Statins have been almost universally hailed as “wonder drugs” by medical authorities around the world. The market for statins was $26 billion in 2005, and sales for Lipitor alone reached $14 billion in 2006. Merck and Bristol Myers-Squib are actively seeking “over-the-counter” (OTC) status for their statin drugs. Statins are prescribed to men and women, children and the elderly, people with heart disease and people without heart disease.
In fact, these drugs have a reputation for being so safe and effective that one UK physician, John Reckless (I’m not kidding – that’s actually his name!) has suggested that we put statins in the water supply.
That’s a bold suggestion, of course, and it begs the question: are statins really as safe and cost effective as mainstream medical authorities claim? The unequivocal answer is no.
Statins don’t increase survival in healthy people
Statins have never been shown to be effective in reducing the risk of death in people with no history of heart disease. No study of statins on this “primary prevention population” has ever shown reduced mortality in healthy men and women with only an elevated serum cholesterol level and no known coronary heart disease. (CMAJ. 2005 Nov 8;173(10):1207; author reply 1210.) Statins do reduce the risk of heart attacks in this population, but the reduction is relatively modest:
Statins don’t increase survival in women
Despite the fact that around half of the millions of statin prescriptions written each year are handed to female patients, these drugs show no overall mortality benefit regardless of whether they are used for primary prevention (women with no history of heart disease) or secondary prevention (women with pre-existing heart disease). In women without coronary heart disease (CHD), statins fail to lower both CHD and overall mortality, while in women with CHD, statins do lower CHD mortality but increase the risk of death from other causes, leaving overall mortality unchanged. (JAMA study)
Statins don’t increase survival in the elderly
The only statin study dealing exclusively with seniors, the PROSPER trial, found that pravastatin did reduce the incidence of coronary mortality (death from heart disease). However, this decrease was almost entirely negated by a corresponding increase in cancer deaths. As a result, overall mortality between the pravastatin and placebo groups after 3.2 years was nearly identical.
This is a highly significant finding since the rate of heart disease in 65-year old men is ten times higher than it is in 45-year old men. The vast majority of people who die from heart disease are over 65, and there is no evidence that statins are effective in this population.
Do statins work for anyone?
Among people with CHD or considered to be at high risk for CHD, the effect of statins on the incidence of CHD mortality ranges from virtually none (in the ALLHAT trial) to forty-six percent (the LIPS trial). The reduction in total mortality from all causes ranges from none (the ALLHAT trial) to twenty-nine percent (the 4S trial).
However, the use of statins in this population is not without considerable risk. Statins frequently produce muscle weakness, lethargy, liver dysfunction and cognitive disturbances ranging from confusion to transient amnesia. They have produced severe rhabdomyolysis that can lead to life-threatening kidney failure.
Aspirin just as effective as statins (and 20x cheaper!)
Perhaps the final nail in the coffin for statins is that a recent study in the British Medical Journal showed that aspirin is just as effective as statins for treating heart disease in secondary prevention populations – and 20 times more cost effective! Aspirin is also far safer than statins are, with fewer adverse effects, risks and complications.
The bottom line
- Statin drugs do not reduce the risk of death in 95% of the population, including healthy men with no pre-existing heart disease, women of any age, and the elderly.
- Statin drugs do reduce mortality for young and middle-aged men with pre-existing heart disease, but the benefit is small and not without significant adverse effects, risks and costs.
- Aspirin works just as well as statins do for preventing heart disease, and is 20 times more cost effective.
So what if you are at risk for heart disease and you’d prefer not to take a statin? Other than aspirin, there are many clinically proven ways to prevent heart disease involving simple adjustments to diet and lifestyle. In fact, the recent INTERHEART study which looked at the incidence of heart disease in 52 countries revealed that over 90% of heart disease is preventable by diet and lifestyle modifications.
I’ll discuss these natural methods of preventing heart disease in my next post. Stay tuned!
To read more about heart disease and cholesterol, check out the special report page.
Recommended links
- Dangers of statin drugs: what you haven’t been told about cholesterol-lowering drugs
- The effect of statins is not due to cholesterol lowering
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{ 24 comments… read them below or add one }
Not being a big fan of Statins i would suggest reading these articles.
Magnesium and Walking Will Always be Superior to Lipitor
Lifestyle changes that allow you to avoid lipitor
LIPITOR: THE POISON THAT CAUSES CONGESTIVE HEART FAILURE
ROBERT JARVIK, PFIZER’S PIMP WITH A PUMP
We should also keep in mind that statins interfere with co-enzyme Q10 production. CoQ10 is extremely important for mitochondrial energy production and is especially important for heart function. It is also a powerful antioxidant which may prevent arteriosclerosis by preventing the accumulation of oxidized fats. It has been shown in clinical studies to modulate high blood pressure, regulate heart rhythm, and increase exercise tolerance in cases of angina and congestive heart failure.
Hi Marc,
Welcome to The Healthy Skeptic and thanks for your comment.
Yes, that’s exactly right. Statins powerfully inhibit CoQ10 production and that is very likely one reason are not effective for more than 95% of the population and actually increase total mortality in many cases – in spite of their anti-inflammatory effect.
This is one of the many “untold stories” of statin drugs. Thanks for bringing it to our attention!
Chris
Can you link me to some of the studies/data showing that they increase total mortality?
I am currently having a discussion with my father, who’s doctor told him that statins decrease total mortality, and he has gone back on them. I can’t find any reputable studies either way… (and sorry for resurrecting a post this old, but…)
They decrease total mortality in men with pre-existing heart disease, but not in women, men or women over 65, or men without pre-existing heart disease. The mortality reduction in men with pre-existing heart disease is small, and in my opinion is better achieved using other means.
Hi Mark
I read your comments on statin drugs a lot of the symtons I have lethargy muscle weakness etc
I spoke to my doctor regarding this and said it is a very small minority of people that have side affects and it was media hype. I would like to know if I can just go off them because my memory is clouded and I am sick of it. I would rather take aspirin.
Is there a safe way to take aspirin without damaging the lining of the stomach.
I am 57 years old
Kind regards
Julia Pogson
Aspirin is a vitamin K antagonist. This means that the low dose aspirin that is so often recommended is preventing vitamin K from ensuring strong, flexible arteries with little to no calcium deposition – which is probably what REALLY causes CVD. Not to mention that aspirin ups the risk of bleeding out.
Aspirin on a daily basis is ill-conceived and is based on the paradigm of CVD occurring as a result platelets sticking together and then hanging up on build-up in arteries. Instead, it appears that calcium build-up is the first action of problems which occurs throughout life from early on – due to insufficient K2 and insufficiency of other calcium metabolism co-factors – and then the build up causes cholesterol to try to repair this problem and then docs think they need to “thin” blood and reduce cholesterol carrier proteins (LDL and VLDL) and they block the vitamin K action of making calcium go to the teeth and bones by hampering the carrier protein of vitamin K (yep, LDL and VLDL are the carrier proteins of vitamin K and beta carotene, among other beneficial proteins) via statins and aspirin. Hence, we have the wrong paradigm, the wrong treatments, and we need less aberrant forms of calcium, more calcium metabolism co-factors and fewer docs prescribing.
The comment by Micki Jacobs is incorrect.
Aspirin is NOT in any way a vitamin K antagonist. Aspirin is not an anticoagulant like warfarin. Aspirin is an antiplatelet drug. It is an irreversible inhibitor of cyclooxygenase, which is an ezyme involved in the production of prostaglandins and, important for this topic, thromboxane.
Thromboxane causes platelets to clump together. This clumping together to repair damage blood vessels is often what leads to heart attacks and strokes. Therefore, Aspirin works to reduce the incidence of stroke and heart attack by blocking the ability of platelets to clump together.
That’s not to say that low-dose Aspirin does not have it’s own potential adverse effects. Even low doses of Aspirin can greatly increase one’s risk for gastrointestinal ulcers. However, everything the aforementioned comment mentioned about it’s effect on Vitamin K is completely false.
Aspirin has absolutely no effect on Vitamin K.
Thanks for this post and comments regarding CoQ10, which most physicians seem to ignore. There’s a very good book related to this discussion — “Drug-Induced Nutrient Depletion Handbook.” It’s not as up-to-date as some of us would like, but it’s still helpful for anyone wondering about how specific drugs can affect our health. (fyi, I have no connection to this book or its authors — just find it useful and thought others might, too.)
Thanks for the heads-up on that book, abolderwoman. Actually I just received an email a couple of days ago from a woman who suffered from muscle damage as a result of taking statins. She was wondering what she can do to address the persistent weakness she’s experiencing – even though she is no longer taking the drugs. I’ll forward this to her.
Here are my numbers:
49 year old female
overweight
normal bp
normal sugar readings
0verall chol: 281
hdl 73
ldl 193
triglycerides 152
crp 7.2
My doctor has been bugging me for the past 2 years about going on statins. The main concern is my ldl and crp readings(which he admits are not always accurate). I’ve had these readings for many years, no matter what weight I am at or exercise level.
Took pravastatin 2 years ago for a feww months and stopped after memory issues and muscle pain.
I’d really appreciate input.
Here are my numbers:
49 year old female
overweight
normal bp
normal sugar readings
0verall chol: 281
hdl 73
ldl 193
triglycerides 152
crp 7.2
My doctor has been bugging me for the past 2 years about going on statins. The main concern is my ldl and crp readings(which he admits are not always accurate). I’ve had these readings for many years, no matter what weight I am at or exercise level.
Took pravastatin 2 years ago for a feww months and stopped after memory issues and muscle pain.
I’d really appreciate input.
Chris,
Above, you state: “Statins have never been shown to be effective in reducing the risk of death in people with no history of heart disease.”
This is what I had thought as this is basically what has been promoted in the popular media outlets.
I’d be interested in your thoughts on the following article published in the NEJM:
“Long-Term Follow-up of the West of Scotland Coronary Prevention Study”
http://www.nejm.org/doi/full/10.1056/NEJMoa065994#Background=&t=abstract
This shows a reduction in (total) mortality in healthy patients (elevated cholesterol as well as no previous MI). I wonder why this hasn’t been cited more in popular media?
Chris,
Above, you state: “Statins have never been shown to be effective in reducing the risk of death in people with no history of heart disease.”
This is what I had thought as this is basically what has been promoted in the popular media outlets.
I’d be interested in your thoughts on the following article published in the NEJM:
“Long-Term Follow-up of the West of Scotland Coronary Prevention Study”
http://www.nejm.org/doi/full/10.1056/NEJMoa065994#Background=&t=abstract
Are you familiar with this study?
This shows a reduction in (total) mortality in healthy patients (elevated cholesterol as well as no previous MI). I wonder why this hasn’t been cited more in popular media?
Last May (2011) my NEW doctor started me on a statin drug after cholesterol came back at 262. HDL (60′s)and Triglycerides (80′s). LDL 170′s. I asked nurse about side effects and was told not to worry about it. I said what the heck and started taking them. 6 weeks later cholesterol numbers fine. continued on statin. couple months later found my hips hurting so bad couldnt sleep. Then found i couldnt run without massive joint and muscle pain. I decided to do research of side effects and found the statin drugs to be the cause. Stopped them and was fine within a short time. My doctor said I HAD to take them. I asked about diet and exercise and she said a man my age (54) couldnt control my cholesterol without drugs.
Well I refused to take the statins again and started educating myself. Through my reading I discovered the importance of Omega 3 (EPA DHA) in our diet and how Omega 6 causes inflammation. Taking 2+ grams a day of Omega 3 (EPA DHA), also take Niacin, 1 gram a day.. 4 months later, without Statins, my total cholesterol is 217, HDL is 67, Triglycerides 71 and LDL 136. Combined with this started eating way better, avoiding the simple carbs, vegetable oil etc etc etc. I have lost 10 lbs without trying ( I am 6′ tall and did weigh about 194)
The biggest thing is I FEEL GREAT!!!!!!
I tell people to read your articles all the time, changed my life. Thank you!!!
P. S. I am looking for a new doctor.
Dave
Your welcome, Dave! So happy to hear I’ve made a difference for you.
How do I know how much COq10 to take each day?
50 mg a day is a standard dose. There isn’t much evidence that higher amounts are beneficial, and they may be harmful.
In the end, we can’t trust most doctors as they recommend what drug companies tell them and not what science tell them. I eat well (most of the time mostly vegetables and very little meat and little sugar) and I have a very good HDL level but a little high LDL level.
I am 47. A doctor specialized in lipid clinic told me right away that I had to take statins even if I do not have any heart problem.
I really am frustrated regarding this doctor urge to prescribe drugs to enrich companies instead of trying to find other ways. Are doctors really independent???
Hi Chris
I understand you are not taking any new patients, but would like to know if you can recommend someone who has a nonstatin approach to lipids. Please don’t tell me to go to the paleo doc site because most of the people on there are chiropracters (not that I have anything against them, but I probably need an MD). I have extremely high cholesterol (61 y.o. thin female) and up until recently have been on 10 mg of lipitor, but stopped it because my blood sugars have been labile and I think I’m one of those who have developed diabetes from statins. I fit the typical profile.
Right now I am trying to control my blood sugar by low carbing (we raise our own grass fed animals/milk/eggs etc), but still not sure what to do about the high cholesterol. Thanks
Chris,
Do you believe a daily low dose aspirin (81 mg) is just as effective as a higher dose at treating heart disease, but with–perhaps–a smaller risk of internal bleeding? My doctor says I would “benefit” from a statin, but I have refused thus far to take one, and am considering aspirin as a part of an approach to reduce the risk of CVD. My Apo-B is 143 with pattern B LDL and high blood sugars and high blood pressure. I definitely have to do something to reduce my risk of CVD.
Thanks Chris
Hi there,
Just came across your information.
I was always against stain-use from the widespread information that gets purported by ‘alternative medicine’ in terms of the issues with myopathy and rhabdomyolysis, and memory problems.
I have just written a report on long-term statin use for a class my cardio class at University and the issue I take with your article is that you look at a few very, very large meta-analyses and then use that to form judgements.
Statins have a strong correlation with reduced heart disease (30-35% reduction in LDL-C and 20-25% reduction in mortality from CHD) and these values have been established across wide number of studies. The problem most people make is they say the cholesterol has very little to do with it (they would be right) but the pleiotropic effects of statins is huge. Reduced inflammation, up-regulated nitric oxide, huge antioxidant benefit and stability of the endothelium is massive. They are marketed as cholesterol lowering drugs (which they do) but the main benefits seem to come from the above beneficial effects.. And so when you tell people to stop taking statins cause they cause muscle degradation or they cause this or that.. Or that cholesterol has nothing to do with it.. It could do a lot of harm (people have heart attacks when stopping statins use due to immediate drop in nitric oxide and spiked blood pressure)..
Take home message – cholesterol has very little to do with CHD other than being a mediator in the process – statins have a wide-spread affect other than just cholesterol. First, you should fix your lifestyle (i.e. start exercising, start taking CoQ10, omega 3s, eating less refined CHOs) and then reduce statin use. The ill-harm that comes from reduced CoQ10 levels can be mediated via a supplement and most people’s muscle pain goes away when they use that supplement.
Also, when you say there is no reduced mortality in people taking the statins vs. placebo, you have to remember that people will die of something, eventually. So sure, they die of cancer, but their quality of life may have been hugely increased by not having CHD.
The way you talk, you are still thinking of statins as a cholesterol lowering drug. Since that it was they are prescribed for it would make sense to assume that when you ask “What do statins do?” the answer would be “lower cholesterol.”, but that is not the case.
There have been several drugs that actually did lower cholesterol(cholestenone, Triparanol, etc) but in each case they never made it to clinical trials or were pulled shortly after they did because they are extremely dangerous. In the case of Triparanol, for example, it increased the blood levels of desmosterol(one of the precursors for cholesterol) which had similar effects to cholesterol, so it didn’t provide any net gain. These drugs also caused lens cataracts and hair loss. Rats tested at high dosage actually went blind.
So if statins don’t inhibit cholesterol, what do they do? Well, they went all the way back to the basic building blocks and blocked it there, by inhibiting the entire mevalonate pathway. Statins interfere with the pathway right near the top, by blocking the Hydroxymethylglutharyl-CoA(HMG-CoA). This is equivalent to trying to reduce the emissions on your car by welding the intake for your gas tank closed.
So what does it block, besides cholesterol?
Well, it blocks all of the following, among many others:
Acetone, Acetoacetic acid, beta-Hydroxybutyric acid, Mevalonic acid, Phosphomevalonic acid, 5-diphosphomevalonic acid, Isopentenyl pyrophosphate, Dimethylallyl pyrophosphate, Geranyl pyrophosphate, Prephytoene diphosphate, Phytoene, Androstenedione, 5-Androstenediol, Testosterone, Dihydrotestosterone, DHEA sulfate, Epitestosterone, Farnesyl pyrophosphate, Squalene, Lanosterol, …
Among the end-points that are blocked are the Dolichols, Ubiquinones, Squalene, Heme A, Sterols, and Prenylated proteins.
So what does that matter? Well, lets take dolichols… While they have many effects, for our purpose here let us examine their function in the brain. As our brains develop the levels of dolichol increase and the substantia nigra gets darker(caused by neuromelanin, of which the major portion is made of dolichols). In Alzheimer patients, they have found that there are decreased levels of dolichols, and several drug companies are testing various drugs(i.e. Ropren) to deal with neurodegenerative diseases by addressing dolichol deficiency. Statins cause artificial dolichol deficiency. Gee, I wonder what that would do…
What about squalene? Well, it is the biochemical precursor to all steroids. It is also vital for vitamin D synthesis… But I guess that none of those are really important, right?
Have you seen the list of side effects for, for example, lipitor?
abdominal pain
acute renal failure
altered liver function
anaphylaxis
angioedema
angioneurotic edema
anxiety
arthralgia
Cataracts
chest pain
chills
cholestatic jaundice
cirrhosis
constipation
cranial nerve dysfunction
decline in cognitive function
decreases in libido
depression
dizziness
drowsiness
dyspepsia
dyspnea
erythema multiforme
fatigue
fatty changes in the liver
fever
flatulence
flushing
fulminant hepatic necrosis
gynecomastia
headache
hemolytic anemia
hemorrhagic stroke
hypospermia
insomnia
leukopenia
liver dysfunction
Loss of apetite
malaise
memory loss
myalgia
myopathy
nightmares
Opthalmoplegia
pancreatitis
paresthesias
peripheral edema
peripheral nerve palsy
peripheral neuropathy
polyneuropathy
rhabdomyolysis
Stevens-Johnson syndrome
thrombocytopenia
thyroid dysfunction
toxic epidermal necrolysis
Transient Global Amnesia
tremors
urticaria
vertigo
vomiting
weakness
How many of their patients do you think doctors are warning about those side effects? How many patients are being prescribed statins when they are in groups that show no benefit to it AT ALL(i.e. women)? Not only that, but there is an abnormally depressed reporting of adverse effects, and it has actually been fairly well documented that doctors are resistant to attributing these adverse effects to the statins and reporting them as such.
Take home message: Statins are really really bad news, and you shouldn’t START taking them in the first place. Granted if you have been on a significant dose for some time you should wean yourself off rather than going cold turkey, but you should still get off them
Hi Chris,
What do you think about the updated Corhane review which do suggests that statins are effective for the primary prevention of CVD? http://www.ncbi.nlm.nih.gov/pubmed/23440795
Also, there have been studies since that show effectiveness for woman as well:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097284/
Finally, what do you think about blood glucose levels as a way to measure CVD risks?
http://www.ncbi.nlm.nih.gov/pubmed/23351551
Thanks Kaspars
P.S. I very much enjoy reading this site and listening to your podcasts, a wealth of information. Thank you for that!
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