When your doctor suggests statins (Part 1: Mechanism of Action)

High blood pressure is statistically associated with cardiovascular risk. Avoiding salt lowers blood pressure, but it does not affect cardiovascular risk.

Inflammation is statistically associated with cardiovascular risk. NSAIDs lower the body’s inflammation, and also lowers cardiovascular risk.

Statin drugs reduce LDL cholesterol levels in the blood and also quell inflammation. Statins seem to reduce cardiovascular risk.  Does this have to do with cholesterol or with inflammation?


For almost everyone, LDL cholesterol levels rise during middle age.  Most doctors will prescribe statin drugs as your first line of defense to lower risk of heart attack. The link between LDL cholesterol and heart disease is not well-established.  And in any case, there are many things you can do to lower heart risk that are both more effective and have less side-effects than statins.  I have become convinced that statins are over-prescribed.

(Too many doctors are still telling patients to cut back on salt.  They are out of touch with an emerging consensus.)


 

Two years ago, I spent a few weeks reading the literature on cholesterol and heart disease, and I reported finding a deep split in the community [Part 1, Part 2]:  There are two camps in the research field, one saying that lowering cholesterol levels is the most effective way to control heart risk, and the other saying that cholesterol levels are completely unrelated to heart risk.  At the time, I didn’t take sides; but now I’m inclined toward the latter group, based on politics as much as science.

It is difficult to get a man to understand something, when his salary depends upon his not understanding it.
         — Upton Sinclair

John Abramson, a professor at Harvard Med and author of Overdosed America, lists statins as America’s #1 most overprescribed drug class.  Even for the class of patients most at risk, he estimates that of every 140 people are taking statins, only 1 of them avoids a heart attack. He tells a story of an entire sub-field of medicine that has been touched by money from the pharmaceutical industry.  Most scientists are smart, honest, and independent.  But I have found in several areas that scientists are not immune from herd mentality.  We tend to be trusting creatures, specialized in a narrow field, with faith to accept others’ findings in areas where we are less expert.  Hence, it is not as difficult as you might think for money to influence a scientific paradigm.  This is especially so in epidemiology, where large studies of diverse humans are amenable to various interpretations.  The specialists in physiology are not good at statistics, and the statisticians are not senior authors, but are hired to put numbers together in support of a thesis  The predominance of private money from drug companies over public money from NIH makes pharmacological science especially vulnerable.

Abramson’s advice is that statins are appropriate therapy only for men who have already suffered one heart attack.  For your reference, I’ve posted the key pages from Chapter 9 of his book here.  What he reports is enough to foment a rebellion against for-profit health care, and especially the corporate role in health research.  After reading it, I was moved to write a column dismissing statin drugs as a well-funded scientific fraud.  I did not find evidence to support that.

What I did find, is that the prevailing theory about LDL cholesterol and CV disease has very little support.  I believe that statin drugs work to lower CV mortality, but that the mechanism for the benefit has more to do with inflammation than with cholesterol.  This leads to the question:  Are there better ways to lower inflammation that do not impose the substantial side-effects of statin drugs?

 

What is a heart attack?

Heart attacks result when an artery feeding the heart muscles becomes obstructed.  Most commonly, deposits (“plaques”) build up on the insides of artery walls over many years, and sometimes pieces of placque break off and become seeds for blood clots that can block the artery enough to cause an attack.

  1. The placques are predominantly cholesterol.
  2. The breakage of the plaques is an inflammation process.
  3. Clotting of blood is frequently the step that pushes the attack over the edge.

Viable therapies interrupt the process at any of these three stages.

  1. LDL the form of cholesterol in the blood that is most likely to form plaquest, while HDL can actually dissolve the plaques and re-metabolize choleserol.  Statin drugs lower LDL.  Exercise, weight loss, a Mediterranean diet, and niacin (vit B3) can raise HDL.
  2. Anti-inflammatories can help keep the artery walls intact.  Lowering inflammation also lowers risk of cancer, stroke and AD.  Common anti-inflammatory agents include NSAIDs, fish oil, curcumin, boswellia, and cat’s claw.  Statin drugs are powerful anti-inflammatories, and there is a school of thought that says that their anti-inflammatory action is more important than their cholesterol-lowering action for preventing heart attacks.
  3. Anti-coagulants, including NSAIDs and fish oil, protect against heart attacks as well.  Side effects include risk of internal bleeding, stomach ulcers, and hemorrhagic stroke.  (13% of strokes are hemorrhagic and come from blood flooding the brain; the rest are ischemic, which means that they are caused by a clogged artery, via mechanisms closely analogous to heart attacks.)

Congestive heart failure is a condition that sometimes precedes or predicts a heart attack, and is a health problem in its own right.  The cause is often partial blockage of arteries feeding the heart, causing the heart to become weak.  Common symptoms include decreased stamina, shortness of breath, fluid retention and swelling in the limbs.

 

Statin Drugs Interfere with the Manufacture of Cholesterol

Starting sixty years ago, medical thinking was that it was most powerful and sensible to interrupt this cycle at Stage 1 by lowering the cholesterol in the bloodstream.  Statins go a step further by actually interfering with the body’s manufacture of cholesterol.

The trouble with this reasoning is that cholesterol is not some unwanted byproduct of the metabolism like lipofuscin or glycated proteins.  It is not, like adipose tissue, the origin of pro-aging signals in the body.  Rather, cholesterol is an essential ingredient in the cell metabolism, which the body manufactures abundantly and uses in diverse waves.  Cholesterol lives in cell membranes, and cholesterol is concentrated in nerve cells, where it plays an essential role as insulator.  Cholesterol is a chemicl precursor to vitamin D and sex and steroid hormones.   Our brains have more cholesterol than any other part of us.  Cholesterol is the substrate for producing the bile acids that we need for digestion.  Here is a tutorial on the biochemistry of cholesterol in the body, its manufacture, uses and dangers.

It should be obvious that shutting off the body’s cholesterol factory is likely to cause many unwanted side-effects.  A smarter, more focused attack on the particular chemistry of deposits in the arteries is needed.

 

Choesterol and CV disease

Here are results from a classic epidemiological study, based on the Framingham Heart database [1993] :

The relationship between total cholesterol level and all-cause mortality was positive (ie, higher cholesterol level associated with higher mortality) at age 40 years, negative at age 80 years, and negligible at ages 50 to 70 years.

[Note: there are a lot more people dying at age 80 than at age 40.  The negative relationship at late ages is both more important and better established – JJM]

The relationship with CHD mortality was significantly positive at ages 40, 50, and 60 years but attenuated with age until the relationship was positive, but not significant, at age 70 years and negative, but not significant, at age 80 years.  Results for the relationship between low-density lipoprotein cholesterol and high-density lipoprotein cholesterol and mortality help explain these findings. Non-CHD mortality was significantly negatively related to cholesterol level for ages 50 years and above.

[Translation: People under 70 who had higher levels of cholesterol had a greater chance of dying of heart disease, but this was compensated by a smaller chance of dying of other causes. – JJM]

In this study, funded by the life insurance industry which ought to have a neutral interest in prediction, only small relationships were found between cholesterol and mortality risk,* and risk was elevated both for low cholesterol and for high cholesterol.  LDL levels had no consistent relationship to mortality.  Average levels of HDL were better than either high or low.  High levels of total cholesterol (TC) presented no additional risk, but very low levels corresponded to a 50-75% increase in mortality.  These findings may be of limited utility because they are uncorrected for smoking or diet or statins, and are only very crudely stratified by age. The “sweet spot” for total cholesterol was about 180-230 for men, 170-220 for women.

These two graphs represent all-cause mortality risk for women and men over 60, graphed against their cholesterol level.  1.5 million life insurance applicants (yes – a huge subject pool) have been grouped by percentile.  The middle half is all lumped together, and the ends of the curve are finely divided.  What I get from this picture is consistent with noise from the 5th through the 95th percentiles.  There is no apparent relationship between mortality risk and either total cholesterol or HDL.  The exception seems to be at the extremes–the highest 1% and the lowest 1% both seem to be at higher risk.  The highest 1% corresponds to about 334 mg/dl (F) and 308 (M).  The lowest 1% corresponds to 146 (F) and 138 (M).  (There is no corresponding graph for LDL in the article, but the authors report, “Using LDL or non-HDL cholesterol instead of total cholesterol does not improve mortality risk discrimination; neither does using total cholesterol or triglyceride values in addition to the total cholesterol/HDL ratio”

Mortality_vs_Cholesterol_Fgt60 Mortality_vs_Cholesterol_Mgt60

 

Anti-Inflammatory action of Statins

  • Of potential interest is the statin-induced reduction of C-reactive protein (CRP), a marker for inflammation; recent data suggests that the CRP-lowering effect of statins might, in addition to lipid lowering, be relevant for progression of disease.
  • Data from experiments in cell culture and animal models show that statins can induce the cellular accumulation of endothelial nitric oxide synthase; inhibit the expression of adhesion molecules and chemokines that recruit inflammatory cells; inhibit expression of pro-coagulant factors and induce anti-coagulant substances; inhibit proliferation and promote apoptosis of vascular smooth muscle cells; and ameliorate platelet hyper-reactivity.  [ref]

 

Evidence for Benefits of Statin Drugs

(1) Here’s an example that is well-researched and well-reasoned with a British pedigree:

Reduction of LDL cholesterol with a statin reduced the risk of major vascular events , largely irrespective of age, sex, baseline LDL cholesterol or previous vascular disease, and of vascular and all-cause mortality. The proportional reduction in major vascular events was at least as big in the two lowest risk categories as in the higher risk categories. [Lancet, 2012]

The size of the benefit they find is a 22% reduction in risk of heart attack for a 40 point drop in LDL.

This finding, solid as it appears to be, is actually not inconsistent with the thesis that LDL cholesterol has nothing at all to do with risk of heart disease.  Statin drugs are both powerful anti-inflammatories and also lower LDL cholesterol.  People who take statin drugs may indeed have lower LDL and also lower inflammation.  The incidental correlation between LDL and inflammation would only show up in people taking statins, but it could completely account for the results of this meta-analysis.

(2) Here’s a trial of Rosuvastatin in which heart attack rates were slashed by more than half and stroke by almost that much, and the trial was stopped after just two years because it could no longer be justified to keep people on placebo.  These were people without elevated LDL going in.  Rather they were chosen on the basis of high C-Reactive Protein.  CRP is an inflammatory marker.

So this study is more evidence, perhaps, that statins are very effective anti-inflammatories, and can be read as consistent with the idea that LDL is a red herring.  Reporting included both CRP and LDL levles, but the body text emphasized LDL.

The trial was stopped after a median follow-up of 1.9 years (maximum, 5.0). Rosuvastatin reduced LDL cholesterol levels by 50% and high-sensitivity C-reactive protein levels by 37%…(hazard ratio for rosuvastatin, 0.56; P<0.00001)…Consistent effects were observed in all subgroups evaluated. The rosuvastatin group did not have a significant increase in myopathy or cancer but did have a higher incidence of physician-reported diabetes. [review of JUPITER study]

Tentative Conclusion

I believe that to resolve questions about statins, their mode of action, and whether their benefit justifies the side-effects, what we need is a large scale study in which patients at high CV risk are randomized to a program of statins or to other anti-inflammatory agents.  There has not been such a study, and at present it would be considered unethical, so large is the presumption in favor of statins.

Next week, I’ll have more cholesterol stories, and suggest some alternatives to statins.

Caveat: I’m speculating on health advice out of my field.  I could well be wrong.  I invite readers who know things I don’t know to please comment, or contact me privately.

————————-

* In this context, “small relationships” mean less than a factor of 2 in death rate.  A doubled risk might not seem a small concern, but ratios less than 2 are difficult to distinguish from noise in actuarial studies. An easy-to-remember rule of thumb: a factor of 2 in mortality corresponds to about 10 years in age.

16 thoughts on “When your doctor suggests statins (Part 1: Mechanism of Action)

  1. I always thought free form niacin was a better alternative if the objective was to lower cholesterol but, of course, many do not like the side effects. I hope you address this in the next post.

    • High does of B3 can also be damaging to the liver. I’m only now researching in hopes of finding better alternatives to statins and/or niacin.

  2. -i read that statins are only most effective with ppl who have already had a heart attack.

    -in ppl who have not had such an adverse heart event, statins increase the risk of diabetes in such pp.

    ppl over 50 yrs of age with higher overall cholesterol levels had significant lower risk of having a heart attack; while ppl over 50 yrs of age with lower overall cholesterol levels are at a greater risk of heart attack..

    the science is indicating that the only bad cholesterol is the small hard ldl cholesterol, not th large fluffy ldl. this cholesterol is made from the accumulation of sugar/carbs not burned as body fuel, but becomes stored as triglycerides; the precursor to the bad small hard ldl. it is said that these small hard ldl act as missiles, banging against, and eventually punching their way into the artery walls. the bodies natural defense mechanism is activated to repair the punctures; activating the “calcium patch repair process”. these calcium patches, overtime, accumulate based on the amount of eaten sugar/carbs that are not effectively burned as body fuel, but stored as triglycerides; arterioslcerosis ensues. the cycle is perpetual as long as the person is not properly burning the sugar/carbs.

    on the other hand, it is widely known and accepted but scientific study that animal fat and omega 3 are the most efficient source of body fuel to burn. our cells walls particularly of the lungs) are made of the same fat of animal fat; saturated fat. the optimum proportion of omega 6s and omega 3, i believe is like 1 to 6 ( i forget actually-just look it up).

    point being, we need saturated fat to have healthy strong pliable cell walls.

    conclusion:
    there is a condition called the spontaneous bifurcation (dissection) of the left anterior descending coronary artery (th widow maker). it is the a smaller branch of that main left anterior descending coronary artery. this is a condition where for no apparent reason, that smaller artery splits lengthwise…& for the vast majority of such ppl, this event is fatal.

    my best friend suffered one over a year ago & by God’s will & grace is still with us today…she had virtually no plague, overall cholesterol 118, hdl 45, ldl 30…but triglycerides at 355…

    many of the millions of heart attacks suffered by ppl in the usa annually, are asymptomatic, sudden and fatal. many of these types of heart attacks are to very health conscious and health practicing ppl, while they are exercising but who unfortunately follow the government’s and fda recommendations of high-moderate carb and low fat diets. (please check out the documentary film ‘the widow maker”, narrated by gillian anderson-x files).

    if overall lower cholesterol levels place older ppl at greater risk of an adverse heart event, then based on the above info, i suggest that weaker cell walls, (due to the lack of sufficient saturated fat intake to produce healthy levels of overall cholesterol) are causing these spontaneous bifurcation (dissections) of the ladca and increasing the risk of heart attacks in older ppl.
    terri a.

    • According to my doctor, spontaneous bifurcation is usually caused from a mineral deficiency of copper. Most heart attacks in general are mostly a deficiency of selenium and/or a deficiency in thiamine. Just as you state, cholesterol is necessary for good heart health. There is really no disease that arises from high cholesterol. Correlation does not imply causation. I eat 6 -10 eggs a day on purpose just so I can get enough cholesterol. I am 52 and I have six pack abs year ’round. I didn’t always used to be this way. Until I was 46 I was chubby. That is when I learned that most of the so-called conventional wisdom regarding nutrition was pure bunk. The myelin sheath of the brain is mostly constructed from cholesterol. Not enough cholesterol eventually equals Alzheimer’s. Low sodium diets will kill you. Sodium Chloride is used by the body to make hydrochloric acid, which is used to digest nutrients so that it can be absorbed. Not enough salt equals not enough hydrochloric acid. Not enough HCI means you won’t absorb nutrients (like copper, selenium, etc.) leading to disease. You aren’t what you eat, you are what you are able to absorb. Additionally, lower HCI levels in the stomach equals hight PH levels. Higher PH levels equals an environment prone to candida and other yeast/fungus conditions. Allopathic reductionism tends to focus on the trees rather that seeing the whole forest.

      • Interesting. What did you change in diet and lifestyle to change your body composition? What does your typical meal/supplement regimen look like?

        • Well it wasn’t an overnight change. I learned as I went. But what eventually emerged was a protocol of daily fasting from 8pm to 12pm (only black coffee or tea and water in that time). I cut out all gluten products. The only grains I eat are brown and wild rice and occasionally oats. The only dairy I eat are cheeses. I eat meats cooked medium or medium rare. I eat eggs poached in order to not damage the cholesterol. I eat salads with dressing that do not contain any bottled oil (yes, olive oil oxidizes and is not really good for you). When I want to lean down, I eat almost exclusively steak and eggs. I take supplements that contain all 90 essential nutrients – 60 minerals,16 vitamins, 12 amino acids and 2 essential fatty acids. According to my doctor, most diseases are the result of deficiencies – and then it is mostly mineral deficiencies. Minerals are important cofactors for enzymes and gene expression. Most people are deficient due to modern agriculture practices. We no longer have the rivers overflowing their banks and depositing mineral rich silt on our farmlands. And farmers only put nitrogen, potassium and phosphorus back in the soil to get the crops to grow. So over time, the soil becomes depleted. Therefore, robust supplementation is a must. For exercise, I don’t do any cardio other than walking. I followed the Stronglifts 5×5 protocol 3 times a week to get in shape. Now that I am in shape I do a similar workout but not as intense. I am 6’2″ with a 54″ chest and a 29″ waist. I am complemented regularly on my physique when I’m out in public. I try to share what I have learned with anyone who will listen. But it is amazing how few people will commit to this lifestyle change. I consider it one of the simplest changes I have made in my life, with the greatest results. Now I am looking at longevity as the next step. So I am looking into everything from methylene blue to C60 to deprenyl to metformin, vasopressin, epitalon, etc. – again, learning as I go…

          • >>Most people are deficient due to modern agriculture practices. We no longer have the rivers overflowing their banks and depositing mineral rich silt on our farmlands. And farmers only put nitrogen, potassium and phosphorus back in the soil to get the crops to grow. So over time, the soil becomes depleted. Therefore, robust supplementation is a must.<<

            I had never stopped to consider this chain of cause for malnutrition in our whole foods.

            Thank you for this insight. I can see this being very likely in the commercial of our foods (even farming).

            I always minimized the consumption of mineral/vitamin supplements mainly because the man-made attempt to repackage nature (even up til today's tech standards) misses out on a lot of the unknowns in nutrition and health science the elements and synergistic benefit of elements (enzymes, undiscovered nutrients, etc) that occur from the natural whole food source.

            Still, a concern in mineral / vitamin supplementation is the body's optimal absorption AND proper management/elimination of excess repacked nutrients we attempt to put into these bottled supplements. Perhaps, a request for comprehensive blood work at a doctor's visit would be better to determine levels of such essential vitamins, minerals, etc. is a better approach than taking in large amounts of vitamins/minerals? And by those results, supplement by foods/supplements accordingly and remeasure 45-60days later?

            *******
            On the note of dissection… i recently heard about this rare risk… On that note, I suspect such risks and other serious issues (disease, etc) are due to lack of optimal nutrition… as well as genetics that add extra variable to the risks we are exposed to.

  3. I just finished reading The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet by Nina Teicholz. Once they found a link between cholesterol and heart disease they used that for a proxy for heart disease. That way they could do a diet study in just a year or so rather than wait decades to see who dies eating what diet. Then they found out there are two forms of cholesterol, HDL and LDL and that HDL is actually good, i.e. the correlation with heart disease goes the other way. Now it turns out that LDL can be divided into “good” and “bad” and eating saturated fats raises the “good” LDL while eating carbs and sugar increase the “bad” LDL. It may take decades before they admit their mistake.

  4. Josh (and any other interested readers):

    The following is NOT a disagreement with your fundamental point (which is, I believe, that the medical profession is MISSING the point) about the underlying nature of coronary artery disease. On the contrary, I admit to avidly following your blog since I discovered it last year. If the new paradigm of aging you advocate (and its implications for the most prevalent of chronic diseases) is correct, it means that a large part of my job as a primary care physician will be obsolete. And good riddance.

    I have been researching the inter-relationship of statins, cholesterol and heart disease since medical school with, I think, an unusually healthy skepticism for someone in my profession. As I am a family practitioner, the issue could hardly be more relevant to me, as it is clearly relevant to my patients.

    Perhaps you have already done so, but if not, I would encourage you to go further back in the history of biomedical research to the study and the man who arguably started us down this blind alley: Ancel Keys and his Seven Country Study, which purported to find a relationship between serum cholesterol and vascular risks (i.e. heart attacks and stroke).

    As it turns out, he and his colleagues “cherry picked” the data: out of dozens of data points, they chose the ones which demonstrated the strongest correlation. If ALL the data points are included, the graph looks like it was hit with buckshot – no meaningful correlation (r pretty close to zero). This finding would likely have ended public funding, and Keys’ name would have sunk into obscurity. He (and his colleagues) made the choice to lie by omission, and secure further funding.

    Fast-forward a few decades: HMG-CoA reductase inhibitors (aka “statins”) start to gain attention as a solution to the perceived problem. Unfortunately, they seem to cause as much trouble as they avoid: increased cancer risk, hepatotoxicity, rhabdomyolysis, etc. Statin manufacturers conjured up a trick (aside from blatant falsification of data) to “stack the deck” and improve the odds of successful, publishable results: they learn to use the “run-in” phase (usually 4-6 weeks) to weed out subjects who show signs of adverse events (elevated LFTs, muscle pain, cognitive impairment, etc). In one study, the Heart Protection Study (investigating simvastatin), fully two-thirds of the patients recruited for the study never made it past the run-in phase. Which means, by the way, that their results were only relevant to a minority of patients. But at least they showed modest benefit, which ultimately accomplished Merck’s main goal: to maintain and increase shareholder value.

    By the way, I understand that 9 of the 14 principal investigators in the JUPITER trials had direct financial ties to Astra Zeneca, the manufacturer of Crestor (aka rosuvastatin).

    [The author of this comment is a prominent doctor who has asked that his name be withheld because it is not safe to express such opinions in his professional community.]

  5. Thanks for the article Josh. I have asked about your opinion on this topic before, maybe that also motivated you to write that piece.
    I am myself also suffering from elevated cholesterol, so I am very interested.
    I did some literature review about half a year ago, and I do think elevated cholesterol is definitely a risk factor. For example there is familiar hypercholesteraemia, genetic disorder causing highly elevated TC (10 times the normal). People with this condition usually die of vascular disease at a young age in their 20s.
    According to the Farmingham study SCORE, cholesterol is a risk factor only coupled with elevated blood pressure and advanced age.
    On the mechanism, extra cholesterol tends to inhibit endothelial function thus it is the starting point of the colonization of the vascular wall.
    All this suggests to me the cholesterol is an important enabler of CVD but it is not enough on its own to cause the disease, it has to be coupled with inflammation, high blood pressure, blod clotting agents, etc.

    My personal strategy is that I would like to avoid statins for a few years. I want to do a coronary imaging when I am 45 to assess how much plaques I have. Then based on this information I could decide whether to start on statins.
    Until then (I am 41 now) I try to do with diet/daily exercise. I have some high hopes on time restricted feeding, in mouse studies it had a good effect on TC.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255155/

  6. Josh,

    I was recently switched from my previous “friendly” statin to atorvatstatin.

    It didn’t take long before I noticed painful swelling in my left breast.

    This required a visit with a surgeon who ordered a mammogram.

    Turns out the swelling is gynecomastia, a benign condition in the sense that is isn’t cancer, but not so benign in that the damn thing hurts!

    I can’t prove that the statin is responsible but I am going to go back to my previous medication. If the gynecomastia resolves it will be a pretty good bet that the statin was the culprit.

    In the meanwhile I still have to pay the bills for the mammo and the surgical consult, so not so benign after all.

    Regards,

    John

  7. Hi Josh, I wanted to drop some additional points for your consideration.

    I like genetic studies because they can elucidate the effect of modifying LDL over a lifetime, rather than a snapshot of LDL levels at one point in time. End-of-life cholesterol levels are especially problematic, because they are confounded by (a) people who are making deliberate efforts to lower their cholesterol because they are already at high risk for a heart attack, and (b) people who have comorbidities such as cancer that produce a rapid decline in cholesterol. These people may have deceptively low cholesterol even though it could have been elevated previously and silently affecting them for decades.

    In a Mendelian randomization study, people with genetically lower LDL cholesterol had a reduced risk of CHD that was 3-fold more powerful than statins per unit lower LDL-C.[1] The protective effect was consistent across 9 polymorphism in 6 different genes, making it likely that LDL reduction – the known common factor in these polymorphisms – was causing the effect.

    There are also drugs besides statins that reduce risk, by lowering LDL cholesterol in other ways. Ezetimibe decreases cholesterol reabsorption from the gut, and new PCSK-9 inhibitors upregulate the LDL receptor to increase clearance from the blood.[2]

    Last year, FDA strengthened its warning that NSAIDs could increase the risk of heart attack, with higher doses imparting greater risk.[3] So I’m not too confident in the claim that anti-inflammatory drugs, as a class, will reduce cardiovascular risk.

    Although cholesterol is an important substance for normal biological functioning, how much is adequate? Newborn babies, wild hunter-gathers, and other free-living primates have an LDL cholesterol level in the 50-70 mg/dL range.[4] This is much lower than the “sweet spot” identified by epidemiological study of Western populations. People with heterozygous hypobetalipoproteinemia have LDL levels as low as 30 mg/dL without any apparent negative effects.

    [1] http://content.onlinejacc.org/article.aspx?articleid=1135650
    [2] https://www.sciencebasedmedicine.org/update-on-cholesterol-and-statins/
    [3] http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm453610.htm
    [4] http://www.ncbi.nlm.nih.gov/pubmed/15172426

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