe that a BMI of > 30 can ever be protective of anything.

          1. weing says:

            @agitato,

            I think age played a role too. But it doesn’t explain the difference between the 18.5-25 BMI category and the 25-30 as the ages did not differ significantly here, being 69 +-19 and 16, respectively in the Kahlon study. The signal also became stronger when nursing home patients were excluded. Live and learn.

  31. MarilynMann says:

    Dr. Hall, thanks for this summary. Dr. Krumholz has written an editorial on the guidelines that was just published in BMJ:

    http://www.bmj.com/content/347/bmj.f7110

    I thought your readers might also be interested in the background on the shift away from LDL targets. I have summarized it in this blog post:

    http://marilynmann.wordpress.com/2012/01/28/hayward-and-krumholz-open-letter-to-the-adult-treatment-panel-iv-of-the-national-institutes-of-health/

    Marilyn Mann

  32. Pooled Cohort says:

    If anyone is interested in calculating their own risk using the Pooled Cohort Equations, I found a good online calculator for it.

    http://www.advcardiologyassoc.com/pooledcohort.htm

  33. Jack Kruse says:

    http://www.bmj.com/content/347/bmj.f6900?ijkey=TpaKlRN20axHgvv&keytype=ref

    Seem others think the ties between big pharma and medicine are a big deal.

    1. charles grashow says:

      Are you the same Dr Kruse who claims he had elective surgery without anesthesia and that he injected himself with MRSA too??

      WOO WOO WOO

      1. windriven says:

        Link us Charles! If this is true it is just too delicious.

        1. charles grashow says:

          http://paleohacks.com/questions/127986/what-are-your-thoughts-on-the-jack-krusequilt-tedx.html#axzz2lzixgbJv

          “He goes on to say that his idea was to do the first “Evolutionarily Directed” surgery. Nodoby would let him do this to someone else – inject bacteria and avoid anesthesia. The secret pathway tells us we have ultimate immunity.

          He decided he had to “make” himself a surgical candidate. So, he had some sort of tummy tuck type surgery and “secretly” gained 25 lbs eating a SAD (PUFA + grains he says). It took 2 months to gain 25 lbs and nobody knew and he hid it.

          On Jan 8th he told his wife about this. The next day he had surgery without anesthesia. Before the surgery he injected MRSA all over his torso (he says it’s nasty stuff). He “woke up” and was in pain. His wife and daughter didn’t know what was going on and even his son at the time of taping didn’t know anything about this. His wife and daughter was ordered to get out a tub while he was sceaming and crying. He told her to get 120 lbs of ice from the freezer and in minutes the ice got rid of his pain. He even flaunted his incisions to his 11 year old daughter.

          He avoided infection and never had pain.”

          http://intoxicatedonlife.com/2012/04/23/fire-up-your-immune-system-the-benefits-of-cold-part-2/

          The often controversial Dr. Jack Kruse completed an astounding bio-hack on January 9, 2012. At the Nashville TEDx conference on March 31, 2012, he apprised the world of his extraordinary self-experiment. Dr. Kruse underwent an invasive elective surgery, but prior to undergoing this surgery he both injected and rubbed himself down with MRSA. MRSA, which causes thousands of deaths a year, is a bacteria which causes an infection resistant to many common antibiotics.

          After his surgery, Dr. Kruse buried himself in ice and never had any complications from infections after his surgery.

          1. charles grashow says:

            http://carbsanity.blogspot.com/2012/04/hof-wim-ania-and-pair-of-dimes.html

            At TEDx in Nashville he dropped the Kruse Missile. If he’s to be believed, Jack intentionally injected MRSA virus and underwent abdominal surgery (to remove intentionally gained fat) to test/prove that his CT would be effective in (a) preventing the infection from taking hold, and (b) managing post-op pain without drugs.

            http://freetheanimal.com/2012/04/jack-kruse-neurosurgeon-leptin-reset-and-cold-thermogenesis-controvery.html

            Jack just gave his talk at TEDx the other day in Nashville. The video should be available soon but I was able to see it, though not live as some others did. He’s also been blogging, leading up to this. But only at TED did he spill the beans that on Jan 9th of this year, he injected himself with a staph infection and had a plastic surgeon colleague remove abdominal fat he’d spent a few months gaining in anticipation of the surgery (he had to create a valid cause for the surgery…because your business is everybody’s fucking business). He did general anesthesia, no local, and no post-op meds. Instead, he went home and settled into a tub of ice for some hours.

            He claims he was screaming in pain prior to entry, but was pain free inside of minutes, has remained pain free, and the staff infection did not take hold. Of course, this wasn’t a one-off deal—he used cold thermogenesis (CT) as an exclusive alternative for his post operative recovery. He has since begun to use CT on patients who were inoperative, in order to rehabilitate them to a state where he could perform surgery (he tells one of those stories in his TED talk). I’m sure he’ll tell others in time.

            Let’s back up to January 9th, the day of his surgery. By coincidence, Jack had been trying to reach me for a few days, and after obligatory phone tag, I settled down to a glass of whiskey on the evening of January 9th and rang him up, having no idea of what was in store. He answered, and something seemed way off…as though he’d been shot and was lying in a puddle of his own blood, bleeding to death. Nope, it was worse. He’d been in 40ish degree water for some hours (under supervision) at that point. He told me all about what he was up to, swore me to secrecy and that was that. I made sure he was under supervision and was eating during the experiment, because he was intending for a long haul in the icy water.

            1. windriven says:

              There is no word that fits this better than insane.

      2. stanmrak says:

        When you don’t like the message, shoot the messenger.

        1. weing says:

          Stasiu,
          You talkin to me?

  34. Andrés says:

    I will try to find a population where I can feel being represented. I will focus on primary intervention trials on mostly healthy people from the Table in the CTT 2005 paper and MEGA and JUPITER added in the CTT 2010 one. My blood pressure is 104/75, TC 368, HDL 97 (not due to excessive alcohol ingestion, mind you), TG 96, fasting blood glucose 81mg/dl. TC/HDL=3.8. I gave up smoking almost 7 years ago.

    WOSCOPS (3.2% mortality in statin group versus 4.1% in control group): 44% current smokers, cholesterol (TC) 272±23mg/dl, HDL 44±10, triglycerides (TG) 163±70mg/dl, likely average TC/TG around 6.18. Nope.

    AFCAPS (0.46% mortality in statin group versus 0.44% in control group): lipid entrance criteria TC in 180-264mg/dl and HDL< 47mg/dl. Nope.

    ALLHAT-LLC (12.2% mortality in statin group versus 12.4% in control group): hypertensives. Nope.

    ASCOT-LLC (3.6% mortality in statin group versus 4.1% in control group): hypertensives. Nope.

    MEGA (2.4% mortality in statin group versus 3.6% in control group): 42% hypertensives, 21% diabetics. Nope.

    JUPITER (2.2% mortality in statin group versus 2.7% in control group): LDL<120mg/dl, C-reactive protein > 2mg/l (I have no idea what my C-RP value is), 41% with metabolic syndrome. Nope.

    Well, not being represented in any of these trials I am not compelled at all to follow any recommendation inspired by them. Moreover, I side with the NNT Group logic and not with the CTT one. I don’t think that lumping together both primary and secondary prevention data and talking only about relative risk reductions instead of absolute ones is meaningful. At least I have being unable to locate specific analysis of primary prevention by the CTT group (I am not alone). Yes, the only group that has all the data to do it.

    Once smoking and hypertension are taken out of the equation, cholesterol is not so a big factor in death by any cause. It has been known from quite a long time. From The Seven Countries Study: Addendum (it seems a trip through archive.org is needed now):

    Long-term prediction. The study was one of the first to examine the relationship between baseline characteristics during health and subsequent longevity, variously defined as survival for twenty-five years or to age 75 or 85. In this instance, cigarette smoking was the main contributor, with a major contribution also from blood pressure, but very little from serum cholesterol and body mass index.

    Since we all are going to die, I would prefer cardiac disease (two uncles, one heavy smoker and diabetic type II the other, and one grandmother, hypertensive; I’m not in a hurry, though) than cancer (mother, one grandfather and other grandmother).I’ll take my chances.

    1. Harriet Hall says:

      “cholesterol is not so big a factor”
      That’s exactly why the new guidelines focus on overall risk.

      ” I side with the NNT Group logic”
      The NNT analysis is by a single ER doc. Why do you think that would be more reasonable than the recommendations of a panel of experts in their field?

      “not being represented in any of these trials I am not compelled at all to follow any recommendation inspired by them”
      Of course you aren’t, and that’s why the guidelines say they are not meant to be used as a “cookbook” mandate, but that clinicians should take other individual patient factors into consideration. You are trying to do exactly what they recommend, but your doctor might be able to do it better.

      1. Antonio says:

        “… the new guidelines focus on …”
        and no responsibilities for the old ones -also made by experts “based-on-(wrong)-evidence”- with cholesterol as a big factor.

        “your doctor might be able to do it better”
        or might not.

        1. windriven says:

          So Antonio, do us all a favor and stop seeing doctors. When your appendix goes hot, when you start bleeding from the butt, when you come down with typhoid, whatever you do, don’t see a doctor.

          1. Antonio says:

            The issue is cholesterol and statins (old guidelines) or statins plus excel and discredit (new ones).
            In fact I DO have followed the indications of a doctor and got statins for five years. Now I don´t. Am I doing wrong?
            I don´t want your favor, keep it for your dog, I just want real science.
            But, as I said, nobody will take any responsibility for that. I know.

            1. windriven says:

              ” I just want real science.”

              No you don’t, you want glib answers.

              This is the way real science works. It gets refined. Sometimes guidelines change. Sometimes they are expanded. Sometimes they are narrowed.

              1. Harriet Hall says:

                The old guidelines were tweaked: the new guidelines are fundamentally similar. The new guidelines will also be changed as more evidence comes in. That leaves us with a choice: be guided by current guidelines, or ignore science and go wherever speculation leads you. I’ll take my chances with the current guidelines, however imperfect they may be.

    2. charles grashow says:

      What is your LDL-C, LDL-P or ApoB??

    3. Andrés says:

      Dr. Hall said:

      The NNT analysis is by a single ER doc. Why do you think that would be more reasonable than the recommendations of a panel of experts in their field?

      Because the document by the experts is not consistent. Let’s take a look at information relevant to my case.

      Excerpt from Section 1.4. Methodology and Evidence Review:

      No evidence was found that titration or combination drug therapy to achieve specific LDL–C or
      non-HDL–C levels or percent reduction improved ASCVD outcomes. Therefore, this guideline does not
      recommend their use as performance measures.

      Excerpt from Section 4.4. Primary Prevention in Adult ≥21 Years With LDL–C ≥190 mg/dL (my bold type):

      It is recognized that maximal statin therapy might not be adequate to lower LDL–C sufficiently to reduce ASCVD event risk in individuals with primary severe elevations of LDL–C. In addition to a maximally
      tolerated dose of statin, nonstatin cholesterol-lowering medications are often needed to lower LDL–C to
      acceptable levels
      in these individuals.

      So they come back to speak of LDL-C levels. I don’t know if they mean ezetimibe (comment by Dr. Briffa about three papers cited at the end) but it is named several times along the document. As far as I know ezetimibe has not been shown to improve hard outcomes (newer comment by Dr. Briffa of a paper cited at the end) at all. I see that Dr. Stone et alter at Table 4 (page 22) admit the evidence is only moderate (B) or inexistent (E, expert opinion) though. And if I haven’t read it wrong all stands on the CTT group conclusions. So let’s take a look at the CTT group methods.

      It would seem that since they have access to all the data of their trials that they have been looking for a dose-response in respect to LDL-lowering and negative-events in the pool of all the subjects of all the trials. That was my first impression when reading statements of theirs like (2005 paper):

      There was a 12% proportional reduction in all-cause mortality per mmol/L reduction in LDL
      cholesterol

      Well, it has not been done. Go take a look at Subsection Statistical analysis in Section Methods. They are simply getting the numbers from the averages/measures (weighted or not) of each trial. I find that to be somewhat deceiving and similar to an ecological fallacy. Perhaps those trials being done on heterogeneous populations grant not pooling all patients together, I don’t know. Nevertheless, on the stratified analysis in subpopulations they do it only for major vascular events (hypertensive or not and the like) not overall mortality and not for a healthy subpopulation.

      Dr. Hall said:

      You are trying to do exactly what they recommend, but your doctor might be able to do it better.

      I have good references of a doctor. I will consider going to him in the future. I am 45 years old now and I am not considering getting an Agatston calcium score before 50. Why a calcium score? It is the difference between population medicine and individual medicine. It is the difference between measuring risk factors and measuring (almost) the real thing. It is the difference between blindly trying to cure something and purposefully taking action driven by actual disease…. Well, I have to confess that I am in the blind group without any Agatston calcium score yet but I am applying several of the actions taken by the Track Your Plaque group (yes, a blog commenting his clinical experience). Why? Dr. Davis has been able to slow-progression/regress coronary plaque growth in his patients. If I ever get to measure my coronary calcium score I will likely accept a lower than 15% annual increment happily.

      Why I am not worried yet? From Importance of HDL cholesterol levels and the total/HDL cholesterol ratio as a risk factor for coronary heart disease in molecularly defined heterozygous familial hypercholesterolaemia:

      In our study, carried out in a familial hypercholesterolaemia group of similar age, sex distribution, body mass index, ACE DD genotype distribution, and LDL receptor null mutations distribution, we found that only low HDL cholesterol levels and high total/HDL cholesterol ratios are associated with coronary heart disease.

      In addition, Hausmann et al.[27] have shown by step-wise multiple regression analysis both in heterozygous familial hypercholesterolaemia and in familial combined hyperlipidaemia, that the strongest predictor of plaque burden in the left anterior descending coronary artery was the level of HDL cholesterol and the total/HDL cholesterol ratio. Sudhir et al.[28] have also demonstrated a strong association between plasma HDL cholesterol levels and coronary ectasia in heterozygous familial hypercholesterolaemia.

      Not that I have familial hypercholesterolaemia AFAIK, but my high HDL gives me some composure.

      What is it that I really don’t like of statins? First, their efficacy has not been proved in healthy people as further as I can see. I consider myself healthy. Second, their efficacy has been proved on secondary prevention with trials of not much more than five years. After five years of treatment you are on unexplored territory.

      Charles Grashow said:

      What is your LDL-C, LDL-P or ApoB??

      I don’t know. My Friedewald estimated LDL-C = CT-HDL-TG/5 = 252mg/dl. We don’t have available NMR profiling around here. Perhaps I will ask for ApoB on a second analysis next year near my annual checkup (they don’t measure it there).

      1. weing says:

        “Because the document by the experts is not consistent.” So it’s consistency you are looking for? Doesn’t matter if the data is right or wrong? That’s balsy.

        You are correct about section 4.4. It is poorly written and does need clarification. I take it to be descriptive of what has been the current practice. Could they be saying to add on something else if the LDL-C is down to 300 from 600? Ezetimibe? I don’t know, there is no data to support it. Is it like a Hail Mary pass?

      2. Harriet Hall says:

        IMHO the apparent “inconsistency” is not in the report itself, but only in your own interpretation.

        The Agatson calcium score is not what you think it is. The panel identified the risk factors that are most significant. Things like calcium scores and ApoB are only useful as additions to the individual decision-making process about statins when the risk is borderline. And there appears to be a better test of cardiac calcifications than Agatson: see http://www.sciencedirect.com/science/article/pii/S1934592510004739 The decision to get a cardiac calcium test should not be taken lightly. It involves exposure to radiation equivalent to 20-40 chest x-rays, and can give false positive and false negative results. For a discussion of the pros and cons, see http://www.webmd.com/heart-disease/should-i-have-a-coronary-calcium-scan-to-check-for-heart-disease#av2273

    4. Andrés says:

      Dr. Hall said:

      IMHO the apparent “inconsistency” is not in the report itself, but only in your own interpretation.

      IMHO we are seeing consensus at work. It is clearly inconsistent saying that LDL levels are not important and at the same time giving credence to the CTT’s analysis lumping together primary and secondary prevention over really independent ones trying to look at primary prevention alone pointed out rightly by Dr. Newman (I don’t know if he is the only author or not of that analysis neither consider it to be relevant) like that by Ray et alter over high risk subjects.

      Dr. Hall said:

      The Agatson calcium score is not what you think it is.

      The Agatston calcium score is not used the way it should. I see that the paper Progression of Coronary Artery Calcium and Risk of First Myocardial Infarction in Patients Receiving Cholesterol-Lowering Therapy is not cited at all. Ok! So I am not an expert at all like Dr. Stone et alter. Nevertheless there are cardiologists like Dr. Davis using the information attained that way to individualize treatment for his patients and improve their health. I much prefer the experiment-tank approach.

      Dr. Hall said:

      The panel identified the risk factors that are most significant. Things like calcium scores and ApoB are only useful as additions to the individual decision-making process about statins when the risk is borderline.

      The committee of experts is irreversibly focused on population medicine and is concerned only about not letting any potential beneficiary of statin therapy without treatment. Any new information that we get about refined risk factors is only applied to add more people to therapy never less. They don’t care about putting people not really at risk under chronic treatment with a xenobiotic substance. I suppose that it would not bring any difference incorporating Dr. Dayspring or Dr. Davis to the committee due to the consensus process itself so I prefer to decide for myself after reading those getting results and not following willful population thinking. I am not waiting to Dr. Davis’s refined-through-time approach being replicated on a (non-blinded) clinical trial when you can measure progress on you by yourself if you decide to.

      Dr. Hall said:

      And there appears to be a better test of cardiac calcifications than Agatson: see http://www.sciencedirect.com/science/article/pii/S1934592510004739

      Perhaps when taking only one measurement into account. I think about measuring progress/regression through at least two annual (if first is non-null) Agatston scores.

      Dr. Hall said:

      The decision to get a cardiac calcium test should not be taken lightly. It involves exposure to radiation equivalent to 20-40 chest x-rays, and can give false positive and false negative results.

      Of course if I get to that I will look for an EBT machine with something like 4 chest X-ray exposure. I think I had located one around here in Spain.

      weing said:

      So it’s consistency you are looking for? Doesn’t matter if the data is right or wrong?

      Consistency is a must in people getting paid for their analysis. I am not interested about population medicine in the least. I am not interested on efficacy of statins on diabetics, prediabetics, hypertensives and/or smokers. Actual data is not accessible as I have already said.

      1. Andrés says:

        I said:

        It is clearly inconsistent saying that LDL levels are not important and at the same time giving credence to the CTT’s analysis lumping together primary and secondary prevention over really independent ones trying to look at primary prevention alone pointed out rightly by Dr. Newman (I don’t know if he is the only author or not of that analysis neither consider it to be relevant) like that by Ray et alter over high risk subjects.

        Actually the CTT group did a meta-analysis somewhat on primary prevention The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials, so I retract that part. Anyway, my initial point of the CTT not analyzing a healthy subpopulation (no hypertensives, no diabetics, no prediabetics, no one with metabolic syndrome) still stands since the main trials with meaningful <5% risk population were MEGA (at least 33% of hypertensives on the <5% group), JUPITER (metabolic syndrome at least in 6% of the <5% group), AFCAPS (HDL<47mg/dl) and ASCOT-LLA (hypertensives) from Table 1. It seems that the more similar analysis they did was on any vascular death / non-vascular death for the populations stratified by risk in Figure 3. Those without previous diagnosed cardiovascular disease and <5% risk under treatment (or bigger dose statin) suffered 31+98=129 deaths while those under placebo (or lesser dose statin) suffered 40+87=127. It seems both populations had more or less the same size (31/0.07=443, 40/0.09=444). So, even including hypertensives and diabetics statins don't seem to bring any benefit for this population. I suppose the <10% risk group has much more hypertensives and diabetics, so I don't see how any conclusion about a healthy subject old enough to qualify within the <7.5% risk category is going to be well represented.

  35. charles grashow says:

    I take 10mgs of Atorvastatin a day. I still eat grass fed/finished ground beef, raw goat milk, full fat goat milk yogurt, 1 raw duck egg yolk and I also eat nuts, seeds, veggies, fruit, etc.

    Last blood test was 10/13

    TC – 126 mgs/dL
    LDL-C – 71 mgs/dL
    ApoB 64
    HDL 48
    TG 36
    non-HDL 79

    I take 200mgs CoQ10/day to mitigate any possible side effects but have experienced none so far

    BTW – I’ll be 60 next July and weigh 160lbs at a height of 6′

    1. Antonio says:

      Last blood test was 10/14

      TC – 318 mgs/dL
      LDL-C – 238 mgs/dL [Friedewald. Estimated, not measured]
      HDL 58
      TG 110
      TC/HDL 5.48
      TG/HDL 1.90 [first time, AFAIK, under 2. With statins and supervised by nephrologist from 4 to 10!!]

      Lost 20kg, now in 75kg. 178cm.

      Of course much better now both physically and mentally.

      1. Charles Grashow says:

        @Antonio

        Your Non HDL-C is 260 – That is a dangerously high level (IMHO)

      2. Antonio says:

        I forgot my CRP: 0.32 mg/L.

        1. charles grashow says:

          http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf

          Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL’s? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB and an inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation: please see Ira Tabas, Kevin Jon Williams, Jan Borén. Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis Update and Therapeutic Implications Circulation. 2007;116:1832-44.

          http://circ.ahajournals.org/content/116/16/1832.full
          Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis

          1. Antonio says:

            “One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis.”

            You would die earlier, it’s the other way around.
            Thanks, cholesterol.

            1. charles grashow says:

              A RECEPTOR-MEDIATED PATHWAY FOR CHOLESTEROL HOMEOSTASIS
              Nobel lecture, 9 December, 1985
              by
              MICHAEL S. BROWN AND JOSEPH L. GOLDSTEIN
              Department of Molecular Genetics,
              University of Texas Health Science
              Center, Southwestern Medical School, 5323 Harry Hines Blvd. Dallas, Texas,
              U.S.A.

              When LDL-cholesterol levels are below 100 mg/dl (equivalent to a total plasma cholesterol level of 170 mg/dl), heart attacks are rare. When LDL-cholesterol levels are above 200 mg/dl (equivalent to a total plasma cholesterol level of -280 mg/dl),heart attacks are frequent. Controversy arises over the middle ground, i.e.,individuals with plasma LDL-cholesterol levels between 100 and 200 mg/dl (total plasma cholesterol of 170 to 280mg/dl). This is the, range in which the vast bulk of heart attacks occur. Somewhere within this range there is a threshold value of cholesterol at which heart attacks begin to become more frequent. In this middle ground how much of the heart attack burden is attributable to plasma cholesterol? There is no definitive answer. In addition to cholesterol, heart attacks in this group are aggravated by smoking, hypertension, stress, diabetes mellitus, and poorly understood genetic factors. However, it seems reasonable to propose that plasma cholesterol does have something to do with heart attacks in these subjects, and that the incidence of heart attacks would be reduced if plasma cholesterol could be lowered .

              The LDL receptor studies lend experimental support to the epidemiologists’ suggestion that the levels of plasma cholesterol usually seen’ in Western industrialized societies are inappropriately high (9). This support derives from knowledge of the affinity of the LDL receptor for LDL. The receptor binds LDL optimally when the lipoprotein is present at a cholesterol concentration of 2.5 mg/dl (28). In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol (118). This is roughly one-fifth of the level usually seen in Western societies (Fig. 16 and ref.119). Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl (Fig. 16 and ref. 120). In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels (9,119). Second, the LDL level in newborn humans is approximately 30 mg/dl (121), well within the range that seems to be appropriate for receptor binding (Fig. 16). Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies (116)

              Once LDL receptors become saturated, the removal rate of LDL is proportional to the number of receptors. Whenever the number of receptors is reduced, plasma LDL levels must rise. Experiments in animals indicate that the consumption of a high fat diet decreases the number of LDL receptors in the liver (123, 124). We believe that this mechanism operates through feedback suppression as described above. That is, when excess dietary cholesterol accumulates in the liver, the liver responds by decreasing the production of LDL receptors (Fig. 13C). The entry of dietary cholesterol into the liver is mediated by a receptor, termed the chylomicron remnant receptor, whose activity is genetically distinct from the LDL receptor (125). The chylomicron remnant receptor is unaffected by cholesterol accumulation (126), and it causes cholesterol to accumulate to high levels in liver when the diet contains excess fat. The combination of saturation and suppression of hepatic LDL receptors contributes in a major way to the buildup of LDL in plasma when a diet rich in saturated fats and cholesterol is ingested. Insofar as such a diet also may increase production of LDL in the face of a fixed or declining removal capacity, the LDL level would rise even higher If the LDL receptor does limit the removal of LDL from plasma, then maneuvers that increase LDL receptor activity might be effective in individuals who have high plasma LDL-cholesterol levels, but who do not have defective LDL receptor genes. Such therapy seems feasible with the development of HMG CoA reductase inhibitors. However, it is still too early to tell whether such therapy would decrease the incidence of myocardial infarctions in individuals with moderately elevated plasma LDL-cholesterol levels in the range of 100 to 200 mg/dl. There is much circumstantial evidence to expect such improvement (127), but unequivocal data are simply not there. Hopefully, with the availability of powerful receptor-stimulating drugs, the hypothesis should be susceptible to testing in the near future. In considering the role of diet and drugs in treatment of high cholesterol levels, physicians and public health authorities must bear in mind the genetic variability between individuals. This variability exists at three levels: 1) The degree of increase in plasma cholesterol upon ingestion of a high cholesterol diet is variable. Not all people develop hypercholesterolemia. Some people, such as the Pima Indians, maintain low plasma cholesterol levels despite ingestion of a high fat diet (10). 2) Even when the plasma cholesterol level becomes elevated, the propensity for atherosclerosis varies. For example, a substantial proportion of FH heterozygotes (10 to 20%) escape myocardial infarction until the 8th or 9th decade despite pronounced hypercholesterolemia from birth (14). 3) Genetic susceptibility to contributory risk factors is variable. Some people can withstand hypertension and cigarette smoking for decades without developing atherosclerotic complications; others are highly sensitive.

              1. WilliamLawrenceUtridge says:

                A Nobel lecture from 1985…convincing!

            2. weing says:

              @Antonio,
              “You would die earlier, it’s the other way around.
              Thanks, cholesterol.”

              I’m sure your life insurance premiums will be dirt cheap with those numbers.

              1. Antonio says:

                With the new guidelines that could change. Life insurance companies are not responsible for the old ones.

                @Grashow, you are still staring at the firefighters in a fire, calling them guilty.
                The formation of plaque is in the first place a consequence of a healing process. What are the underlying causes? Would you prefer at that moment be lacking of cholesterol? I don’t.

                BTW, you missed Ranvskov’s article above, with your two nobel prizes as appeal to authority.

              2. Harriet Hall says:

                Calling the firefighters guilty? Yes, what if the fire department improves its firefighting methods: do you criticize them for having used the old methods? Do you accuse them of lying when they said that the old methods would work to fight fires? Or do you congratulate them for what they have learned and for being better able to protect your home?

              3. Antonio says:

                So: High cholesterol, just by itself, don´t cause atherosclerosis
                http://www.ravnskov.nu/cholesterolwashealthy

              4. Harriet Hall says:

                The source you cited is a very disreputable one, but we all know that high cholesterol does not cause atherosclerosis all by itself, but in conjunction with other risk factors like age and blood pressure: that’s precisely why the new guidelines emphasize total risk assessment rather than cholesterol numbers.

                High cholesterol is one of the risk factors, and when it is lowered by statins, the reduction in risk increases with the reduction in LDL-C; hence, higher risk statin doses are given to higher risk patients. It has been suggested that reduction in LDL-C might be just a marker for the anti-inflammatory and other effects of statins; if so, that still means it is a useful guide.

              5. Antonio says:

                @Harriet Hall

                I have accused nobody of lying. Just of being wrong.
                And I thinks is fair to ask for some responsibility. After all I was taking statins for five years without good evidence.

                “we all know that high cholesterol does not cause atherosclerosis all by itself”

                Ok then. But not everybody knows that already.
                And you still overlook the damages of statins.

                Now, keep the new guidelines with it’s discredited (already) calculator for you and your family.
                No offense, yoy agree with that.

                I repeat it: thanks cholesterol.

              6. Harriet Hall says:

                The previous guidelines weren’t “wrong.” The new guidelines are better. Scientists do take responsibility. You were not taking statins without good evidence; you were taking them based on the best evidence available. What, do you expect scientists and doctors to have some kind of crystal ball to predict what science will discover in the future? And I do not “overlook” the damages of statins: I look at the best evidence on side effects from controlled studies rather than the hype from anecdotal evidence. And my article answered the criticisms about the (not actually discredited) calculator.

              7. Antonio says:

                Of course the old guidelines were wrong. You´re just ideologically biased and allergic to any sense of responsibility. Anything “official” must be not-wrong.
                And the new ones are also wrong, just in a diffrente way. More convenient. Better to keep avoiding any responsibility.
                The “the best evidence available” was very evidence. Of course there were criticisms against them but you never paid attention. You keep thinking those criticisms were wrong anyways.
                So good for you. You are infalsifiable.
                The only thing I expect (ideally, I know) is more humility before sending guidelines to everybody with such high confidence. We don`t yet enough knowledge to justify such guidelines.
                But… you just feel irresponsible. Anything they do will be correct if it’s done witrh the best intentions.
                I don’t agree with that and I don’t feel you have the right to have such a great influence on people with such poor evidences and besides overlooking the side effects so badly.
                You did answer nothing. Just a few cherry-picked arguments at your convenience.
                In the comments you received better arguments you didn’t answered, nor even tried to.

                Anyways, un cordial saludo.

              8. charles grashow says:

                @Antonio

                Why did you take a statin drug for 5 years and then quit?

                Curious

              9. Antonio says:

                Because after several check-ups with high lipids (ex.: CT=270; TG=192; LDL= 186) my doctor explained to me his science-based-on-evidences-and-statins.
                And I did not revised his opinion until 5 years later, with cholesterol restrained a little above 200, triglycerides also above 200, fatter, weaker and lazier than ever.
                Eventually I took interest in this issue and began reading papers and opinions of experts from each side (because where there is science it usually happens there is debate too), and realized that there is intellectual life outside of guidelines.
                With the invaluable help of people like Andrés who showed me a lot of papers of other investigators also honest but with different opinions.
                So for five years I (blindly yes, but that`s the more usual for majority of people) followed the best opinions and guidance from one side (simplifying) and after that I decided to give a try to the other experts opinions, equally legitimate, also based on partial evidences, hypotheses and criticism. In general (there could be exceptions) all of them deserve to be taken seriously, even if at the end some should be proven wrong.
                Science is about that in geat extent: challenging (with respect) and not being conformist.
                And a little sceptic about our own opinions.
                Now I`m certain (subjective we can say) that I`m much better than before. And I`m also witnessing the changes already comming.
                Last comment, for your curiosity.
                And good luck at your sixties when the calculator will tell you it’s your turn to start with statins (just kidding, Charles).

              10. weing says:

                @Antonio,

                “And a little sceptic about our own opinions.”

                That’s funny. You don’t seem at all sceptical of your own opinions. I have no problem with you not taking statins. It’s your life, not mine. Meanwhile, science marches on.

                http://www.nature.com/ng/journal/v45/n11/full/ng.2797.html

            3. weing says:

              @Antonio,

              “With the new guidelines that could change. Life insurance companies are not responsible for the old ones.”
              Right. Let me know when your premium drops. They rely on what makes them money. If they didn’t have to pay out to beneficiaries of high cholesterol clients, the premiums would have dropped a long time ago to reflect that.

              1. Antonio says:

                What`s the point. Should I take statins putting my health innecesarily at risk just for a few bucks in my pocket?

              2. weing says:

                The point is the insurance companies know something you don’t. You and your Rafi guy will not make them charge you less for coverage because, according to their analyses, based on payouts and actuarial data, you are wrong.

              3. Antonio says:

                Well, actually I’m right and old and new guidelines are wrong suggesting with such high confidence the use of statins.
                And, anyways, I don`t have any issue with anybody nor company here in Spain.
                Yours is just a fictional argument. But if it should happen such a conflict I would stick againsta the guidelines and in favor of my health. Based on evidences, of course.
                Period.

              4. Harriet Hall says:

                “Well, actually I’m right and old and new guidelines are wrong suggesting with such high confidence the use of statins.
                And, anyways, I don`t have any issue with anybody nor company here in Spain.
                Yours is just a fictional argument. But if it should happen such a conflict I would stick againsta the guidelines and in favor of my health. Based on evidences, of course.
                Period.”

                Well, actually I’m right and old and new guidelines are right to suggest high confidence in the use of statins.
                And, anyways, I don’t have any issue with anybody or any company.
                Yours is just a fictional argument. I stick with the guidelines in favor of my health. Based on the evidence, of course.
                Period.

                How does it sound when I reverse your statements? I know my saying this isn’t going to change your mind; why would you imagine your saying this has any chance of changing mine?

              5. windriven says:

                “Well, actually I’m right and old and new guidelines are wrong ”

                Wow, I didn’t realize that you were such an expert! Or are you in fact an astonishingly arrogant guy with just enough information to be dangerous?

              6. Antonio says:

                No, I’m not the author of the guidelines.
                And I didn’t have to change my criteria in such a way without any apologies.
                I am not the arrogant here, boys. Just a patient who took statins for 5 years based on nothing.
                Now, good night from here.

              7. Harriet Hall says:

                “based on nothing.”

                If you really believe that, you are delusional. And if it were true, you would be at fault for taking a medicine based on no evidence. Are you saying you were gullible and stupid for 5 years and suddenly have become wiser?

              8. Antonio says:

                Well, I’m gomma stop this impolite (from your part) conversation.
                Just I will answer this.
                No.
                We just to rely to some extent in our fellow citizens and institutions. I can`t know everything. So you don’t either, probably.
                So I rely in doctors (in general I still do) but finally, in this particular issue, for whatever reasons, I came to discover how fragile -and eventually wrong- was the “lipid hipothesis”. That`s all.
                It’s easy to understand. No need to insult.
                Now we know that this is just a question of time. The new guidelines are indeed a “tectonic shift” (Dr. Steven Nissen).
                We need more work. Much more.

                Have a nice week end.

              9. weing says:

                “So I rely in doctors (in general I still do) but finally, in this particular issue, for whatever reasons, I came to discover how fragile -and eventually wrong- was the “lipid hipothesis”. That`s all.”
                So you had an epiphany? You are showing us all the light of truth? Only you have the necessary background and ability to discern the truth with Raffi, for whatever reasons?

              10. Harriet Hall says:

                The lipid hypothesis has now been accepted as fact by the majority of the scientific community. The only lipid hypothesis that was wrong was the one that said a high cholesterol diet was the cause of atherosclerosis. It’s the lipids in your blood that are important. The composition of your diet is only a minor factor, and trans fats have replaced cholesterol as the dietary villain.

              11. weing says:

                “Well, actually I’m right and old and new guidelines are wrong suggesting with such high confidence the use of statins”

                So you are saying that the companies that make a profit selling life insurance are wrong in charging higher premiums to people with high cholesterol levels or even refusing to insure some of them? What do you consider high confidence? There are patients that cannot benefit from statins because of side effects.

    2. interested party says:

      It may be that with your healty diet, you don’t need to take any statins. Did you ever test your blood after a 6 month statin fast?

      I don’t take any statins and my LDL-C is slightly over 200 which is lower than it was 16 months ago when I was still eating a lot of carbs. Now that I eat very little carbs and lots of saturated fat, my LDL is lower and the rest of the indicators are about the same as before and normal. I also am 6′ and weigh 153. Previously I weighed170. The low carb high fat diet was just an experiment to see what happens. The though of taking statins to lower my LDL never crossed my mind.

      Why are you taking statins?

    3. Andrés says:

      charles grashow said:

      I take 200mgs CoQ10/day to mitigate any possible side effects but have experienced none so far

      I don’t know which risk factors you had before deciding taking statins but as I have already said it is not clear at all for healthy people. Moreover, CoQ10 and cholesterol are not the only ones being downregulated when interfering with the mevalonate pathway like geranylgeranyl diphosphate needed to convert vitamin K1 to K2-MK4 (vía George Henderson). Experimental data supports only statins for 5 years. As I see it afterwards you are on your own.

  36. Flower says:

    A closer examination of the data from the most recent Cochrane review was completed by Dr Uffe Ravnskov earlier this year. Dr Ravnskov stated:

    “without statins your chance to be alive after a few years without treatment is 94.8 %, but if you take a statin every day you can increase your chance to 95.6. … In the control group 5.17 % had died, and in the treatment group 4.41% – a difference of 0.76 %”

    Dr Ravnskov’s study: Cholesterol Was Healthy in the End (http://www.ravnskov.nu/cholesterolwashealthy – also indexed in PubMed), outlines the faulty science behind the lipid theory and lists research indicating that LOW cholesterol levels are detrimental to health.

    Dr Ravnskov took a closer look at the data from the most recent Cochrane review and concluded from the data that:

    “without statins your chance to be alive after a few years without treatment is 94.8 %, but if you take a statin every day you can increase your chance to 95.6. … In the control group 5.17 % had died, and in the treatment group 4.41% – a difference of 0.76 %”

    Moreover, according to the British Medical Journal, “All of the randomised controlled trials included in the CTT (Cholesterol Treatment Trialists) meta-analysis were funded by the manufacturer of the statin being studied.

    A recent Cochrane review found that industry sponsored clinical trials are significantly more likely than non-commercially funded studies to report favourable efficacy and safety results and conclusions.” 22

    BMJ 2013;347:f6123

    Weighing the pros and cons of taking a statin for life, and the health risks involved, the evidence points to doing nothing is healthier than taking the drug.

    1. WilliamLawrenceUtridge says:

      That 0.76%, on a population level, translates to an enormous number of people not dying. Not to mention, the appropriate comparison isn’t the raw number of people who died in the population and those who didn’t, it’s the difference between the number of people who died and those who didn’t.

      Also, there’s a reason why meta-analyses have pre-determined rules about which studies are included and which are not, along with search criteria. It reduces the bias, such that questions about influence are less of an issue.

  37. Helge says:

    A little about the Jupiter study:
    “The most recent attempt to increase statin sales is the Jupiter study funded by statin maker AstraZeneca. Dr. Paul M. Ridker, in charge of the study, reports financial ties with more than ten pharmaceutical companies. Although 90,000 people were screened, less than 18,000 people were selected to participate in the Jupiter study that took place in 1315 sites in 26 countries. “If you extrapolate that, it means there are not all that many people exactly like those who were studied,” said Dr. Nieca Goldberg, Director of the women’s heart program at New York University Longone Medical Center.
    As a former pharmaceutical rep. turned whistleblower, let me cut through the boloney and give you the actual facts that came from this study. All the people selected for the study were at a low risk of serious heart problems. The absolute difference in risk (the drug-company-paid researchers only talk in relative terms, not absolute) between the study’s statin group and placebo group was actually less than one percent. The New England Journal of Medicine editorial about the Jupiter study concluded that treating 120 people who have the same health profile as the study participants for about 2 years would benefit only one person. In other words, 120 people, with a specific health profile, have to take the drug daily for about 2 years in order for one person to benefit. All 120 people would be susceptible to the multitude of the drug’s side effects. The two lead selling statins, Lipitor and Zocor, are in the top fifteen drugs for severe side effects in the FDA reporting system.
    A serious fact from the Jupiter study that is not widely publicized is that the statin group developed diabetes at a higher rate than the placebo group. The development of diabetes in people taking statin drugs has also been reported inprevious statin studies.
    The Jupiter study was stopped early, less than two years, ostensibly so that the people in the placebo group could be offered statins. Since the negative outcome of the trial – the higher rate of diabetes, a disease that often leads to heart disease, in the statin group – was more significant than the positive outcome of one person out of 120 benefiting from the drug, I suspect the study was stopped early because the drug company was fearful of how high the diabetes numbers would climb if the study continued. Drug companies create studies to sell more drugs, not to disclose
    the truth.” From : http://diaryofalegaldrugdealer.com/the-great-cholesterol-myth/

    Then my doctor wanted me to take statins I did some research, and changed my diet
    to http://diaryofalegaldrugdealer.com/the-great-cholesterol-myth/ and my health got better,as the science say: https://www.dietdoctor.com/science

    1. weing says:

      “As a former pharmaceutical rep. turned whistleblower, let me cut through the boloney and give you the actual facts that came from this study.”

      Really? You worked for AstraZeneca and were instrumental in running the study, involved in selection of patients for the study and advised stopping the study early in order to hide the diabetes risk? Wow. And I thought pharmaceutical reps were just eye candy.

      1. Interested party says:

        Weing, do ever have anything intelligent to add to the debate? I all see are irrelevant remark intended to discredit by intimidation. Try to add something that is supportive to your cause that is somehow base on science.

        1. weing says:

          @Interested party

          “I all see are irrelevant remark intended to discredit by intimidation. Try to add something that is supportive to your cause that is somehow base on science.”

          I’m sorry but my stupidity is great. Could you point out the science that Helge was basing her screed on?

    2. Harriet Hall says:

      @Helge,
      “As a former pharmaceutical rep. turned whistleblower, let me cut through the boloney and give you the actual facts that came from this study”

      As a medical doctor who just possibly may know more about interpreting studies than a former pharmaceutical rep, I took my own look at the Jupiter study when it first came out. See:
      http://www.sciencebasedmedicine.org/statins-are-better-on-jupiter/

      The purpose of the JUPITER study was to determine whether there was a benefit to using statins in otherwise low-risk patients whose CRP was elevated. Only 18,000 were selected out of the 90,000 screened because this study rejected anyone with an LDL-C of greater than 130 or a high-sensitivity C-reactive protein level of less than 2.0 and they rejected people with possible confounding factors, just as any good study does.

      The finding of an increase in diabetes diagnoses WAS highly publicized. In fact, it led to the FDA issuing a warning, advising doctors to weigh the patient’s risk of diabetes against the benefits of statins.

      The study was NOT “stopped early.” It was designed to continue until 520 confirmed primary end points had been documented, to provide a statistical power of 90% to detect a 25% reduction in the rate of the primary end point, with a two-sided significance level of 0.05. The stopping boundary was crossed at the first prespecified efficacy evaluation, and the study was terminated exactly as the protocol had planned. The report does say it was “stopped early,” but that only meant that since the endpoint was reached early on, the median followup was less than 2 years, and for that reason they continued monitoring side effects in a blinded fashion after the study. It was NOT stopped so they could offer statins to the placebo group: they only say the data should be considered when deciding whether the use of statin therapy among those with low LDL cholesterol levels but elevated high-sensitivity C-reactive protein levels would be cost-effective if applied widely.

      In fact, an accompanying editorial said “At this point, the current guideline for measurement of high-sensitivity C-reactive protein remains reasonable: a measurement may be obtained in asymptomatic individuals who have an intermediate level of risk, as estimated on the basis of standard clinical risk markers, if the decision to initiate drug treatment might change depending on the high-sensitivity C-reactive protein level. In my view, the evidence still favors this selective strategy for measuring high-sensitivity C-reactive protein, not routine measurement.”

  38. weing says:

    “Statin drugs deplete the heart muscle of coenzyme Q10, a fundamental cofactor for mitochondrial energy production (the heart muscle cells have one of the highest mitochondrial densities (approximately 5,000 mitochondria per muscle cell, versus 50 for skeletal muscle), and therefore are most susceptible to statin-induced coenzyme Q10 depletion, and subsequent mitochondrial dysfunction.”

    What is the NNT for CoQ10 and avoiding fructose?

  39. Reading With Interest says:

    For people like @goodnightirene, the use of statins seems to be a no-brainer, potentially providing her with a modest risk reduction benefit over 5 years.

    http://www.ti.ubc.ca/newsletter/statins-benefit-secondary-prevention-confirmed-what-optimal-dosing-strategy

    However, for primary prevention, could someone please direct me to the systematic meta-analyses that were used for these new guidelines to see what the NNT were? I understood that statins for primary prevention provided zero benefit:

    http://www.ti.ubc.ca/letter77

    Thanks.

    1. Harriet Hall says:

      That article is 3 years old, and even then 2 out of the 5 meta-analyses showed a benefit in primary prevention. Newer data and newer meta-analyses support a clear benefit. Here’s a few links to get you started:
      http://www.ncbi.nlm.nih.gov/pubmed/23447425
      http://www.ncbi.nlm.nih.gov/pubmed/23440795
      http://www.ncbi.nlm.nih.gov/pubmed/23186103
      http://www.ncbi.nlm.nih.gov/pubmed/23095240
      http://www.ncbi.nlm.nih.gov/pubmed/22674150
      http://www.ncbi.nlm.nih.gov/pubmed/22387091

      1. Self Skeptic says:

        Dr. Hall,
        Thanks for offering this list of references.

        Most of these are behind a paywall, so readers not associated with a med school library or other such service, can only read the abstract. (Dr. Hall, this isn’t a criticism, just an observation.)

        Here’s a list of free full text articles that are related, obtained by using the PubMed sidebar options for finding related papers:
        http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed_citedin&from_uid=17408535

        Note to newbies to PubMed: When you have the abstract view of a paper up on the screen, look at the right sidebar.

        There is a list titled “Related citations in PubMed” at the top, that can be expanded, and sorted by various criteria. I usually sort it by “pub date”, which puts the newest papers at the top of the list. You can scan this list for those articles that say “Free full text” in red. Otherwise, unless you’re in a medical center, you can only read the abstracts, and not look at the data (though some journals let you preview the figures as well as the abstract.) (Of course you could pay $30 to $40 for an article.)

        There is also list titled “Cited by x PubMedCentral articles” (where x is a number), which will give you only free full text papers, that have cited the paper whose abstract you have up.

        The advantage this method has, over using the References section of a paper, is that you’re getting a less personally, more randomly selected, list of references. The references in a paper are always somewhat biased (some more than others, of course) to support the authors’ point of view. Not in some sinister or intentional way, usually; just in the same way, that all of us are unavoidably biased by our culture.

      2. Self Skeptic says:

        Here’s one of the of the interesting articles I found, while using PubMed this way:
        http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093765/#__ffn_sectitle
        It’s a consideration of a proposal to offer medication relevant to CVD, to [i]all[/i] adults over the age of 55, as a prophylactic measure. More specifically, it’s about “polypills.”

        Am Heart J. 2011 Apr;161(4):719-25. doi: 10.1016/j.ahj.2010.12.019.
        Projected impact of polypill use among US adults: Medication use, cardiovascular risk reduction, and side effects.
        Muntner P, Mann D, Wildman RP, Shimbo D, Fuster V, Woodward M.
        Source
        Department of Epidemiology and Medicine, University of Alabama at Birmingham, 35294, USA.
        Abstract
        BACKGROUND:
        Polypills, which include multiple medications for reducing cardiovascular disease (CVD) risk in a single pill, have been proposed for population-wide use. The number of US adults eligible for polypills and potential benefits are unknown.
        METHODS:
        The National Health and Nutrition Examination Survey 2003-2004 and 2007-2008 were analyzed to estimate treatment rates for medications proposed for inclusion in polypills (aspirin, statin, an angiotensin-converting enzyme [ACE] inhibitor, and a thiazide-type diuretic for those without and a β-blocker for those with a history of myocardial infarction) among US adults. The number of coronary heart disease (CHD) and stroke events potentially prevented through polypill use was projected by published meta-analyses and 3 large population-based cohort studies. Two polypill eligibility criteria were analyzed: (1) US adults ≥55 years and (2) US adults with a history of CVD.
        RESULTS:
        There are 67.6 million US adults ≥55 years and 15.4 million US adults with a history of CVD and, thus, eligible for polypills using the 2 outlined criteria. In 2007 to 2008, 37.3% of US adults ≥55 years and 57.0% of those with a history of CVD were taking statins. Use of other polypill medications was also low. Polypill use by US adults aged ≥55 years is projected to potentially prevent 3.2 million CHD events and 1.7 million strokes over 10 years. Among those with a history of CVD, the potential to prevent of 0.9 million CHD events and 0.5 million strokes is projected.
        CONCLUSIONS:
        Polypills have the potential to lower CVD incidence substantially among US adults.
        Copyright © 2011 Mosby, Inc. All rights reserved.
        PMID: 21473971 [PubMed - indexed for MEDLINE] PMCID: PMC3093765 Free PMC Article

        I’m not exactly shocked, but…well, I guess I am shocked. I thought my GP was joking, when he said to another doctor about statins, “They should just put it in the water,” 10 years ago. [He may have been joking; but I didn't know any of the details about how drug recommendation policies are made, then. Now I would ask for more details.] But maybe it’s a predictable result of EBM combined with drug enthusiasm, carried to an extreme by one end of the spectrum. (The other end of the spectrum would be strong advocates of personalized medicine and individual clinician and patient judgment.) This “all adults over 55″ would be the ultimate in huge, undifferentiated subgroups, being treated according to the group’s average risk. Slim, fit people with normal BP and no family history of CVD would be given the same prophylactic treatment with statins or polypills, as obese, sedentary people with high BP and a high family history of CVD, according to this recommendation.

        Whenever I’m shocked, I know I should refrain from forming a quick opinion, or at least from expressing one vehemently. It means I’m being confronted with a different way of looking at things, than I usually use. So I’m not pushing any snap judgment about “good” or “bad” here, though you can tell where my bias led me (because I’ve tried to make my bias transparent, so you can allow for it. This is part of Feynman’s “bending over backwards to show how you might be wrong.”) Just passing along the information, for your consideration.

  40. Jack Kruse says:

    This why the calculator is a problem. http://mobile.nytimes.com/2013/11/30/opinion/statins-by-numbers.html?from=opinion

    Just because the lipid hypothesis is accepted by a large majority has nothing to do with it being correct. It is just today’s prevailing belief.

    There are moments in life when knowledge and myths are all turned inside out–what is real becomes unreal, what is unreal becomes tangible, and all your levelheaded efforts to keep a tight ontological control are rendered silly and indulgent. Today we are on that ledge with statins. The real difference in this thread of comments is we can see who accepts the majority and who remains skeptical because the mathematics don’t add up. Mathematics is the language of nature. To those who do not know mathematics it is difficult to get across a real feeling as to the beauty, the deepest beauty, of nature … If you want to learn about nature, to appreciate nature, it is necessary to understand the language that she speaks in……..many in medicine don’t. I think this is self evident here.

    1. weing says:

      ‘Just because the lipid hypothesis is accepted by a large majority has nothing to do with it being correct. It is just today’s prevailing belief.”

      And your belief today is ……? That you have a touchstone?

    2. windriven says:

      So now you offer an opinion piece in an aging newspaper that resonates with what we imagine your view* to be. On what basis is that supposed to change minds?

      The Reader’s Digest version of the op-ed is that there are all sorts of calculators out there and you can get different results depending on which you use.

      This is more of the usual nut bag nonsense that offers nothing constructive, only the sophomoric glee of urinating on the prevailing wisdom; frat boys venting against an imagined Dean Wormer in the campus rag.

      There is considerable evidence of the benefits of controlling cholesterol in citations scattered throughout these pages. The question becomes: how do we determine who will be most likely to benefit from statin use and how do we best balance the therapeutic benefit and the rare but real ADRs? This calculator is the most recent embodiment of the current consensus. It is not the word of god, it is not infallible, it is not even likely that the calculator 10 years from now will use the same algorithm**. It is a guide to be used as part of the package in assessing a patient’s suitability for statin therapy.

      If you have a superior guidance algorithm supported by significant clinical research and accepted by a substantial cross section of experts in cardiology and epidemiology, why haven’t you shared it with the ACC?

      *One of the hallmarks of cranks is that they typically do not set out reasoned arguments articulating their specific objections and offering specific solutions. Instead, they fog the conversation with innuendo and aspersion.

      ** Science works that way, Jack. We know more about statin therapy today than we did in 1985. We’ll know more still in 2025. And we’ll apply that knowledge to better the algorithms and better the outcomes.

    3. charles grashow says:

      Tell us why we should listen to someone who infected himself with MRSA?

      Tell us why we should listen to someone who writes about coherent water?
      http://www.jackkruse.com/quantum-biology-4-coherent-water/

      “Bulk liquid water is therefore a two-fluid system consisting of a coherent phase. Close to 40 percent of total volume of water at room temperature is actually capable of being coherent. The remainder 60% is present as an incoherent phase of water.

      Key Point: In the coherent phase, the water molecules oscillate between two electronic configurations in phase with a resonating EMF.”

      Why should we listen to someone who writes crap like this?
      http://www.jackkruse.com/emf-rx-the-top-ten-emf-faqs/

      “1. What is the real cause of low carb paleo flu?

      It’s called dehydration of your carbon nanotubes and you can not rehydrate on fluoridated water. You can use Lugol’s or potassium iodide to ‘knock down’ the fluoride effect of water. It acts as a dielectric in the CSF of the central nervous system to cause avalanche discharge. This is why fluoride is bad. You can not rehydrate with bad water. If you live in the southwest or California pay deep attention to it.”

      4. So fluoridated water blocks semiconduction by blocking the doping mechanism in the DHA of the human nervous system. So what is the ion responsible for proper doping?

      http://www.jackkruse.com/emf-5-what-are-the-biologic-effects-of-emf/
      There are many forces at play to keep this information from you. If you were to understand its full power the economy of the world would likely collapse. This is why this info is systematically kept from you.

      Dr Kruse – please go away

      1. weing says:

        He also has a thing for Dr. Nissen. Yes. Dr. Nissen is surely a Big Pharma tool. Look at the role he played in the Vioxx and Avandia matters.

    4. WilliamLawrenceUtridge says:

      Jack, “just today’s belief” is a convenient, lazy way of discounting all the information that led up to the belief. But the nice thing is – if you are right, the iterative nature of science will eventually come to realize this. The solution is more studies. Not dogma.

      All of your blah-blah-blah high-minded blather about nature being numbers and whatever is great, if you’re attempting to dispense with the evidence without engaging with it. There’s a reason why doctors and medical experts believe what they do, and it’s the existing evidence. If your beliefs are true, I’m very curious why all the doctors and expert committees haven’t come around to it. I’m sure you’ll claim conspiracy, which is just another lazy way of discounting without engagement.

      Also, if you’re such an expert, why not submit a journal article for review, summarizing the totality of the evidence as it should be analyzed? Don’t forget to review the objections of the peer reviewers and adjust your submission accordingly!

  41. Dave says:

    I’m not quite sure why there are so many comments, now more than 200, about these revised guidelines and perhaps someone can explain this to me.

    Statins are mostly off patent, so they’re cheap. Nobody’s trying to sell something here, or the guidelines would be pushing ezetemibe. Most patients have no side effects from these drugs. Any medicine has rare dangerous side effects – even aspirin causes anaphylaxis and bleeding in some folks. Compared to something like nonsteroidal anti-inflammatory agents statins seem to me to be pretty benign. There’s no uproar about Aleve or Motrin, though I’ve seen renal failure and GI bleeding a number of times from them. The vast majority of the patients who get side effects from statins are ok if they stop the statins. Many will be able to take a different statin if they choose to do so. If you fall into a low risk category, or if you are in a high risk category but don’t like the NNT data, nobody’s forcing you to take them. It’s not like refusing antibiotics for meningitis, you won’t automatically die. These are just guidelines.Good lord, people refuse medical advice all the time, or there would be no smokers.

    Just realize that preventive medicine involves treating a number of people to prevent disease in a few, and recognize that this is the advice of experts who have studied this carefully and weighed the various studies before revising the guidelines, and have come out with what they think is the best advice given the present state of knowlege.

    I do sympathize with those who are upset that the authorities change the recommendations – we would like to think the knowlege base is such that recommendations are set in stone, but that is (unfortunately) not how things work. The recommendations will undoubtedly be different in another couple of years as more data becomes available.

    1. Interested party says:

      Dave,
      Interesting question and well balanced commentary. It seems that if there is no money in something, there should not be much incentive to deceive. I would buy that arguement. However, perhaps because the patents are running out, big pharma is desperately trying to find replacements. If the value of Statins in general is discounted, newer Statins would not be so well received. I would think that big pharma is still very interested in maintaining credibility in the role of statins for their there own well being. Of course this is private enterprise and I respect such activity. Just saying.

    2. Self Skeptic says:

      Making money on the cholesterol hypothesis:
      Part 1: PCSK9 inhibitors and RNAi

      There is plenty of money to be made, as long as cholesterol reduction is seen as an important goal. I’m quoting a variety of sources, including the Motley Fool investment site, to show the business angle. I broke it into two parts: I hope each part is small enough to get posted promptly.

      http://www.reuters.com/article/2013/11/15/fda-pcsk-idUSL2N0IZ2NZ20131115

      U.S. FDA says new cholesterol drugs may not need outcome studies
      Thu Nov 14, 2013 7:31pm EST

      Nov 14 (Reuters) – Members of an experimental class of cholesterol-lowering drugs could get U.S. regulatory approval based on their ability to lower “bad” cholesterol, and may not need to show that they reduce the risk of heart attack and stroke, the Food and Drug Administration said on Thursday.

      The statement eased industry concerns that the agency would require more onerous “outcome” studies before approving the drugs, known as PCSK9 inhibitors.

      Those concerns emerged earlier this week when two leading U.S. medical organizations recommended that doctors drop their emphasis on specific targets for lowering “bad” LDL cholesterol levels. They also recommended only statin drugs for patients at high risk of heart attack or stroke.

      http://www.forbes.com/sites/larryhusten/2013/11/25/slouching-toward-phase-3-progress-report-on-new-cholesterol-drugs-at-the-aha/

      This is from investment site the Motley Fool (great name, isn’t it?): http://www.fool.com/investing/general/2013/10/14/this-new-cholesterol-treatment-has-blockbuster-pot.aspx

      Since generic statin cholesterol treatments are now widely available from companies like Teva Pharmaceutical and Dr. Reddy’s Laboratories, it is unlikely that a new statin treatment for high cholesterol will become the next blockbuster. In addition, statin can cause muscle and liver damage, digestive problems, increased blood sugar and diabetes, and neurological side effects — causing the drawbacks to outweigh the benefits.

      Therefore, investors should look to new kinds of high LDL treatments for a clearer glimpse into the future.

      Could this new treatment be safer and more effective?
      One new approach to treating high cholesterol is to silence certain genes. A top contender in this space is Alnylam Pharmaceuticals (NASDAQ: ALNY ) .

      Alnylam is focused on creating a new class of drugs, which interfere with RNA expression, known as RNAi treatments, which can directly silence disease-causing genes in the body. Alnylam’s experimental high-cholesterol drug, ALN-PCS, reduced patients’ LDL levels by an average of 40% and up to 57% on a higher dose during a phase 1 trial. It also reduced LDL cholesterol levels by 68% during a test on primates. By comparison, Pfizer originally claimed that Lipitor reduced high cholesterol in 39% to 60% of patients.

      If ALN-PCS can make it through mid-stage and late-stage trials, it could become a revolutionary next-generation treatment for high cholesterol, since its side effect profile compares favorably to statins, with muscle pain and memory loss being the most common problems reported. In addition, no serious adverse events occurred.

      Alnylam is currently partnered with critical care treatment company The Medicines Company (NASDAQ: MDCO ) , which will fund clinical trials of ALN-PCS from phase 2 onwards and commercialize the treatment if successfully approved.

      1. Harriet Hall says:

        The fact that cholesterol-lowering drugs are profitable is irrelevant to the question of whether they are safe and effective.

        1. Interested party says:

          @Dr. Hall
          I think that we alreay know that they are not “safe”, if you define safe as not actively contributing to your death. The real question becomes: Is it in the interests of the pharma group to downplay the risk? Judging by the potential profits that are already in jeapordy, it would be unwise to assume otherwise. That IS relevant.

          1. Harriet Hall says:

            You missed my point. It was in the best interests of companies making penicillin to downplay risks and hype the effects, but whatever the companies said about penicillin was irrelevant to the truth that it was a lifesaving advance over older treatments.

            1. Self Skeptic says:

              I wonder if Kassirer is right, in his sense that both medical and corporate culture have changed since then. It seems likely that they would have, in the 6-7 decades since the introduction of penicillin.

              I wonder what the NNT and NNH are, for penicillin as currently used, in comparison to statins. (This is assuming that we include all the people on statins or penicillin, even for prophylaxis. And include number of days used, not just number of prescriptions.) Even if we use current drug company data for the statin NNT and NNH, I think this might turn out to be a rather far-fetched comparizon.

              Although, there is also the problem of overuse of penicillin for respiratory infections which may be viral, which would increase the NNT. But then, this use probably prevents cases of fatal complications, like bacterial pneumonia in the elderly. And the NNH can’t measure the cost to society of overuse, which is the primary driver now toward discouraging such use.

              The problem of what to include in benefits and harms is a big one. How do you balance the harm of possible diarrhea from penicillin, with the benefit of preventing possible complications from strep and other secondary or undetected infections?) When one starts thinking of all the unmeasurable confounders, NNT and NNH start looking as problematic as some of those economic numbers that externalize too many important factors, like environmental costs and social harm from unemployment. If we have a commitment to cutting through illusions, we’d recognize that numerical terms are more likely to give us a false sense of knowledge here, than to accurately represent reality. At that point we have to fall back on common sense. Which, as we all know, isn’t really common, as it depends on our values.

              So, am I just giving up? No; I’m recognizing that value judgments (qualia) are unavoidably part of these calculations. I’m giving up an illusion about numbers which make something look science-y, but don’t really answer the question. I’m recognizing an element of cargo-cult science, that needs to be kept in mind when using simplified numbers like NNT and NNH, especially from COI-affected sources, which now includes a significant portion of the mainstream medical literature. (Though I suspect simple-mindedness is the more common fault here, than the greed or status-seeking of experts.)

              This puncturing of illusions is all to the good. It acts like a vaccination against gullibility. Not an extremely effective vaccine, but one like the flu vaccine. Imperfect, but arguable still worthwhile, especially for those in positions where they would be likely to infect the vulnerable public. ;)

              1. weing says:

                “Although, there is also the problem of overuse of penicillin for respiratory infections which may be viral, which would increase the NNT. But then, this use probably prevents cases of fatal complications, like bacterial pneumonia in the elderly.”

                I doubt it. I haven’t seen any evidence of prevention of bacterial pneumonias in viral infections. The pneumonias that do occur in these cases are more likely to be penicillin resistant.

              2. Harriet Hall says:

                Don’t try to divert this into a discussion of NNH for penicillin! My point was that what a drug company says may be true, so we shouldn’t automatically reject the arguments just because of their source. We all know value judgments are involved, and I don’t think we are being simple-minded; in fact, I think it is simple-minded to demonize Big Pharma. In no way could this be called “cargo-cult” science: that refers to not following the scientific method at all, rather than to following scientific evidence that is less than ideal when it is the only evidence we have. We seldom have the evidence we want, but we have to treat patients based on the evidence we have today: we can’t just sit back and wait for more perfect data.

              3. Self Skeptic says:

                Weing said: “I doubt it. I haven’t seen any evidence of prevention of bacterial pneumonias in viral infections. The pneumonias that do occur in these cases are more likely to be penicillin resistant.”

                @Weing,
                I don’t want to discount the value of clinical experience, so if you find this to be the case in your practice, I’ll note it as an anecdote. Thinking back, I first encountered the idea that viral infections may preceded bacterial pneumonia, when I was researching past epidemics. In the process, I read John Barry’s book “The Great Influenza,” and that’s where I saw that secondary pneumonia, not the flu itself, was a frequent cause of deaths in that epidemic. I don’t remember now if there was a discussion as to what kind of pneumonia.

                So I went looking for more information. I’ll break this up into parts, so it will post promptly.

                (Someone might ask, what does this have to do with the statin guidelines? Simple; the real debate in this thread is whether we should accept expert consensus at face value, or whether we should make it a habit to question authority. This 3-part post will demonstrates how one can gather information in order to assess an expert opinion, on a medical matter. This should be a welcome addition to any Skeptic’s toolchest.)

                Pneumonia secondary to acute respiratory infections,
                Part 1

                From the CDC:
                http://wwwnc.cdc.gov/eid/article/14/8/07-0751_article.htm

                Evidence from laboratory, clinical, and epidemiologic studies suggests that bacterial co-infection contributes substantially to the illness and death that occurs in pandemic and seasonal influenza.
                snip
                Bacterial Pneumonia and Seasonal Influenza
                Pandemics are relatively rare; therefore, more data are available about bacterial infections associated with seasonal than pandemic influenza A strains. Secondary bacterial pneumonia is a common cause of death in persons with seasonal influenza; co-infections have been found with ≈25% of all influenza-related deaths (4,5). Pathogen-specific data are summarized below.
                Streptococcus pneumoniae
                Of laboratory-confirmed cases of community-acquired pneumonia, ≈30% involve bacterial–viral co-infection (6–8). S. pneumonia is the most common cause of community-acquired pneumonia and bacterial co-infection with influenza A (9–12). Invasive pneumococcal disease is a term used when the organism is isolated from a typically sterile site, such as blood or pleural fluid. This definition therefore underestimates pneumococcal pneumonia where isolation of the organism is not possible (13). Notwithstanding, a number of studies have documented the temporal association between influenza and invasive pneumococcal disease, which suggests synergism. Grabowska et al. (14) recently used 2 epidemiologic methods based on Swedish surveillance data to estimate the excess cases of invasive pneumococcal pneumonia associated with seasonal influenza at 12%–30%.

                This doesn’t say whether the bacteria were penicillin-sensitive. Here’s something about that, also from the CDC.
                http://www.cdc.gov/pneumococcal/drug-resistance.html
                “In 2011, there were about 37,000 cases of invasive pneumococcal disease. Available data show that pneumococcal bacteria are resistant to one or more antibiotics in 31% of cases.[3] How common drug-resistant Streptococcus pneumoniae (DRSP) is depends on what part of the country you live in.”

                I seriously doubt that 37,000 figure; pneumonia isn’t that rare. If the reporting for that is as bad as for, say, Lyme disease, it could be low by 10-fold. They really should qualify where they got that number, instead of stating it as a fact. (The footnote isn’t very helpful.) Otherwise, people (including doctors) with a merely average level of skepticism, will believe it, since it came from the CDC.

              4. Self Skeptic says:

                Pneumonia secondary to acute respiratory infections,
                Part 2

                I went looking for other estimates and, amusingly, one of the first ones that came up was from Pfizer, which is sells pneumonia vaccine
                http://www.reportlinker.com/p01009245/Global-Pneumococcal-Vaccine-Market.html
                “Key vendors dominating this market space include GlaxoSmithKline plc. Merck and Co. Inc. and Pfizer Inc.”
                Here’s the Pfizer site:
                http://www.knowpneumonia.com/cases-pneumococcal-pneumonia
                “How Common
                In the United States alone, as many as 442,000 cases of pneumococcal pneumonia are caused by Streptococcus pneumoniae (S pneumoniae) bacteria every year.
                Many of those cases can be serious enough to cause hospitalization. In fact, pneumococcal pneumonia puts as many as 302,000 people in the hospital each year. And between 5% and 7% of people who are infected with pneumococcal pneumonia in the United States die from it each year.”

                As Dr. Hall has rightly pointed out, just because drug companies often are untruthful, doesn’t mean that everything they say is untrue, and I don’t know whether this particular number is inflated, or not. The value of this source, is that we can assume they made an effort not to err on the side of under-reporting. ;)

                Here’s more info from the CDC about pneumonia:
                http://www.cdc.gov/nchs/fastats/pneumonia.htm
                “snip
                Health Care Use
                Hospital inpatient care
                Number of discharges: 1.1 million
                Average length of stay: 5.2 days

                Source: National Hospital Discharge Survey: 2010 table, Average length of stay and days of care – Number and rate of discharges by first-listed diagnostic categories [PDF - 58 KB]

                Nursing home care
                Number of residents with pneumonia: 33,700
                Percent of residents with pneumonia: 2.3%
                Source: 2004 National Nursing Home Survey, Residents, table 33B [PDF - 719 KB]

                Mortality
                Number of deaths: 49,597
                Deaths per 100,000 population: 16.1
                Source: Deaths: Final Data for 2010, tables 10, 11 [PDF - 3.1 MB]

                Percent of hospital inpatient deaths from pneumonia: 3.4%
                Source: National Hospital Discharge Survey: 2006 Annual Summary, table 25 [PDF - 2.8 MB]”

                Hmm…looks like I was right about that 37,000 number, also from the CDC, being suspiciously low.

                I must emphasize that we don’t know how many of these cases followed a viral ARI, were bacterial vs. viral, nor antibiotic-resistant, nor penicillin-resistant. I’d go look, but this is enough info to make the point, that it’s not entirely silly to consider that penicillin treatment of ARI may prevent some pneumonia deaths.

                I guess the simple-minded might say, well, if even the CDC contradicts itself that much, then there’s no way we can know what’s true. So I’ll just have to pick some expert to believe.
                Not at all. Buyer beware: “expert” in medicine, is often someone who is willing to make authoritative-sounding statements, based on insufficient information. I’m beginning to classify high-profile medical expertise as a performance art. it certainly isn’t science. (They can get away with this, because medicine doesn’t cultivate the habit of public skepticism and informed debate, among its practitioners. Dr. Hall even says that it’s irresponsible for an expert to critique guidelines issued by panels. I find that idea so anti-scientific, that I hardly know where to begin explaining.)

                The key is to suspend judgment, while seeking more detailed information. Then when you do make a decision, it won’t be based on mere confirmation bias that you’ve foisted upon yourself, by having made a snap judgment and then (unconsciously, of course) having given undue weight to information that supports it.

              5. Harriet Hall says:

                “it’s not entirely silly to consider that penicillin treatment of ARI may prevent some pneumonia deaths”

                Are you recommending penicillin treatment? Don’t you realize the downside of doing that?

                “The key is to suspend judgment, while seeking more detailed information.”

                OK, so you would just suspend judgment and do nothing? Doctors don’t have that luxury. We can’t just say “We don’t have enough detailed information to know whether statins or antibiotics might work for you, so we refuse to prescribe anything.” Medicine is an applied science and we have to act with incomplete information.

              6. Self Skeptic says:

                Pneumonia secondary to acute respiratory infections,
                Part 3

                Here’s a 2013 paper where a group (in England) attempted to determine what happens in the real world, with antibiotic prescriptions for acute respiratory tract infections (ARIs):
                http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601395/#!po=31.2500

                Risks and Benefits Associated With Antibiotic Use for Acute Respiratory Infections: A Cohort Study
                snip
                The cohort included 1,531,019 visits with an ARI diagnosis; prescriptions for antibiotics were given in 65% of cases. The adjusted risk difference for treated vs untreated patients per 100,000 visits was 1.07 fewer adverse events (95% CI, −4.52 to 2.38; P = .54) and 8.16 fewer pneumonia hospitalizations (95% CI, −13.24 to −3.08; P = .002). The number needed to treat to prevent 1 hospitalization for pneumonia was 12,255.

                This rate of antibiotic prescription seem very high; I don’t even know anyone who goes to the doctor for a cold or flu. Maybe more of these cases in the study, were really bad colds that looked like they were developing into something worse, and that’s why antibiotics were given so often.

                But, I’m admittedly surrounded by highly educated people. Things may look quite different to a GP in a less rarified community. To be fair, with regard to flu, I gather that it can be so bad that one fears for one’s life, and of course we all hear that some (frail?) people die of seasonal flus. Most of us will go to the doctor for strep throat, a months-long chronic cough, or a painful sinus infection. So I may be too selective in what I’m calling a “cold” that doesn’t tempt one to seek medical attention.

                Getting back to this study; even though there was a (tiny) benefit seen in the treated group, the NNT is huge. So those of us who don’t want antibiotics for our ARIs that look like mere colds or flu, are justified (by this one study, at least). But if it starts to feel like something worse, maybe we should brave the wrath of the antimicrobial stewards, and try to get treatment.

                And what does this have to do with the statin guidelines? That’s easy. I’m countering the “learned helplessness” that the SBM regulars are exhibiting, regarding medical knowledge. This is an example of how to do research, on any medical question of interest.

                Before you again accuse me of “hubris,” let me just say that for a scientist, this is run-of-the-mill background research. There are plenty of intelligent lay people who can suspend judgment until they’ve done this too. I could dignify it as “due diligence,” to be exerted when making important health decisions for one’s family – but I’m tempted to consider it mere common sense. Why on earth would people who claim to be interested in “science-based medicine” not take these elementary steps?

                Before the web, this kind of research was laborious; now, it takes much more time to write it up, than to do it. The clicking-around stage took about 20 minutes. I’ve taken the trouble to write it up, because very few of you seem to know how to approach it. Consequently, you’re wasting your time making repetitive arguments about how “we must trust the experts,” when you could spend the same amount of time, or less, gathering information that would allow you to make informed decisions. Then one is learning something about the real world, instead of merely defending a bias toward faith in authorities.

              7. Harriet Hall says:

                You have demonstrated exactly why we shouldn’t do our own research. Anyone can look up studies, and you can find a study to support almost any point of view. This study shows that prophylactic antibiotics rarely improve patient outcomes and we know they can cause significant harm if overprescribed. You say “if it starts to feel like something worse, maybe we should brave the wrath of the antimicrobial stewards, and try to get treatment.” but you can’t base a treatment decision on whether you think it starts to feel like something worse. That would be just as idiotic as giving everyone with a cold an antibiotic. Experts have the knowledge and judgment to put all the available research into perspective; laymen don’t.

                For the umpteenth time, we are NOT demonstrating “learned helplessness.” We are helping ourselves by consulting experts who know more than we do. If my car breaks down, I consult an expert mechanic. I don’t try to read a manual for myself. And I certainly don’t ask YOU what I should do.

              8. Dave says:

                Your comments on pneumonia demonstrate how dangerous a little reasearch on the internet can be. There are guidelines for communty acquired versus hospital acquired pneumonia but the treatment is much more nuanced. If the patient has a swallowing problem or a history of a recent seizure he could have aspiration pneumonia. If from a nursing home or alcoholic, gram negatives are in the picture. A high fever and other organ system dysfunction raises the spectre of Legionaire’s disease. If a patient has AIDS, is on immunosupporessive therapy or has had a transplant opportunistic oganisms must be considered. If he’s got a sick pet bird he might have psittacosis. If he’s been exposed to pigeon shit, as when scraping a bridge to repaint it, he could have histoplasmosis. Some pneumonias are not infectious, and go by a variety of terms, cryptogenic organizing pneumonia, bronchiolitits obliterans and usual interstitial pneumonia being a few. And God forbid you should miss TB! Not to mention the atypical mycobacteria. Younger folks might have a mycoplasmal pneumonia. But I’m sure in your research on pneumonias you learned all this.

                Sore throats are usually regarded as a no-brainer by lay people. Get a throat culture and if it shows strep, give penicillin. Of course, the patient with acute epiglotitis may die with this approach (when I was a medical student I witnessed that) and if the patient has a fusobaterial infection he won’t be soing so hot either.

                The most important quality a physician can have is to know what he doesn’t know. If you were a physician you’d not do well.

                I still don’t get all the comments on the cholesterol guideline topic. Personally, if I have 500 patients in my practice with coronary disease, and I can prevent a few of them from having another heart attack and dying or winding up a cardiac cripple by putting them on statins, I’d grab the chance. Few moments of my life have been as miserable as when I’ve had a patient with a bad MI going down the tubes (telling the family their loved one has died is worse), and NO moments have been worse for the patient.

                Once again, these are recommendations based on the data we have available. And you can bet the experts are aware of all the studies.

                One other point, SS. Doctors are responsible for making recommendations that have real consequences for living breathing human beings. It’s a lot harder being at the wheel than in the back seat second guessing the driver. If you had the responsibility to advise someone as to the best way to increase their chances you might see this in a different light. Or maybe not – maybe you’d tell your MI patients you don’t agree with the guidelines and they don’t need a statin. Of course, that’s not standard of care.

          2. WilliamLawrenceUtridge says:

            I think that we alreay know that they are not “safe”, if you define safe as not actively contributing to your death.

            So, interested party, what you’re asking for, are drugs with no side effects, that can never cause any harm, that are only beneficial.

            Sign me up! That’s kinda what everybody wants. Unfortunately, the human body (like all products of evolution), is sloppily designed, is self-regulating in ways that can be bad for long-term health, and has duplicated receptors in multiple parts of the body – particularly between the brain and the gut.

            Unfortunately medicine is about finding a pretty fine line between maximum protectiveness and minimum adverse effects with only imperfect statistical information and an inability to predict effects and adverse effects on an individual basis.

            When you’ve got a way of perfectly predicting all outcomes in a chaotic system, please let medicine know. Doctors are keenly interested.

      2. Sawyer says:

        I wonder if the “Follow the Money” meme merits a post from one of the ScienceBasedMedicine contributors at this point? It is used so often by the critics of modern medicine, and almost always used incorrectly. They don’t seem to understand the huge difference between an imperfect incentive structure and “let’s kill people for money”. There are multiple motivations for doctors, scientists, regulators, and share holders. Some are good, some are bad, and it takes a lot of experience to tease out which ones are driving decisions. Unless of course we’re talking about quacks, who can only have the purest of motivations.

        One could also write a topic about how using the Scientific Method in reverse is not very useful. I think the Follow the Money conclusion is a prime example.

        Just a thought.

        1. Dave says:

          Absolutely. There may be biases in reporting, withholding data, or trying to put a spin on the data, but te data is still data. If the science is done correctly, it’s still correct science regardless of the source of funding. Like it or not, government funding for studies is not going to increase. Most research will fall o the private sector.

        2. weing says:

          “I wonder if the “Follow the Money” meme merits a post from one of the ScienceBasedMedicine contributors at this point? It is used so often by the critics of modern medicine, and almost always used incorrectly.”

          I think it’s a great example of the Ad hominem fallacy. Because someone stands to make a profit, they automatically have to be wrong.

    3. Self Skeptic says:

      Making money on the cholesterol hypothesis:
      Part 2: Combination pills

      Then there’s the strategy of winning patients currently on generic, off-patent drugs, back on a brand name drug, by making combination pills. These are said to increase adherence because they are more convenient.
      (Zetia is still on patent, either until 2014 or 2017).

      http://www.fool.com/investing/general/2013/05/03/fda-approves-powerful-new-cholesterol-drug.aspx

      Merck (NYSE: MRK ) gained Food and Drug Administration approval for its powerful new cholesterol drug Liptruzet, a combination of two already-approved drugs, Pfizer’s (NYSE: PFE ) Lipitor and Merck’s Zetia.

      Merck already sells a combination drug containing Zetia and Zocor called Vytorin. Zocor and Lipitor are in the same class of drugs called statins, but Lipitor is considered more powerful.

      In a clinical trial, Liptruzet taken for 12 weeks lowered LDL cholesterol — that’s the bad kind — by 53% to 61% depending on the dose. Lipitor alone in the same trial reduced cholesterol by 37% to 54% depending on the dose. Zetia by itself reduced LDL cholesterol by just 20%.

      Interestingly, despite Lipitor being a better statin than Zocor, the LDL cholesterol data doesn’t look that much better than for Vytorin.

      In the clinical trial supporting the approval of Vytorin, the combination pill reduced LDL cholesterol by 45% to 60%. It’s difficult to compare results between trials since there may be a different makeup of the subjects enrolled in the trials, but there’s somewhat of an internal control because both trials tested Zetia alone. In the Vytorin trial, the group that got Zetia by itself had a 19% reduction in LDL cholesterol, similar to the 20% seen in the Liptruzet trial.

      One advantage of Liptruzet over Vytorin seems to be at the lowest dose — 53% vs. 45% — which could be helpful for patients that can’t tolerate high doses of statins due to side effects including muscle aches.
      snip

      Then there’s the polypill: not just two drugs combined, but a whole raft of them.

      Here’s the famous proposal to give a version of this combination medication to everyone over 55, from 2003:
      http://www.ncbi.nlm.nih.gov/pubmed/12829553

      “The formulation which met our objectives was: a statin (for example, atorvastatin (daily dose 10 mg) or simvastatin (40 mg)); three blood pressure lowering drugs (for example, a thiazide, a beta blocker, and an angiotensin converting enzyme inhibitor), each at half standard dose; folic acid (0.8 mg); and aspirin (75 mg).”

      Here’s a newer 2012 version which contains amlodipine 2.5 mg, losartan 25 mg, hydrochlorothiazide 12.5 mg and simvastatin 40 mg, in a PLOS paper, also by Wald et al:
      http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0041297

      A recent paper pushing the “polypill” in 2013:
      http://www.ncbi.nlm.nih.gov/m/pubmed/24288261/?i=1&from=polypill

      Here’s a Medscape discussion from 2011, titled
      “Experts Debate Merits of Polypill”

      http://www.medscape.com/viewarticle/748818#1
      Note that no disclosures are given on this one. I looked them up separately:

      Salim Yusuf, MD, DPhil

      Professor of Medicine, McMaster University; Executive Director, Population Health Research Institute, McMaster University, Hamilton Health Sciences; Vice President, Research, Hamilton Health Sciences; Heart and Stroke Foundation of Ontario/Marion W. Burke Chair in Cardiovascular Disease, Hamilton, Ontario, Canada
      Disclosure: Salim Yusuf, MD, has disclosed the following relevant financial relationships:
      Served as an advisor or consultant for: Boehringer Ingelheim Pharmaceuticals, Inc.; Bristol-Myers Squibb Company; GlaxoSmithKline; Merck & Co., Inc.; Novartis Pharmaceuticals Corporation; sanofi-aventis
      Served as a speaker or a member of a speakers bureau for: Boehringer Ingelheim Pharmaceuticals, Inc.; Bristol-Myers Squibb Company; GlaxoSmithKline; Merck & Co., Inc.; Novartis Pharmaceuticals Corporation; sanofi-aventis
      Received grants for clinical research from: Boehringer Ingelheim Pharmaceuticals, Inc.; Bristol-Myers Squibb Company; GlaxoSmithKline; Merck & Co., Inc.; Novartis Pharmaceuticals Corporation; sanofi-aventis

      Allen J. Taylor, MD
      Washington Hospital Center
      Washington, DC
      Disclosures:
      Consultant Fees/Honoraria
      Abbott
      Research/Research Grants
      Resverlogix

      Valentin Fuster, MD, PhD
      Director, Zena and Michael A. Wiener Cardiovascular Institute, Marie-Josee and Henry R. Kravis Center for Cardiovascular Health; Richard Gorlin, MD/Heart Research Foundation Professor of Cardiology, Mount Sinai School of Medicine, New York, New York
      Disclosure: Honoraria: Bristol-Myers Squibb Company, Cordis Corporation, GlaxoSmithKline, Sanofi-Synthelabo Inc., Schering AG; Grant Support: Bristol-Myers Squibb Company, Cordis Corporation, GlaxoSmithKline, Sanofi-Synthelabo Inc., Schering AG; Consultant: Bristol-Myers Squibb Company, Cordis Corporation, GlaxoSmithKline, Sanofi-Synthelabo Inc., Schering AG.

      This does not look good for Dr. Hall’s view that experts account and correct for big pharma bias in the literature, when they express opinions in their area of expertise. In real life, experts are the preferred conduits that pharma uses, to ensure that its biased data and conclusions comprise the centerpiece evidence, in any expert discussion of an intervention. This is described in detail in Kassirer’s “On the Take,” and many other sources.

      1. Harriet Hall says:

        Correction: I do not claim that experts completely account and correct for Big Pharma bias, or that they are unbiased themselves. I do have confidence that they are aware of those issues and are trying to eliminate those biases from their recommendations. I am confident that in the natural course of the scientific process, the truth will eventually come out despite the biases. Meanwhile, we have no “better” way to determine how to treat patients than the recommendations of panels of experts, and we can use them while realizing they are not definitive answers and will be modified as better evidence comes in. Otherwise, we are left to our own devices (and biases) or the non-mainstream views of a minority who have their own biases.

        1. Interested party says:

          @ Dr. hall
          Well yes we do have a better way, and that is to carefully evaluate research studies and check study protocol, possible bias, methodology, accuracy of data analyis, and anything else that might influence the reader in an unwarranted manner. Perhaps we need to be more SKEPTICAL. It would help if research studies were published in an open forum and made available to peer review on-line for all to see. It just might stimulate higher quality analysis and reporting.

          1. weing says:

            “Well yes we do have a better way, and that is to carefully evaluate research studies and check study protocol, possible bias, methodology, accuracy of data analyis, and anything else that might influence the reader in an unwarranted manner.”

            That’s what I do when I read or review papers and that’s what I expect the experts do. I can only penetrate to a certain depth, they can go much further than I can. You may not like it, but there is an element of trust involved. I trust them, you don’t. That’s your prerogative. Yes we can be fooled for a while by frauds like Wakefield, but they are eventually brought to light. I seriously doubt you have the background to be able to judge peer-review, public or otherwise.
            If you ask me, I think there is a problem with the data and not the experts. Big Pharma should be forced to release all studies on drugs they have done and not just those that showed the effects favorable to them. That would allow all of us, including experts, to have access to more complete data and give us better guidelines.

            1. interested party says:

              @ weing
              I believe everything you said is correct. I am not kocking the peer reviewers. I just believe that more review is better than less.

          2. WilliamLawrenceUtridge says:

            Well yes we do have a better way, and that is to carefully evaluate research studies and check study protocol, possible bias, methodology, accuracy of data analyis, and anything else that might influence the reader in an unwarranted manner. Perhaps we need to be more SKEPTICAL. It would help if research studies were published in an open forum and made available to peer review on-line for all to see. It just might stimulate higher quality analysis and reporting.

            Well, your first sentence just sounds like science, and in particular how I would go about reviewing the evidence to come up with an expert recommendation.

            Your second is a good idea, one called for by many researchers, doctors and regulators. Ben Goldacre’s Bad Pharma goes into this somewhat.

      2. weing says:

        @Selfie,
        Are you perhaps looking for experts that don’t exist in the real world? Some independently wealthy researcher who won the Lotto and is using his winnings to fund studies and research on treatment and prevention of cardiovascular diseases? Coming out with drugs and then distributing them freely to those that need them? Better yet, coming to the “unbiased” conclusion that there is no way of preventing the diseases other than a low-carb diet and exercise? No meds needed.

  42. There are two kinds of LDL cholesterol: Small, dense particles, called “Pattern B”; and large, less-dense particles, called “Pattern A.”

    Pattern B is associated with increased risk of atherosclerosis; Pattern A is not.

    According to one study (at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929871/ ), statins do not reduce the levels of Pattern B LDL-cholesterol, which would mean that by monitoring TOTAL LDL cholesterol we’ve been watching the wrong thing.

    1. charles grashow says:

      What about Pattern I?

      LDL particles less than 258 Angstroms can get through the holes between cells quite easily and are therefore can be quite “atherogenic” (that is, cause blockages in the arteries). Those larger than 263 Angstroms are much less likely to cause blocked arteries. Now, we all have LDL particles that range from 200-300 Angstroms. It is the “peak” LDL size that has much to do with determining our atherosclerotic risk. If we have predominantly large LDL, we’re called “Pattern A”, if we have lots of the nasty small LDL we’re called “Pattern B”. Those with LDL between 258 and 263 are intermediate, or “Pattern I”.

    2. charles grashow says:

      Antonio says:
      November 29, 2013 at 4:46 am

      Last blood test was 10/14

      TC – 318 mgs/dL
      LDL-C – 238 mgs/dL [Friedewald. Estimated, not measured]
      HDL 58
      TG 110
      TC/HDL 5.48
      TG/HDL 1.90 [first time, AFAIK, under 2. With statins and supervised by nephrologist from 4 to 10!!]

      Using the Iranian formula
      http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm

      Your LDL is now 234.3!

      The optimum ratio (TC/HDL) is 3.5 – yours is 5.48!

      Your non HDL-C is 260!

      I do not understand your position re statins?

      BTW – which statin were you taking and at what dosage?

  43. Interested Party says:

    Harriet, you said that the study was terminated exactly as the protocol had planned. However, a report written by several MD’s and Phd’s in June 2010 entitled
    Cholesterol Lowering, Cardiovascular Diseases, and the Rosuvastatin-JUPITER Controversy : A Critical Reappraisal,
    http://archinte.jamanetwork.com/article.aspx?articleid=416101
    stated that “The JUPITER trial was prematurely terminated. Although having prespecified early stopping rules is a well-accepted feature of clinical trials, it is critical that the rules truly be prespecified. In the case of the JUPITER trial, the prespecified rules were not detailed in the published description of the study protocol.22 Indeed, we still do not know which end point was used to define them, or which level of benefits—unexpected on the basis of the a priori calculated hypothesis22—was required to justify early termination.

    Further, the authors said ”In defending the decision to end the trial early, the JUPITER investigators stated that the decision was not made by them but by members of an independent safety-monitoring board.24 However, the chairman of this board—an investigator of the Clinical Trial Service Unit of Oxford University, Oxford, England—has been, and still is, involved in many other industry-sponsored lipid-lowering trials, raising issues of conflict of interest”.25,26

    This report appears to me to be well written and contains many valid points that should have been addressed by anyone commenting on the value of the Jupiter trial today. I note that in writing your current blog you made mention of what Dr. Mercola said, but nothing about the report referenced above. These doctors who wrote the report called the Jupiter report FLAWED and they backed it up with many points that strike me as worthy of, at least, rebuttal.

    There is also the clip that appeared in the LA times http://articles.latimes.com/2010/jun/29/science/la-sci-statins-20100629
    The article ends with the following paragraph:
    “Editorializing in the Archives, Dr. Lee A. Green of the University of Michigan acknowledged that physicians faced with advising their still-healthy patients on the use of statin medications “really must admit that we do not know” what their best course should be. But the research that will inform those consultations in the future, Green wrote, “must be free of incentives to find any desired answer.”"

    I would suggest that anyone who is seriously wondering whether the new cholesterol guidelines are based on sound science should review the referenced report on the Jupiter trial as well as the LA Times article.

    1. weing says:

      @Interested,

      If you are truly interested, forget about newspaper articles and opinion pieces. Read the actual guideline article in JACC, and review the rationale and references. It shouldn’t take a bright guy like you longer than 5 minutes. Me, I’m not so bright, I’m slowly plodding through it at my turtle pace ever since the guidelines were announced.

      Some of you guys are big on HDL. Here’s a recent study for those with very high HDLs.
      http://breast-cancer-research.com/content/15/5/R87

      1. Self Skeptic says:

        I agree, examining the actual science takes time.
        Be sure to do the same analysis of the dissenter’s papers, too.
        Otherwise, you’ll be reviewing a biased set of references, that is sure to justify the new guidelines, but may not include other infomation that should be considered.

        I’m not saying the new guidelinew are detectably sub-optimal, BTW. I think they might be better, in the sense that they have eliminated the former intensification of therapy in pursuit of an LDL numerical goal (target), that may not have been relevant to outcomes, after all. You can see this pursuit in the earlier literature, and maybe you know about it from your practice.

        I’m just saying that lots of questioning eyes and minds on new guidelines, are good. One of the main complaints is that the recommendations were formulated behind closed doors, and then “sprung” on the medical community (and patients) as a fait accompli, without a period for review and evaluation. There’s no process for correcting the “groupthink” that often afflicts panels that are closed to outside input, when it’s done that way.
        It may have worked in the old, patriarchal days of medicine, but with the web providing easy access to the medical literature, it may not be an appropriate process, now.

        1. Interested party says:

          Well said Self Sceptic. Personally I think that the advancement of science would benefit if ALL research reports were available on the internet much like blogs are, allowing interested parties to comment. I must assume that the authors are not really interested in receiving dissenting comments, even though they may be coming from very qualified sources. Is there another reason for the secrecy ?

          1. Self Skeptic says:

            IP, you said: “I think that the advancement of science would benefit if ALL research reports were available on the internet much like blogs are, allowing interested parties to comment.”

            Yes, that would be the scientific thing to do. There’s no self-correction in a field where there is no vigorous discussion. (The traditional letters to the editor in the pre-web era, are too little, too late.)

            Yours is the model that Richard Smith, former chief editor of the BMJ, has proposed. He thinks that pre-publication peer review is such an obvious failure, that he proposes abolishing it entirely, in favor of post-publication peer review, in the way you’re suggesting. I doubt that it would be considered practical to completely abolish pre-pub review (in fact, I doubt it is practical) but I do take his point.

            My impression is, that it is so important for doctors to feel confident and knowledgable, that most of them prefer to follow dominant experts and to ignore, or even stifle, dissent. It’s understandable, but this is one of those areas where the doctor’s psychological comfort can be in direct conflict with what is physically best for the patient.

      2. Self Skeptic says:

        That should have been “dissenters’ papers,” not “dissenter’s.” (There’s more than one dissenter.)

    2. charles grashow says:

      http://www.medscape.com/viewarticle/724339#2

      Did the Early Stopping of the Trial Exaggerate the Benefits?
      The most detailed scientific arguments are made in the paper by Kaul et al. They note: “Prematurely truncated trials are notorious for being vulnerable to implausibly large (too-good-to-be-true) estimates of treatment benefits that later exhibit ‘regression to the mean’ on longer follow-up.” On this basis, they conclude that “the treatment benefit in JUPITER, although real, is likely to be overestimated.”

      They point out that estimates from a given trial that seem implausibly high can be moderated using Bayesian methods to incorporate information from earlier trials. They report a Bayesian analysis of JUPITER, showing that the treatment benefit is reduced from 20% to 8% with respect to mortality; from 47% to 13% with respect to the combined end point of cardiovascular death, MI, or stroke; and from 54% to 27% with respect to MI, estimates that they say are in alignment with the results of subsequent rosuvastatin trials. They further note that the number needed to treat increases from 119 to 434, which they say has important implications for clinical practice, cost-effectiveness assessment, and policy and public-health discussions.

      Ray et al express a similar opinion in their paper. In their meta-analysis of all the primary-prevention statin data, they did not find a significant reduction in all-cause mortality. They write: “The present data suggest that the all-cause mortality reduction of 20% reported in JUPITER is likely to be an extreme and exaggerated finding, as often occurs when trials are stopped early.”

      Kaul told heartwire that he “strongly disagreed” with the decision to stop the trial early. “This will probably be the last placebo-controlled statin trial. About one-quarter of patients had very low LDLs (below 45 mg/dL). We will never know for sure now the long-term safety in this group.” Kaul said trials should only be stopped for two reasons–safety or futility. “Stopping for benefit usually occurs when there is an implausibly large benefit, and it serves the purpose of the sponsors. Some may argue that ethically they had to stop, but what about the larger ethical issue of overestimating the benefit and exposing society to a therapy that might be dangerous? We still don’t know on what basis they stopped this trial. Was it because of mortality or the primary end point? If it was mortality, it certainly wasn’t cardiovascular mortality, because that was not significantly different. If it was for other mortality, then is there a plausible mechanism? If they had been more transparent, then we might not be having these arguments.”

      Ridker strongly defends the decision to stop the study. “We had a very conservative DSMB. The p value that was published as <0.0001 was actually 10-8. This is not some random error. The DSMB looked at all the subgroups and waited for the results to become positive in all these subgroups before making the decision to stop." He added: "Even if I did capitulate to these arguments, which I don't–say there was a 10%, 20%, or even 30% overestimation of benefit in JUPITER–the results would still show a large benefit. It's okay with me if these physicians want to ignore the data. I just don't want them taking care of my patients or my family."

      Was the Benefit Anything to Do With Lowering CRP?

      A separate issue raised in Kaul's paper is whether lowering CRP played any role in the benefit seen in JUPITER. Kaul and colleagues note that although the lowest cardiovascular event rate was achieved in JUPITER subjects who attained the "dual targets" of LDL <70 mg/dL and CRP <2 mg/L, CRP is not recommended by the guidelines as a secondary target of therapy because of the lack of clinical-trial evidence that targeting a particular CRP level results in clinical benefit.

      They also point out that without including both a low- and high-CRP arm in JUPITER, it is not possible to fully evaluate the impact of CRP level on treatment response. They cite a post hoc analysis by the FDA that showed that when patients were stratified according to CRP level, the treatment effect was consistently greater in the below-median than in the above-median CRP subgroup. "These data appear to challenge the guideline recommendation that higher concentrations of CRP might predict preferential benefit from statins," they write.

      Kaul et al provide three take-home messages: do not stratify treatment decisions by CRP level; do not expect 50% risk reductions in outcomes; and do not forget diet, exercise, weight loss, and risk-factor control (lifestyle modification trumps pharmacologic intervention for primary prevention, but if patients do not modify their lifestyle, statins can be used judiciously). They say these recommendations should suffice, at least until the next generation of guideline recommendations reignites the controversy.

      In response, Ridker cites new JUPITER data from an American Journal of Cardiology paper published online [5], which he says shows that increasing baseline CRP levels are associated with increasing vascular risk. In the paper, he and his coauthors add that "the relative risk reduction associated with rosuvastatin was similar in magnitude across the tertile and threshold levels of entry CRP," and "as the absolute risk increased with increasing CRP, the absolute risk reduction associated with rosuvastatin within JUPITER was also greatest among those with the greatest entry CRP levels."

      Confusion Over Cardiovascular Mortality Data

      Meanwhile, de Lorgeril et al spend much of their paper arguing that the lack of significant effect on cardiovascular deaths in JUPITER does not fit with the strong effect on nonfatal complications and total mortality, which in turn are inconsistent with other data from primary-prevention trials. They write that although an "unequivocal reduction in cardiovascular mortality was announced in March 2008 as the main justification for the premature trial termination, the absence of cardiovascular mortality data in the published article is striking.

      "If readers calculate the rate of cardiovascular mortality from the data in the paper, it's clear that the CV mortality in JUPITER is actually 'unexpectedly low' compared with total mortality–between 5% and 18%, depending on the means of calculation–whereas the expected rate would have been close to 40% in a non-Japanese and non-Mediterranean population," they write. "These mortality data are not epidemiologically consistent, and the early termination of the JUPITER trial likely was, at least partly, responsible for that lack of consistency."

      Ridker Responds

      I have counted 29 factual errors in this paper alone. I find it hard to believe that it could have been peer reviewed.

      In response, Ridker said the de Lorgeril paper contains so many factual errors that it should never have been published. "How it has been published under the title 'original investigation,' I don't know. There are no new data in this paper. It is just their opinions," he said, adding that some of the coauthors are known to be antistatin. "I have counted 29 factual errors in this paper alone. I find it hard to believe that it could have been peer reviewed," Ridker continued, and he questions the journal's agenda in publishing the paper.

      Ridker believes that the reduction in cardiovascular mortality in JUPITER was not significant because of the extremely rigid criteria used to define cardiac death. "If we couldn't guarantee that it was cardiac, it was classified as noncardiac. That is the way clinical trials should be conducted. The important thing is that total mortality had a hazard ratio of 0.80 with rosuvastatin and was significant. Cardiovascular mortality had a hazard ratio of 0.82, and although this was not significant, it is totally consistent with the overall results. Why are people so unhappy that we saved lives?"

      On the idea that the results are inconsistent with other data, Ridker said: "de Lorgeril et al are saying other trials haven't worked, so JUPITER shouldn't have either. These are kindergarten arguments. Many of the trials they mention are of different drug classes. They are taking statements completely out of context."

      On de Lorgeril et al's accusation that drugs are being used in preference to lifestyle, Ridker commented: "We all concur that diet, exercise, and smoking cessation are the most important aspects of primary prevention. I run a prevention clinic, and I am known as one of the most aggressive doctors on lifestyle changes. But our data show that individuals who eat healthily, exercise, and don't smoke but have raised CRP and are at high vascular risk can still reduce their risk of cardiac events and stroke with rosuvastatin. Why would you ignore data that would have a substantial impact on your patients?"

      Jupiter Patients Were Not Low Risk

      He continued: "The fundamental error many people make is that they think JUPITER patients were low risk. They were not. The actual event rate in the placebo group was substantially higher than in AFCAPS/TEXCAPS and in some hypertension trials. The number needed to treat (to prevent one event) is actually smaller than in several previous primary-prevention trials of hyperlipidemia and hypertension. Are these authors actually suggesting we shouldn't be treating these conditions as well?"

      He added: "I understand that the data may have come as a surprise to some. Atherosclerosis has always been thought of as a cholesterol disorder, but we have shown a larger benefit of a statin in patients with low cholesterol levels than in patients with high cholesterol levels. That can be disconcerting. It makes you have to reevaluate the understanding of the disease. But as physicians, we have to do that."

      Editor of the Archives, Dr Rita Redberg, provided the journal's perspective to heartwire , defending the decision to publish these papers.

      "Every article in Archives is peer reviewed and carefully edited. We are committed to publishing high-quality science; that is our only 'agenda.' " On the four papers concerning JUPITER published this week, Redberg said: "We published a meta-analysis of primary-prevention trials, a critique of the science (not a personal critique) of the JUPITER study, and two accompanying editorials, one focused on cholesterol lowering and one on JUPITER. . . . Finally, in terms of balance, the overwhelming number of articles advocate for statins (often beyond the evidence), so by publishing these submitted papers, we are offering clinicians a more balanced view."

      Final Rebuttal From De Lorgeril

      Offered the chance to make a final rebuttal, de Lorgeril said he would "be very happy" to hear about the factual errors in his paper and that he stands by the questions his paper raised, specifically those surrounding the anomalies they identified in the JUPITER papers and some of the changes as to how data were presented in different articles. "Instead of speculating on our feelings and sentiments, Paul Ridker should first explain the many anomalies we . . . can find in his report."

      On the accusation that de Lorgeril and his coauthors were predisposed against drug therapy, he responded: "The four cardiologists who cosigned the present article use pharmacotherapy in their patients on a daily basis when necessary and for as long as it is in accordance with truly evidence-based medicine." But he added that they are in the process of critically reviewing the positive trials of agents used for the prevention and treatment of atherosclerotic disease and will show that most of these indicate biases similar to those seen in JUPITER.

      Of note, De Lorgeril and one of his coauthors are members of a group called The International Network of Cholesterol Skeptics (THINCS), who oppose the belief that animal fat and high cholesterol play a role in the causation of atherosclerosis and cardiovascular disease–a footnote reported Tuesday on Cardiobrief.

    3. windriven says:

      @interested

      I wonder if you actually read the paper that you cited? Have a close look at Table A. When they pulled the plug the statin group had just over half as many MIs, strokes, unstable angina, etc. as the placebo group. Do I understand that you’re having a cow because many of the excess MIs weren’t fatal? Really? The excess strokes didn’t leave most of the sufferers on the coroner’s slab? So you think it would have been ethical to continue???

      If I’m misunderstanding your objection or mischaracterizing you position please state it with more clarity.

      The authors of this mess say,”Furthermore, there was no difference in the incidence of serious adverse events (total hospitalizations, prolongations of hospitalizations, cancer*, and permanent disability) between the 2 groups.” 62 nonfatal MIs in the placebo group, 22 in the statin group. Apparently the authors believe MIs are only serious if they’re fatal. Do you believe that too, Interested?

      64 strokes in the placebo group. 33 strokes in the statin group. But I guess surviving a stroke means it was a casual adverse event not a serious one. I’ve known a few stroke survivors and every one of them thinks their stroke was a pretty serious event. I guess the authors of this study didn’t talk to any of them.

      *cancer. WTF? I didn’t know cancer was a cardiovascular disease.

      1. interested party says:

        @ windriven
        Sorry for the delay in response. You said “Do I understand that you’re having a cow because many of the excess MIs weren’t fatal? Really? The excess strokes didn’t leave most of the sufferers on the coroner’s slab? So you think it would have been ethical to continue???

        No, that is not the reason. Somewhere in one of Dr. Halls blogs or maybe comments she made the statemtent that the trial was terminated early in agreement with the trial protocol….”
        My research suggested that maybe that was not correct and I supplied the de Lorgeril reference. Then Charles Grashow did a great job on expanding this issue and a lot more. Also, in the original blog comments of Dr. Hall’s blog in 2008, there is another commenter who has this to say:
        http://www.sciencebasedmedicine.org/statins-are-better-on-jupiter/
        I guess I am not the only one “having a cow…”.

        1. windriven says:

          @ip

          In my comment I quoted the actual data from the study. The reduction in negative events was stark. Many of the events were not fatal – a ‘confounding factor’ that may owe something to the fact that these were people in a study and perhaps had better or more frequent care than those in the general population.

          I asked, based on the data shown, if you were having difficulty because the adverse events weren’t fatal. Your response as best as I can understand it is:

          “My research suggested that maybe [the assertion that the study was terminated early in conformance with protocol] was not correct and I supplied the de Lorgeril reference.”

          I asked a simple question and your answer was, essentially, that you prefer de Lorgeril’s questionable pickings. Do I have it right now?

          So let me ask the question slightly differently: looking at the raw data, does a difference of 62 nonfatal MIs in the placebo group versus 22 in the statin group suggest that it might be unethical to proceed with the study? How about 64 strokes in the placebo group versus 33 strokes in the statin group? If you think not, where would you draw the line?

          1. interested party says:

            @weing
            You are now asking me questions that I believe I am not qualified to answer. I do not understand all of the nuances related to trial termination. However, I have gleened from credible sources that terminating a trial could lead to more favorable (for the researchers) results than continuing the trial. This has been done before. So I asked for some comment and explanation about a statement by Dr. Hall which conflicted with a statement by the Dr. De Lorgeril team. I think a discussion about this issue is important and relevant. It seems there are others who agree.

            1. Harriet Hall says:

              I think the confusion is because the report itself said it was “terminated early.” But the original plan of the experiment was to monitor the progress of the findings and to terminate the study at an “early” midpoint rather than a later endpoint if the conclusion was clear and further study would not change the findings. This is a common practice in experiments: if one group is doing enough better than the other, to the point that no matter what else happened later, it would not change the conclusions, then they stop the experiment so they can offer the treatment to everyone. Conversely, if it is showing harm, they would want to take everyone off the treatment.

            2. Andrey Pavlov says:

              I think a discussion about this issue is important and relevant. It seems there are others who agree.

              Of course there are others who agree! And who disagree. No matter what your stance is! I mean seriously, how many times in the history of ever have you even heard of a room full of people getting together and all just uniformly agreeing on something? That sort of should be how science works, but the real world is messy and so are real people. In science we argue about everything! That’s the whole point. And whoever wins the argument – with the evidence! – is “right” at the time. That can change. But over time things become more and more certain and we can be more and more sure that “right” won’t change.

              But the burden is on the minority to prove it. If you fail to, then sorry – you don’t get to claim you are still right. Yes, certain correct and good ideas get blown off by this process. But rather few compared to the number of bad ideas that get rejected. And, eventually, if there really is something to the idea the evidence will win out. But that is key, you need to have the evidence – you don’t get to claim you are right because “some people disagree” and look for the holes in our knowledge and try to assert that is what proves your idea right and the consensus wrong. That’s simply not good enough.

              It is OK to disagree – that is the fundamental nature of science. To survive the gauntlet of criticism. But when you do, you should do it intellectually honestly and with the readiness and willingness to change your mind just as we are.

              I say that the consensus is most likely correct and that there are multiple lines of converging evidence to support it. I recognize that there are things we don’t know, circumstances change, harms may be realized, and the overall calculus may change. I recognize that cholesterol is a surrogate marker of what we are really trying to characterize and accept the inherent problems with any surrogate marker. It may be found that statins work indirectly and that a more efficient way to achieve the same goals may be found. But until that actually happens, I provisionally accept the evidence we have and act in accordance.

              You, on the other hand, are convinced that the consensus is wrong, that we should stop acting in accordance with the consensus, and that the holes in our knowledge are sufficient to support your assertion. You leave no room to be convinced otherwise, because if you did, you already would be and have a much more nuanced stance.

  44. Reading With Interest says:

    Finally, – I found the NNT I was looking for:

    http://www.bmj.com/content/347/bmj.f6123

    “ . . . 140 low risk people must be treated with statins for five years to prevent one major coronary event or stroke, without any reduction in all-cause mortality. The five year absolute reduction in myocardial infarction and stroke for the lowest risk patients (< 5% risk over the next five years) was 0.6%. This means that 167 such people needed to be treated with a statin for five years to prevent one hard cardiovascular event.”
    “Only three of the five largest trials included in the meta-analysis (JUPITER, ASCOT, and LIPID) reported data on serious adverse events, none of which found a reduction associated with statins.”

    “ . . . with no reduction in all-cause mortality and no evidence of reduction in total serious adverse events for patients with five year cardiovascular risk of <10%, the net benefit-harm equation has zero overall benefit (the small reduction in serious cardiovascular events is counter-balanced by a non-specified increase in other serious adverse events) and ignores the clear evidence of harm that has been demonstrated in clinical trials and observational studies. A retrospective cohort study found that 18% of statin treated patients had discontinued therapy (at least temporarily) because of statin related adverse events. Forty per cent of the adverse events were related to musculoskeletal symptoms.”

    I think Dave's comment is the wisest statement on this entire blog:

    “If you fall into a low risk category, or if you are in a high risk category but don't like the NNT data, nobody's forcing you to take them.”

    My question is, do those of you who follow these guidelines and prescribe statins to these low risk patients, actually give them this information?

  45. windriven says:

    @Reading

    “140 low risk people must be treated with statins for five years to prevent one major coronary event or stroke”

    It would be interesting to compute the cost of daily statins for 140 people versus the cost of treating the one major event. A generous estimate of a generic statin at 30 cents per would give a prophylactic treatment cost of (140*365*5*.3) equals $76,650. I don’t know what the going rate for, say, a double CABG and lifetime med costs would be but I’m guessing that $76,650 would be a bargain. Of course not all MIs get CABGs, some get stents. But there are still considerable medication and followup care costs to say nothing of lost productivity.

    1. Reading With Interest says:

      Your reply is interesting, however, you forgot to factor into your total cost, the cost dealing with the “increase in other serious adverse events”.

      No matter, do you believe that it is good medicine to inform patients of all of the data? the absolute risk reduction as well as the risk of SAEs? so they can make their own decision regarding this drug?

      1. windriven says:

        “No matter, do you believe that it is good medicine to inform patients of all of the data? the absolute risk reduction as well as the risk of SAEs? so they can make their own decision regarding this drug?”

        No, probably not. Data requires context to become information and most patients lack the context to use the data as is. That is not the same as being in favor of denying patients access to data about ADRs or anything else. But it should be part of a conversation with their physician who, hopefully, does have the context to process the data into useful information.

        I will remind you again that the new guidelines are not a cookie cutter; the algorithm is to be used as one component in the clinical decision-making process.

        1. Reading With Interest says:

          You said:

          “I will remind you again that the new guidelines are not a cookie cutter”.

          Agreed.

          Do you believe it would be correct to say the following to your low risk patient, and have them choose what they would like to do? (in general of course, because every cookie is different)

          “If you take this drug, statistics say that you have a 1 in 140 chance of this drug helping you prevent a heart attack or stroke over 5 years. On the other hand, you have a 1 in about 40 chance of having muscle pain that will stop when you stop using the drug. As well, taking this drug will increase your chances of having diabetes to the tune of 1 in 200, or if you are a woman, 1 in 100 within 2 years. There could be other side effects associated with this drug.”

          Most patients I believe, can understand numbers like that in order to make an informed decision. No?

          1. Harriet Hall says:

            There’s a problem with simply telling patients the NNT or NNH: there is no single answer, but several answers depending on which study or studies they are looking at. And clinicians ought to look at the individual patient for factors that could be expected to increase or decrease the risks beyond the average.

            This study http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2517983/ showed that 22% of patients on statins developed muscle pain, but so did 16.7% of people not on statins. (I think that works out to an NNH of 18).

            1. Self Skeptic says:

              Dr. Hall, Did you mean “an NNH of 18″ instead of NNT?

              Though maybe NNH is usually confined to deaths; I’ll have to see how NNT and NNH are typically determined. Now that I think about it, it seems like a can of worms, methodologically, unless you’re just measuring mortality from any cause. This is known to be one of the bones of contention, in interpreting the existing statin studies. The JUPITER trial has been critiqued, on that basis. Arguably, the only thing that is an absolutely hard, objective end point, is all-cause mortality. (Maybe instead of “arguably,” the word should be “discussably,” to emphasize that differences in opinion don’t have to be “argued,” in the hostile sense. But “discussably” isn’t a word. :) )

              You have to dig into the known problems with determining cause of death, to get a sense of how biased that factor that can be. See my post, below, about the problems with “cause of death” in the absence of autopsies. The gist is, that death due to heart disease is overestimated in official statistics like the CDC’s, by as much as 100%, because it is so often used as the default cause, when filling out death certificates. If these figures are used at any step, when computing lives saved by statin use, they’re going to be way off.

              it would difficult to try to compare soft outcomes like “not feeling well,” when considering that people undergoing atherosclerotic damage that could have been alleviated by statins may not feel well, either, in ways that aren’t as obvious as angina. In other words, the statins may prevent some types of discomfort in the people they are helping, and cause some types of discomfort in the people they aren’t helping, and I’m guessing there’s no way to do an EBM-acceptable study on that. Well, let me rethink that. How could you?

              Maybe you could have a large number of people wear pedometers every day, and track their physical activity? The pedometers should transmit to a computer, and log the timing of activity, so you could check that they were wearing them. I have one that does that.

              This is all based on a legitimate concern that people whose muscles are uncomfortable or frankly painful, or who feel unusually tired, will become more sedentary, and this will cause more harm than the statin is theoretically preventing. So it’s important to not gloss over the issue of statin side effects, without making a rigorous effort to detect and measure them. This would all have to be government funded, not industry funded, for the obvious reasons. They should be done by people with no financial COIs and no preconceived notions of what the answer should, or will, be (= nonfinancial COIs). Read Peter Gotzsche’s book “Mammography Screening” to understand why.

              These studies are tricky, because once doctors believe in prophylactic statin use for primary prevention in healthy people, they can’t in good conscience randomize people to statin or placebo.

              Maybe you could do the study on healthy people with borderline high LDL, whatever that number is thought to be, by the large number of experts who still are sure that it matters. Then you could justify it by saying that there is inconsistent evidence as to whether this subpopulation could benefit from the statin, so we need to find out. You’d collect the usual mortality data, but also be looking intentionally for evidence of side effects, in as rigorous a way as can be devised. I feel like this is a missing piece of science, in helping patients and their doctors make the choice of whether to take statins for primary prevention, if their risk of CVD isn’t obviously high.

              There will be people who will exercise no matter how awful they feel, and people who won’t exercise no matter how well they feel, and then a population in the middle of that bell curve, who are more likely to exercise if they feel well. That’s why it has to be a fairly large study, to get any realistic results.

              The study participants should also keep a daily account of how they feel, including muscle discomfort along with a list of other questions (to avoid biasing their attention solely toward perceiving muscle discomfort.)

              I wonder if there is some technological way to make diary-keeping easier to monitor; they could fill it out online, every night, from their computers or phones. You could decide to only enroll people who have the habit of checking their email every night, and then they’d be confronted by an email every night that would give them a really fast way to record their experience; a set of lines they could put an x on, to rate aspects of their relative sense of physical well-being, and then hit the reply button. Anybody know what’s being done in this area?

              I suppose there are those who don’t believe that subjective symptoms that can’t be measured, like pain, discomfort, fatigue, relative mental sharpness, etc. have any place in EBM, no matter what. That’s where the pedometers come in. Some small pilot studies should be done, on how to get maximum adherence, and how to know whether adherence is occurring, or not. I have a pedometer call a Fitbit that tracks daily activity by time of day, and downloads it wirelessly to my computer, automatically. Something like that should be used, with addition software to transmit the data to a study monitor, who can check in with the patient immediately if they stop wearing the pedometer.

              Well, I’m sure you all get the idea.

              1. Harriet Hall says:

                Yes, of course I meant NNH and I have corrected it.
                I am also concerned about the reports of “soft” side effects from statins. Yes, there certainly are ways to test for them with controlled studies, and I hope those studies will be done. On the other hand, the reports of equal numbers of serious side effects in patients on placebos is reassuring, and I have every confidence that if the “soft” side effects are real, the scientific method will find out the truth eventually. It has a good track record of doing that.

              2. Andrey Pavlov says:

                @ Self Skeptic:

                I sadly do not have the time to comment here as much as I used to (I used to comment under my ‘nym, NYBGRUS but lately just use my real name) because you and I would certainly tangle quite a bit. I’m currently interviewing for my residency and flying all over the country while trying to sneak in some time for family and holidays, but if you stick around till after the New Year I’ll have some time to get down to it again.

                Every once in a while though, you come up with a few comments that truly belie your shortcomings in understanding and applying medical science and that coincides with a bit of free time I have (surf conditions are pretty crap today, else I would be out in the water right now).

                In general, though, you do seem well versed in science and scientific things. Your problem essentially boils down to a combination of the Nirvana Fallacy and hubris. You seem to not only think that if something isn’t demonstrated in the same way and to the same certainty as particle physics it is crap and that you know everything you possibly need to know about how science is done in order to indict whatever medical science you personally disagree with. You are, of course, completely wrong on both counts. You’d do well to heed Lawrence Krauss’ comment as to why he does theoretical physics than biology – it’s easier. (His words, not mine).

                Though maybe NNH is usually confined to deaths; I’ll have to see how NNT and NNH are typically determined

                No, it isn’t just deaths. That is why it is called “number needed to harm” rather than “number needed to kill.” You can calculate an NNH for anything you define as harm. It just so happens that, in general, death is a pretty easy harm to measure. NNH and NNT are the exact same statistic applied to different things. They are not calculated separately. And the calculation is exceedingly simple (despite the fact that even most med students can’t seem to wrap their heads around it). It is the inverse of the absolute risk reduction (or absolute risk increase) for whatever you happen to be looking at. If you reduce the risk of something by 10% then your NNT becomes 10. (1/0.1=10). It is basically a distributed statistic that asks “How many people will need to have their risk reduced in order for 1 full case to be prevented?” So if you reduce the risk of heart attack by 10% then you would need to do so for 10 people in order to prevent 1 heart attack.

                Of course, this ties in to the fact that probabilities are not the same as frequencies, and there is always random variation in even in normal values, so the number is still more of a yardstick than a reflection of reality (you can see how well the risk reduction and NNT map to reality by doing a Hosmer-Lemeshow goodness of fit analysis which would add information as to how robust the actual ARR is in real populations rather than study populations).

                But of course, you don’t even understand that basics of what NNT/NNH actually are nor the nuances of how they would apply to real populations and how to determine that, yet still feel qualified enough to poo-poo consensus guidelines as though you have authority on the matter. Hubris – one of your downfalls.

                I suppose there are those who don’t believe that subjective symptoms that can’t be measured, like pain, discomfort, fatigue, relative mental sharpness, etc. have any place in EBM, no matter what.

                Of course we do. And the rest of your rant about pedometers and exercise demonstrates you don’t understand why those aren’t in the literature or factor into EBM as prominently. It isn’t that we don’t see a place for them, or value in understanding them, or think that we can’t understand them scientifically. (Well maybe some people do, I don’t and most reasonable scientists wouldn’t either). The reason is that they are very, very, very, muddied statistics that are so difficult to tease out that they are simply impractical to study. The moment you ask people to keep a diary about how they feel you’ve completely skewed the outcome. You even seem to recognize this on some level, by attempting to use pedometers as a surrogate marker, but don’t delve into the fact that this multiplies the amount of noise in the signal. To be able to derive anything useful you’d have to have an amazingly massive data set to work with – one that would be horrendously expensive and a logistical nightmare to work with that would be almost pointless by the time we actually answered the question.

                It is an important question and we will be able to answer it, eventually. But the further reality you miss is that if it takes that much effort to answer the question, it likely isn’t nearly as important to answer! If the effect size is that small, in the face of readily recognized beneficial effect sizes in terms of CVS disease, it becomes academic. Yes, we can (and should) hone our administration to as fine an edge as possible, but you ignore the limits of reality in your rants.

                There is an art to medicine and that is working with incomplete information. Physicists abhor that, which is fine. They need – and can get – a lot more certainty than we do. But if we had your attitude we’d still be 60 years in the past in terms of medicine. There is always a trade off and a balance and even if the next generation demonstrates harms we never imagined at greater levels than we’d hoped from statins, we can rest assured that we did, on the whole, more good than bad by using the drugs. Exactly how much more is “discussable” (as is the question of whether the economics actually made it worthwhile) but the fact that it is more beneficial is not. That question has been settled.

              3. Self Skeptivc says:

                Yes, cell phone is the way to go. You’d need to select your study subjects from among people who carry and use their cell phones all the time, but that’s common now.

            2. windriven says:

              @Andrey Pavlov

              Nicely said.

              I’ve drifted away from the Selfie thread as being endless and increasingly pointless. But your discussion of the pedometer sparked an idea. One might map ‘how people feel’ by using random alarm generators and a visual analog scale similar to the ones used in pain management. The idea is that several (random) times each day a subject’s cell phone will receive a prompting text to which the subject responds with a 1-9 response based on the visual analog scale. The entire process could be run on a computer with the data automatically collected and collated. This could be used to map data on any number of subjective judgments: pain, happiness, thirst, hunger, sexual interest, fatigue, etc.

              1. Andrey Pavlov says:

                @windriven:

                Thanks. I still do read through the comments (though not all of them – I use the general RSS feed that takes all the comments from all of SBM and dumps them into my reader, and for whatever reason not all of them make it through – the new interface is difficult for me to follow so I greatly appreciate you tagging me at the top of your response) and certainly read all the articles. Everyone once in a while I have a chance to comment.

                As for your idea – seems interesting. I think with the younger generation it may be more feasible as they (we?) have all sorts of reminders and things popping up on our mobile devices and you could actually make it unexpectedly random. I’d imagine that grams and gramps would not have anything else popping up so that even if it were random it would still be anticipated to a degree and known what it is before even looking at the notification.

                But in any event this is where “Big Data” can come in. The equivalent of doing GWAS studies but on social media and smartphone sourced data. There is a lot of noise in GWAS which is why they us a much high sigma and it would be the same with this sort of data. There was actually an interesting TED talk I watched a couple years back on the idea of using social network nidus information to do epidemiology. Basically, you ask (or query) who your friend most popular friend is and keep doing that until you get to a person with the largest nidus and use data streaming in and out of those connections to determine sources of infection and detect outbreaks significantly earlier. The CDC has already partnered with Google to do something similar by tracking when people start googling things like “cold remedies” or “local pharmacy” and such stuff.

          2. windriven says:

            @Reading

            Dr. Hall gave you a much better and more nuanced answer than I might have. I would have generally agreed with your premise though I might have quibbled with your ADR rates.

  46. BryanB says:

    Here are some blog posts by medical ethicists on the new guidelines
    http://brodyhooked.blogspot.com/2013/11/new-cholesterol-guidelinesthe-devil-in.html
    “The panel realizes that there’s no good evidence to recommend a particular target level of cholesterol. But they are impressed (as we’ll see) with the studies that show that lower LDL cholesterol is associated with lower risk. They then urge the physician to prescribe a “moderate” or a “high” intensity dose of their favorite statin, with the idea that the end result will be a certain percentage drop in the LDL level—with the additional proviso that if you don’t achieve that level of drop, you will need to up the dose. So the idea of treating to a target level went out the front door and snuck back in the rear window.”

    “Bottom line—it looks worrisomely like what I concluded with CTT—even if these guidelines were not written by people in the pay of the drug industry, they could just as well have been. And somehow, while important new evidence against the routine use of statins, and suggesting that we really don’t know much about the true mechanism by which these drugs work in the cases where they do, crept into the guidelines for the first time, the bottom line is largely unaffected by such enlightened thoughts. We’re back to putting statins in the water supply.”

    http://brodyhooked.blogspot.com/2013/11/new-cholesterol-guidelines-part-two.html

    “So if the guidelines were true to the evidence, what message would emerge? The message would certainly be: the grounds on which we used to prescribe statins were all wet; there are a bunch of folks now taking statins who probably don’t need them; we need to be much more refined in selecting the smaller subsets of people who might actually benefit from taking statins.

    What message is actually being disseminated? It seems to be: If you took statins under the old guidelines, have faith and keep taking them. If you were not on statins previously, don’t worry, because our new, flawed risk calculator will probably say that you too need to be on statins.

    As I said, if the drug industry had been allowed to write the script for this, it would have said exactly the same thing.”

    http://hcrenewal.blogspot.com/2013/11/confused-thinking-about-new-cholesterol.html
    “Guidelines for management of a very common problem promulgated by a major medical society and a major disease oriented non-profit organization suggested a strategy that would vastly increase drug treatment of currently healthy patients. The strategy appears not to have been based on good evidence. When some of the problems with this evidence were pointed out, the guideline developers responded with illogic. Apparently many of the guideline developers have financial relationships with the drug companies that would most profit from increases in drug treatment as recommended by the guidelines Implementation of the new guidelines might results in millions of people in the US receiving unneeded drugs, with resultant side effects and costs. .

    Do we need more examples of how conflicts of interest are causing the poor outcomes and excess costs that are wrecking our health care system? Do we need more excuses not to eliminate conflicts of interest from guideline development? Do we need more delay implementing the standards provided by the Institute of Medicine report on trustworthy guidelines? Do we need more excuses not to drastically reduce conflicts of interest affecting academic medicine, medical societies, and disease specific non-profits, specifically starting with the earlier (and so far generally disregarded) Institute of Medicine report on conflicts of interest in medicine?

    While we in the US argue incessantly in the details of minor reforms of our supposed free health care market, we ignore the rot at its foundations. True health care reform would attack the conflicts of interest that have put money, not patients at the center of health care. “

    1. Harriet Hall says:

      “if the drug industry had been allowed to write the script for this, it would have said exactly the same thing.”
      That doesn’t mean the script is wrong.

      1. interested party says:

        @ Harriet Hall
        Just a little philosophical side-bar. You said ““if the drug industry had been allowed to write the script for this, it would have said exactly the same thing.”
        That doesn’t mean the script is wrong.”

        If 100 scripts were written and they overwhelmingly sounded like they were written by the drug industry, that would make a stong correlation. Would that change anything regarding right or wrong? I don’t think so, so I agree with your statement. But for some reason when it comes to drug trials, correlations indicate rightness.

        1. Harriet Hall says:

          “But for some reason when it comes to drug trials, correlations indicate rightness.”

          False analogy. We have said over and over that correlations don’t prove causation. But correlations from different studies that cohere and that are based on plausible rationales are sometimes the best we have for guiding patient care.

    2. weing says:

      “Do we need more examples of how conflicts of interest are causing the poor outcomes and excess costs that are wrecking our health care system?”

      I don’t understand. What examples have you given for poor outcomes of coronary artery disease?

      “Do we need more excuses not to eliminate conflicts of interest from guideline development?”

      I think we need to figure how to do that.

      “Do we need more delay implementing the standards provided by the Institute of Medicine report on trustworthy guidelines?”

      I’ll have to check out whether they are practical or not. Thanks for pointing them out.

    3. WilliamLawrenceUtridge says:

      I find it interesting that these, like so many other criticisms, takes as a starting point that statin use is inherently wrong and harmful. It seems like the data, with all its complications and nuances, doesn’t matter – since the decision has already been made that statins are only prescribed by doctors to make Big Pharma richer.

      Which says more about the critic than it does about the guidelines.

  47. Self Skeptic says:

    Now the apple industry has gotten into the act:
    (just kidding)

    http://www.bmj.com/content/347/bmj.f7267
    RESEARCH
    A statin a day keeps the doctor away: comparative proverb assessment modelling study
    BMJ 2013; 347 doi: http://dx.doi.org/10.1136/bmj.f7267 (Published 17 December 2013)

    Adam D M Briggs, academic clinical fellow, Anja Mizdrak, researcher, Peter Scarborough, senior researcher
    Author Affiliations

    1BHF Health Promotion Research Group, Nuffield Department of Population Health, University of Oxford, Headington, Oxford OX3 7LF, UK
    Correspondence to: A D M Briggs adam.briggs@dph.ox.ac.uk
    Accepted 27 November 2013

    Abstract
    Objective To model the effect on UK vascular mortality of all adults over 50 years old being prescribed either a statin or an apple a day.

    Design Comparative proverb assessment modelling study.

    Setting United Kingdom.

    Population Adults aged over 50 years.

    Intervention Either a statin a day for people not already taking a statin or an apple a day for everyone, assuming 70% compliance and no change in calorie consumption. The modelling used routinely available UK population datasets; parameters describing the relations between statins, apples, and health were derived from meta-analyses.

    Main outcome measure Mortality due to vascular disease.

    Results The estimated annual reduction in deaths from vascular disease of a statin a day, assuming 70% compliance and a reduction in vascular mortality of 12% (95% confidence interval 9% to 16%) per 1.0 mmol/L reduction in low density lipoprotein cholesterol, is 9400 (7000 to 12 500). The equivalent reduction from an apple a day, modelled using the PRIME model (assuming an apple weighs 100 g and that overall calorie consumption remains constant) is 8500 (95% credible interval 6200 to 10 800).

    Conclusions Both nutritional and pharmaceutical approaches to the prevention of vascular disease may have the potential to reduce UK mortality significantly. With similar reductions in mortality, a 150 year old health promotion message is able to match modern medicine and is likely to have fewer side effects.

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