Should Everyone Be Taking Cholesterol-Lowering Drugs?

Simvastatin-650x376

For everyone?

Should everyone over 50 be treated with cholesterol-lowering drugs, regardless of whether they suffer from heart disease?

A new review of previous research shows that even people with no history of heart disease may slightly lower their risk for heart disease with preventative statin medication*.

Independent.co.uk: ‘Millions’ more to be prescribed statins to beat high cholesterol

There are three reasons to be skeptical of mass medication of the healthy population:

1

All studies included in the review were sponsored by pharmaceutical companies, that sell the drugs involved. It’s not controversial that this leads to positive effects being exaggerated and negative side effects being silenced.

When big money like this is at stake, pharmaceutical companies will use every trick in the book. One of the more obvious examples was when the gigantic JUPITER trial was prematurely terminated by AstraZeneca, just when the figures for their drug happened to look good.

2

These are not harmless vitamin pills we’re talking about. Statins come with relatively frequent side effects, such as muscle pain, muscle weakness, fatigue, a slightly reduced cognitive functioning (on average) and an increased risk of diabetes.

3

The reduction in risk of heart disease in previously heart healthy individuals is hardly great. According to this review the chance of preventing a heart attack, or a similar event, by taking a drug for five years is 1.8 percent! Thus, there is a 98.2 percent likelihood that taking the drug for five years doesn’t protect against such health problems. The risk of troublesome side effects? Significantly greater than the chance of any benefit.

Note that a 1.8 precent chance of benefitting from five years of medication only applies if we blindly trust the pharmaceutical companies’ own studies. Most likely the results are exaggerated, so the chance of a benefit would likely be significantly less than 1.8 percent.

1+2+3+=

Most people probably wouldn’t accept the risk of side effects and long-term medication if told about the 98 percent (at least) risk of having done so in vain.

Would you?

More

Cholesterol-Lowering Drugs Heavily Criticized in Australian TV Documentary

Statins May Cause Diabetes

29 Billion Reasons to Lie About Cholesterol

Dr. Oz Changes His Mind on Cholesterol

*/ If this is caused by a lower total cholesterol, a lower LDL cholesterol or a reduction in the number of small, dense LDL is impossible to tell. But my guess is the latter.

Another way to reduce small dense LDL particles, without using statin drugs? A low carb diet.

84 Comments

Top Comments

  1. Christin K
    I finally got health insurance and went to a doctor. He threatened me with statins because my levels were high, in his mind. After research, I felt my ratios were fine. Because of my research I went on a LCHF diet. A year later at my checkup my total cholesterol drop 32 pts, LDL &TRIg went down, HDL went up. My doctor said medication was not warranted now and to keep doing what I'm doing. At the 2nd appointment he asked if I had been following a low fat diet....I said not exactly:)
    Read more →
  2. FrankG
    Thanks goodness Charles is here to provide the much needed balance. Lawd knows that the pharmaceutical companies are hard-done by and so poorly represented by the conclusions of research and publications, especially to the prescribing medical profession. They need a reliable spokesman to put forward their point of view.... after all, they are just trying to help us poor ignorant saps.. let's give them a break guys :-P
    Read more →
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All Comments

  1. Paul the rat
    This is a secod year University biochemistry course excercise - I demonstrate this to my students using mice as a model, come to my class, you will see it with your own eyes, but Iguess:
    1) you already know it but this knowledge is in conflict with your $$$ income
    2) you will say that mice are not humans.
  2. FrankG
    Science 101 Charles.. correlation does not prove causation -- even if the values listed in the above studies are taken at face value (and I don't ever do that) all you have is an association between neurological tissue damage and dyslipdemia... you have no proof that one caused the other or even vice versa.

    A plausible alternate scenario: may be that other factors which led to the nerve damage also led to the dyslipdemia, or that the dyslipdemia (as measured) was part of the body's defense against such damage...

    ALL such alternate scenarios need to be considered and if possible, dismissed, before a firmer conclusion can be drawn... science is not about picking your pet theory.. especially just if it helps you to sell drugs.

    And why present the same study twice Charles? Trying to skew the data in your favour.. or the favour of your paymasters, I should say :-P

  3. charles grashow
    SO - is the study valid or not??
    Reply: #55
  4. Boundless
    Speaking as a lay person who has had an MD try to push statins to me based on worthless lipid (vs. lipoprotein) testing, and has has looked into the matter, statins should be prescribed only very rarely.

    With some steps almost never done:
    - careful attention to total outcome statistics for the specific patient population,
    - full disclosure on side effects, and
    - stern advice on supplementation,
    statins might have some benefit in a few cases, such as:

    * people with a genetic predisposition to heterozygous hypercholesterolemia, such as apo E4

    * middle-aged males who have already had one heart attack (and even they need to be informed of the benefits of simply changing aisles at the supermarket).

    Prescribing statins in any other scenario is in my view borderline criminal malpractice.

    Statins are likely to be a near-future target for the class-action ambulance-chasing segment of the legal fraternity. Doctors need to worry about whether the defendants listed in the complaint will be limited to pharmaceutical companies, particularly if the doctor has been routinely prescribing statins to all and sundry.

  5. FrankG
    "SO - is the study valid or not??"

    "Answering a question with a question is not a good response." ...your own words Charles :-P

  6. Murray
    To FrankG's point, cholesterol is for reparations. People with plaque damage should have higher cholesterol just as a city with more house fires should have more fire trucks. The study fails to isolate cause and effect, including the lack of a plausible metabolic connection from high LDL-C to plaque formation. I recall a study showing people who lived less long slept more hours per night and the researchers concluded too much sleep caused earlier death. How about people near death need more sleep to stay alive as long as they do. The statin industry would have us use the study to justify putting wake-up pills in the drinking water.

    See Nietzsche, Twilight of the Idols, The Four Great Errors, reversal of cause and effect.

  7. @lowcarb_zealot
    Don't feed the trolls, they thrive on a diet of pure sugar and statins....
  8. Galina L.
    Charles,
    You are missing my main point again . I was criticizing the attempts to improve health by micromanaging markers of diseases by taking drags. You think that a trail about the positive association between cholesterol levels and the low possibility of Alzheimer is the argument toward the take of statines. The study would be valid during the discussion about the possible effect of total cholesterol on a brain health. You know you can low it through more exercise and regular fasting. I guess, high cholesterol may be an indicator of being constantly well-fed while being too sedentary (in some cases at least). At least I had a chance to observe such association in my husband. Hi is a very dedicated bicyclist, but takes a weather-brake for colder months , which exists even in a North Florida.
    The people in the study didn't take statines, they were different genetically or had a different diet/life style. I think that such differences were reflected in their brain health.

    The use of statines is not associated with a good mental health, and memory loss and depression are from the list of standard complains, as I understand.The first thing which came from Google was that one http://www.thecholesteroltruth.com/how-statins-affect-brain-function/ - it was impossible to copy citations, so check it yourself.

    From a common-sense perspective taking a drag which worsens memory to prevent Altzhaimer is counter-productive.

  9. Mark
    Someone who has hypocholesterolemia most definitly should not be taking any kind of cholesterol lowering drugs. (If they are not taking any such drugs and are still hypocholesterolemic then cholesterol RAISING drugs would make rather more sense. Assuming such drugs exist.)

    Too low a level of cholesterol appears to be rather more dangerous than too high.

    Interestingly a 164 country BHF/WHO study gives a healthy total cholesterol range of 200-240 mg/dl (5.2-6.2 mmol/l).

    A possible issue with any cholestetrol lowering drugs, especially HMG-CoA reductase inhibitors, is that reductions in LDL-C may shift LDL towards pattern B (small LDL particles). With the type of LDL particles along with their number being far more relevent to CVD than the amount of cholesterol they are carrying.

  10. Lisa
    Not a chance that I'd take this. These drugs belong in the same dumpster as psychotropic drugs. Run for your life!

    I hear and or see people saying all the time it seems "my doctor threatened to put me on x, y or z"

    Are these doctors holding a gun to your head while they shove it down your throat?

    Really you can take the prescription, say thank you upon leaving then rip it up. No one has to take anything they don't want to.

  11. Henri
    The Fat Loss Jumpstart Program By Metabolic Effect
    http://www.youtube.com/watch?v=cR1TCrww9Eo
  12. charles grashow
    Went for some blood work today

    NMR
    Cardio IQ™ Lipoprotein Fractionation, Ion Mobility

    Essential Fatty Acid Profile C:12-C22
    hsCRP
    HA1C

    Let's see what happens

    Reply: #63
  13. Paul the rat
    as far as I know only two fatty acids are classified as essential for humans:
    ALA (C18:3n-3) and LA (C18:2n-6), maybe I should go back to the books
    Reply: #65
  14. Zepp
    Go back to the book!

    Its rather C20:5n-3, C22:6n-3 and C20:3n-6, thats essentiall for us.

    Or in letters, EPA, DHA and DGLA.

    Reply: #66
  15. Pingo
    Wikipedia agrees with you: http://en.wikipedia.org/wiki/Essential_fatty_acid

    A healthy liver should produce the other fatty acids for us in the amounts that we need. However by eating statins or lots of other medications the liver might not do it's job so well and these people might benefit from other fatty acids.

  16. Paul the rat
    @Zepp
    our body can make them(EPA, DHA and DGLA) from ALA and LA so applying principles of biochemistry the precursors (ALA, LA) are always regarded as essential not the final product. (Having said that , I always go back to the books regardless)
    Reply: #67
  17. Zepp
    Yea.. in theory yes.. but one have to consider our defiency of elongase ensymes.. so it comes out that we need to eat 20 carbon elongated and desaturated fatty acids anyhow!

    "In summary, the conversion efficiency from ALA to DHA is very limited in healthy individuals; furthermore, the apparent inefficiency of the conversion from ALA to DHA is markedly variable between individuals within different sectors of the populations such that the lack of sufficient dietary DHA could compromise optimal health in those with very minimal conversion capacities. The very low conversion efficiencies and wide variation in capacities lend support to serious consideration being given to dietary DHA as an 'essential' fatty acid and/or a 'conditionally essential' fatty acid depending upon the conversion capacity of individuals within the population."

    http://www.dhaomega3.org/Overview/Conversion-Efficiency-of-ALA-to-DHA...

    Reply: #68
  18. Paul the rat
    We discussed term 'essential' not biochemistry, individual variability et cetera et cetera associated with conversion of these essential precursors into final products.

    By the way how the authors of the above paper know that this "very limited conversion rate" is not sufficient?. Some patients when supplement with dietary EPA and DHA get leaky gut.

    Reply: #69
  19. Zepp
    I think its well established in biochemistry that it is the need for elongated and desaturated 20 carbon fatty acids of Omega-3 and 6 for our eicosanoid system that make it essentiall?

    http://en.wikipedia.org/wiki/Eicosanoid

    But its a fairly new part of understanding of human biochemistry.. soo I dont do any safe predictions.. its was in the 90ies they got Nobel prise for detecting our Eicosanoid system!

    Replies: #70, #74
  20. Zepp
    Long chain essentiall omega-3 and 6 acids is 20 carbons!

    The mother acid of those is 18 carbons.. and not essentiall!

    Its still the need for Eicosanoid system thats make it essentiall.

    Its a big differens.. its altso complicated.. and then its dificult to understand too.. and its a new discovery to that.

    I dont have that book.. but I read a lot!

    Is there another explanations in that book?

  21. Zepp
    Heres an more complete discussion of our need for LCPUFA and there implications on different persons and healt outcomes!

    "SUMMARY

    Human plasma and tissues are responsive to dietary intake of the long-chain n−3 fatty acids, and levels increase in plasma and tissues in a dose-dependent manner. The most effective way to increase a particular n−3 fatty acid is to provide that specific dietary fatty acid, because interconversion of the n−3 fatty acids is limited in humans. ALA accumulates only to a minor extent, most likely as the result of increased oxidation at higher doses, and modestly raises EPA but not DHA. Plasma phospholipid EPA concentrations increase in a linear manner in response to dietary EPA, whereas dietary DHA causes a dose-dependent, saturable increase in plasma phospholipid DHA concentrations with doses up to ≈2 g/d. Both DHA and EPA similarly reduce ARA concentrations in plasma. Tissue contents of long-chain n−3 fatty acids increase in response to dietary DHA or EPA. Human milk content of DHA depends on maternal intake of this nutrient, and infant plasma DHA concentrations are responsive to the DHA amounts in their milk or formula feedings. The dose-response information provided herein should be useful in predicting efficient doses of n−3 fatty acids for supplementation studies and for developing recommendations for intakes of specific n−3 fatty acids."

    http://ajcn.nutrition.org/content/83/6/S1467.long

    Reply: #73
  22. Paul the rat
    @Zepp
    I do not argue that our bodies do not need EPA and DHA; we do need them. Eye retina, heart muscle, brain, kidneys would not function without them.

    We seem to miss on terms understanding.

    Let us use two terms to make it clear : ESSENTIAL and NECESSARY. In common English these terms carry more or less the same meaning, however in biochemistry (and nutrition) the term ESSENTIAL is reserved for nutrient which can not be synthesized by the body and as such has to be supplied with diet (as for example ESSENTIAL AMINO ACIDS). EPA and DHA are NECESSARY for our bodies but these compounds are not ESSENTIAL in biochemical terminology because they can be synthesized by the body from precursors.

    It is true that the conversion rate is very poor, in some individuals almost not existent, but this does not make EPA and DHA ESSENTIAL nutrients, it makes them NECESSARY to be supplemented with diet because body can not synthesize enough of them from ESSENTIAL precursors. If our bodies could synthesize ALA, LA say from stearic acid but was unable to synthesize stearic acid than stearic acids would have to be supplied with diet and in biochemical terms would be ESSENTIAL.

    It is in these terms that I originally responded.

    Reply: #80
  23. charles grashow
    http://www.itmonline.org/arts/lox.htm

    REDUCING INFLAMMATION WITH DIET AND SUPPLEMENTS:
    The Story of Eicosanoid Inhibition

    Replies: #75, #77
  24. Paul the rat
    When dietary carbohydrates are reduced to less than 10% of total energy, inflammation disappears. Please read work of Prof. Jeff Volek (and related ) on the subject. People on LCHF do not need to take supplements to quench inflammation, diet itself does the job.

    Also arachidonate, portrayed by omega-3 supplements industry as villain, is in fact necessary compound, which does us plenty of good under LCHF. It might be problematic on SAD or high carbohydrate diet - but than again under such conditions more or less whole biochemistry is out of whack.

  25. Paul the rat
    Lipids. 2008 Jan;43(1):65-77. Epub 2007 Nov 29.

    Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation.

    Forsythe CE1, Phinney SD, Fernandez ML, Quann EE, Wood RJ, Bibus DM, Kraemer WJ, Feinman RD, Volek JS.
    Author information

    Abstract
    Abnormal distribution of plasma fatty acids and increased inflammation are prominent features of metabolic syndrome. We tested whether these components of metabolic syndrome, like dyslipidemia and glycemia, are responsive to carbohydrate restriction. Overweight men and women with atherogenic dyslipidemia consumed ad libitum diets very low in carbohydrate (VLCKD) (1504 kcal:%CHO:fat:protein = 12:59:28) or low in fat (LFD) (1478 kcal:%CHO:fat:protein = 56:24:20) for 12 weeks. In comparison to the LFD, the VLCKD resulted in an increased proportion of serum total n-6 PUFA, mainly attributed to a marked increase in arachidonate (20:4n-6), while its biosynthetic metabolic intermediates were decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid ratio also increased sharply. Total saturated fatty acids and 16:1n-7 were consistently decreased following the VLCKD. Both diets significantly decreased the concentration of several serum inflammatory markers, but there was an overall greater anti-inflammatory effect associated with the VLCKD, as evidenced by greater decreases in TNF-alpha, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and PAI-1.

    Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3 are commonly viewed as pro-inflammatory, but unexpectedly were consistently inversely associated with responses in inflammatory proteins. In summary, a very low carbohydrate diet resulted in profound alterations in fatty acid composition and reduced inflammation compared to a low fat diet.

  26. Paul the rat
    See charles grashow, your whole-grains ain't working' (but you can still enjoy them).

    I would like to draw your attention to the statement and the end of Conclusions: "…than for low-GI/GL diets. …"

    Brainwashing that fat is bad is so profound that we see often that authors are simply scared to say it outright that high fat diets are better than multi-grains diets, so they resolve by using terms like "low GI, low GL" et cetera.

    Am J Clin Nutr. 2014 Feb 19. [Epub ahead of print]

    Association between carbohydrate quality and inflammatory markers: systematic review of observational and interventional studies.

    Buyken AE1, Goletzke J, Joslowski G, Felbick A, Cheng G, Herder C, Brand-Miller JC.
    Author information

    Abstract
    BACKGROUND:
    Chronic low-grade inflammation is a likely intermediary between quality of carbohydrate and chronic disease risk.
    OBJECTIVE:
    We conducted a systematic literature search to evaluate the relevance of carbohydrate quality on inflammatory markers in observational and intervention studies.
    DESIGN:
    MEDLINE, EMBASE, and the Cochrane Library were searched for studies on associations between glycemic index (GI), glycemic load (GL), dietary fiber or fiber supplements or whole grain intake, and high-sensitivity C-reactive protein (hsCRP) or interleukin 6 (IL-6). Included studies had to be conducted on adults (healthy, overweight, with type 2 diabetes or metabolic syndrome features, but without inflammatory disease) with ≥20 participants and a 3-wk duration.
    RESULTS:
    In total, 22 of the 60 studies that met our inclusion criteria examined GI/GL: 5 of 9 observational studies reported lower concentrations of hsCRP or IL-6 among persons with a lower dietary GI/GL; 3 of 13 intervention studies showed significant antiinflammatory effects of a low-GI/GL diet, and 4 further studies suggested beneficial effects (trends or effects in a subgroup). For fiber intake, 13 of 16 observational studies reported an inverse relation with hsCRP or IL-6, but only 1 of 11 intervention studies showed a significant antiinflammatory effect of fiber intake, and a further trial reported a beneficial trend. For whole-grain intake, 6 of 7 observational studies observed an inverse association with inflammatory markers, but only 1 of 7 intervention studies reported significant antiinflammatory effects, 1 further study was suggestive (in a subgroup) of such, and another study found an adverse effect (trend only).
    CONCLUSIONS:
    Evidence from intervention studies for antiinflammatory benefits is less consistent for higher-fiber or whole-grain diets than for low-GI/GL diets. Benefits of higher fiber and whole-grain intakes suggested by observational studies may reflect confounding.

  27. charles grashow
    I don't eat whole grains - white/sweet potato, lentils, black/kidney beans, sprouted brown rice.
    Reply: #79
  28. Paul the rat
    Enjoy it !!. Do not forget your anti-inflammatory supplements !! (and then supplements to supplement supplements to supplement supplements…)
  29. Zepp
    Well now I have read up about it.. you are right, I use essentiall in a to wide definition.. I mean both essentiall and nessecery.. and conditionaly essentiall!
  30. Johnny D.
    I quite my cholesterol drug in January of this year, and I feel great! My doctor still thinks I need one, but I feel too good to agree with him. I'm up 51 points but my skin isn't dry anymore and I'm sleeping better and I have less depression. I think something is working for a change. LOL
  31. Boundless
  32. Robert of cape town
    Hi. Where do I find, how do I get hold of, more information about the benefits / side effects coming from radomised controlled trials and statins. As we all know statins are widely prescribed, and many suggest unnecessarily over prescribed. My purpose is the trials that support wide statin prescription, or don't. Moreover, at what levels of which cholesterol fraction should the statin prescription be targeting.
    Thanks Robert
    Reply: #84
  33. Zepp
    You can start here.. Ravnskog is one of the leading statin skeptics!

    http://www.ravnskov.nu/cholesterol

    And both him and Dr Eenfeldt know that there is a few that need statins anyway.. mostly those with FH or those that got CVD and there risk markers dont get better!

    Statins is not a very good drug.. everybody would like if there was a better!

    But.. it could have benefits if one is at emediate high risk.. but it dont revers anything.. that can only life style changes do.. and for some few even that is a very long shot!

    Statins are mycotoxins that inhibit your intra cellular cholesterole production, that make cells dying if they dont suck up cholesterole in your blood for its demand.

    Heres a krasch course on cholesterole!

    http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-p...

    Heres an Islandish cardiologist!

    http://www.docsopinion.com/category/heart-disease/statins-heart-disease/

    I think you got reading for the whole weekend?

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