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The battle against cholesterol -

statins are not the only viable option

The majority of those who are mindful of cholesterol have been lead to believe that they must reach a certain set of low measurements in order to avoid cardiovascular disease (CVD). In fact, most of us believe that when it comes to cholesterol levels, the lower the better.  This in turn leads to the fact that around a quarter of western population above the age of 45 takes cholesterol lowering statin medication, disregarding the associated risks and side effects which are usually grossly understated.


The way statins work is by blocking an enzyme in the liver that is responsible for making cholesterol.  The liver wouldn’t be making cholesterol if it was not vital for our survival.  By its nature, cholesterol assists in the production of cell membranes, as well as takes a part in hormone production (including testosterone, progesterone and oestrogen), and bile acids that assist in digesting fat, as well as vitamin D.


Cholesterol is also indispensable to our brain which contains about a quarter of the cholesterol in our body.  In addition, it is crucial for the formation of synapse (neuron connections) which enables us to think, learn and remember.

There is no doubt that statins are effective in reducing cholesterol levels, but we should be careful of rushing into wrong assumptions that since levels of cholesterol are dropping, it must mean that our health is improving and that we are getting better.  There is a ‘bigger picture’.

There is much more to consider in respect of our risk of CVD than just our cholesterol levels, and there is evidence that in some cases statins may actually worsen our heart health.  Furthermore, if you are taking statins you should be aware that certain recent studies show that statins are not as effective or safe as initially thought.

Skewing the Statistics – Making Statins Seem Safer And More Effective Than They Realy Are

A recent report published in the Expert Review of Clinical Pharmacology established that those promoting statins used a statistical tool called relative risk reduction (RRR) to amplify statins’ trivial beneficial effects.[1]


According to this report, the director of clinical trials appears to have been successful in minimising the significance of a large number of negative effects that ensue from treatment with statins.

Let us see how statistics can be abused to deceive us about the effectiveness of statins. If we consider the absolute risk, statins benefit only 1% of those who use it.  Effectively what this means is that out of 100 patients treated with statins only one will be prevented from having a heart attack.

Since this result is not as impressive as statins advocates would like it to be, they use a different statistic presentation called Relative Risk (RR). And magically, statins suddenly become beneficial to 30-50% of the patients taking it.

In respect of side effects, the report notes that they are greater than reported by the media and medical conferences and that the relatively small benefits resulting from the use of the drug   are outweighed by the consequential risks which includes cancer, diabetes, musculoskeletal disorders, cognitive impairment and cataracts.

The study authors noted:[2] “In the Jupiter trial, the public and healthcare workers were informed of a 54 percent reduction in heart attacks, when the actual effect in reduction of coronary events was less than 1 percentage point… 

In the ASCOT-LLA study, which was terminated early because it was considered to have such outstanding results, there were heart attacks and deaths in 3% of the placebo (no treatment) group as compared to 1.9% in the Lipitor group.

The improvement in outcome with Lipitor treatment was only 1.1 percentage point, but when this study was presented to the public, the advertisements used the inflated (relative risk) statistic, which transformed the 1.1% effect into a 36% reduction in heart attack risk.

The inflated claims for statin effectiveness, and minimized portrayal of the adverse effects, has played a role in the health care providers and the public's enthusiasm for cholesterol-lowering drugs, say the authors.”


It is very important to understand how a different presentation of statistical results can be used to deceive us especially where effectiveness is stated in terms of relative risk.  Absolute risk reduction is the decrease in risk of a treatment in relation to a control treatment. Relative risk reduction is calculated by dividing the absolute risk reduction by the control event rate.

To simplify, here is an example:  let us say we have a study of 400 men, half of whom take a drug and half take a placebo, in order to examine the effect of the drug on testicular cancer risk.

After seven years, four men in the drug group develop testicular cancer, compared to eight who took the placebo. This data could lead to either of the following headlines, and both would be correct:

"New Miracle Drug Cuts Testicular Cancer Risks by 50%"  or alternatively, "New Drug Results in 2% Drop in testicular Cancer Risks".

You can now see why clinical trials, and in particular those which are funded by pharmaceuticals, will refer to relative risk reductions rather than absolute risk reductions, and as patients and potential consumers of these drugs, we need to be aware that statistics can be easily skewed and manipulated. The bottom line is that relative risk tells you nothing about the actual risk.

Statins Might Stimulate Atherosclerosis and Heart Failure

In a separate study published in Expert Review of Clinical Pharmacology it was revealed that, contrary to the current belief that cholesterol reduction with statins decreases atherosclerosis, statins may instead actually stimulate atherosclerosis and heart failure.[3]


There were several physiological mechanisms which were discussed in this study that demonstrate how statins may worsen cardiovascular health:[4]


  • Mitochondrial damage: Statins are toxic to the energy cores of the body’s cells, called mitochondria. They impair heart muscle mitochondria function, interfere with ATP production (adenosine triphosphate, the energy molecules of the body), and alter intracellular signalling proteins.


  • Interfere with coenzyme Q10 (CoQ10): Statins deplete the body of CoQ10, which accounts for many of their devastating results.[5]


  • Inhibit vitamin K2 functionality: Statins inhibit the function of vitamin K2 in the body. This vitamin protects the arteries from calcification. Without it, plaque levels increase.


  • Interfere with selenium-containing proteins: Selenoproteins such as glutathione peroxidase are crucial for preventing oxidative damage in muscle tissues. As reported by Wellness Resources:
    “Blocking the selenoprotein enzyme glutathione peroxidase is akin to pouring gasoline on the fire of inflammation and free radicals, which damages muscle tissue. In fact, the scientists described this blocking of the selenoproteins reminiscent of selenium deficiency induced heart failure, known as Keshan’s disease first identified in the 1930s.”


Considering the substantial risks associated, the authors concluded:[6] “...the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically re-evaluated.”

Statins Are Not As Beneficial For Parkinson’s Disease As They Would Make Us Believe

Pharmaceuticals endeavoured to portray statins as a ‘magic-bullet’ for an array of diseases including Parkinson’s.  Past research by Xuemei Huang[7], suggested a link between high cholesterol levels and lower rates of Parkinson’s, yet some epidemiological evidence suggested a lower risk of Parkinson’s associated with use of statins.


In a new study conducted by Huang and colleagues, they attempted to ascertain if the lowered incidence of Parkinson’s could indeed be due to statins.  The results demonstrated that statins were not protective of Parkinson’s and, instead, were linked with an increased risk.[8]  Furthermore, high total cholesterol and LDL were associated with a lower risk of Parkinson’s disease. The study concluded, “Statin use may be associated with a higher PD [Parkinson’s disease] risk, whereas higher total cholesterol may be associated with lower risk.” As for why past studies may have shown a link between statins and a lower Parkinson’s risk, Huang suggested:[9]

“One possibility, is that statin use can be a marker of people who have high cholesterol, which itself may be associated with lower [Parkinson's] risk. This could explain why some studies have found an association between use of these medications and low incidence of [Parkinson's]. Most importantly, this purported benefit may not be seen over time."


Are You at Risk for Heart Disease?

Total cholesterol practically tells us nothing about risk of CVD, unless it is extraordinarily elevated (above 330 or so, which most likely is indicative of familial hypercholesterolemia (This is a condition characterized by abnormally high cholesterol, which tends to be resistant to lowering with lifestyle strategies like diet and exercise), which in the view of many Functional and Integrative Medicine doctors, would be about the only incidence where a cholesterol-reducing drug would be appropriate). Two ratios that are far better indicators of heart disease risk are:


  • Triglyceride/HDL ratios: should ideally be less than 2


  • HDL/total cholesterol ratio: HDL percentage is a very effective heart disease risk factor. It is calculated by dividing HDL level by total cholesterol. This percentage should ideally be greater than 24%. Below 10%, it's a significant indicator of risk for CVD


Additional risk factors in relation to heart disease that should be considered, include:


  • Fasting blood sugar level: Studies have shown that people with a fasting blood sugar level of 100-125mg/dl  (5.55-6.95mmol/L) had nearly a threefold increase in the risk of having coronary heart disease than people with a level below 79mg/dl (4.39mmol/L)


  • Fasting insulin level: Food high in carbohydrates like fructose and refined grains produces a swift rise in blood glucose followed by elevated insulin to compensate for the rise in blood sugar. Insulin which is released from carb rich food consumption, promotes fat and makes it more difficult for the body to lose extra weight and fat (particularly around midriff section). It is one of the major contributors to CVDI


  • Iron level: Iron can potentially be a very powerful oxidative stress, therefore excess iron levels can damage blood vessels and increase risk of CVD. Ferritin levels should be regularly monitored and ideally should be not much above 80ng/ml. High levels may be lowered by donating blood or alternatively by undergoing therapeutic phlebotomy.



Optimising Cholesterol Levels

The strategies outlined below are not intended to be used to lower your cholesterol level as low as you can but rather to be used to optimise your cholesterol level so it is in sync with the rest of your body’s systems.


Most of the cholesterol is produced in the liver, which is influenced by insulin levels. Hence, if you optimise your insulin level, cholesterol level almost invariable will follow suit.  Therefore my key recommendation for safe regulation of cholesterol levels is making the following dietary and lifestyle modifications (low cholesterol diet is not required):


  • Eliminate (or at least significantly reduce) consumption of grains and sugars. It is extremely important to stop consuming grains which contain gluten as well as harmful sugars especially fructose and HFCS (High Fructose Corn Syrup, contained in many foods and beverages) until your insulin resistance is in check.


  • A large proportion of your diet should come from raw foods and stay hydrated with plenty of water.


  • Take plenty of high-quality, animal-based omega 3 fats. Fish oil is good but krill oil is better.  There is ample evidence suggesting that as little as daily amount of 500mg of krill oil is likely to improve total cholesterol and triglycerides levels as well as increase HDL (‘good’) cholesterol.


  • Use healthy oils such as olive oil, coconut oil or butter instead of harmful vegetable oils or transfats. However, olive oil should be used cold only, whereas coconut oil is safe to be used for cooking and backing.


  • Consume fermented foods daily. This will optimise the intestinal microflora in your inner garden as well as introduce beneficial bacteria into your mouth. This will boost your overall immunity. Poor oral health is another indicator of increased risk of heart disease.


  • Ensure your vitamin D levels are adequate.  Ideally through safe exposure to the sun or by taking supplements, as this will allow your body to create vitamin D sulphate - another factor that may play a leading role in the prevention of arterial plaque formation.


  • Exercise regularly. Ensure to incorporate HII (high intensity interval) exercise in your routine.  This will also optimise the production of HGH (human growth hormone).


  • Avoid smoking, taking drugs or consuming high quantities of alcohol or caffeine.


  • Get as much sleep as you can.


Following the above guidelines should allow you with time and under the supervision of your doctor to reduce the dosage of your medication and often to reverse your condition where you could avoid statins altogether. 

Supplement Statins With CoQ10 or Ubiquinol

If you do decide to follow your doctor’s recommendation and take a statins, you need to make sure you take coenzyme CoQ10 or Ubiquinol (the reduced form) with it. The majority of patients are not told they need to take coenzyme Q10 to shield against some of the most harmful side effects of the drug.  As discussed above, statins block not only cholesterol production pathways, but several other biochemical pathways, including CoQ10 and squalene—the latter is considered essential in preventing breast cancer.

Squalene reduction caused by the statin can also raise the risk of immune system dysfunction. The depletion of CoQ10 caused by the drug is why statins can increase your risk of acute heart failure. You should discuss the recommended dosage of CoQ10 with your healthcare provider.


One study in the European Journal of Pharmacology showed that ubiquinol effectively rescued cells from the damage caused by the statin drug Simvastatin, thereby protecting muscle cells from myopathies.[10]


Another study evaluated the benefits of CoQ10 and selenium supplementation for patients with statin-associated myopathy.[11] Compared to those given a placebo, the treatment group reported experiencing significantly less pain, decreased muscle weakness and cramps, and less fatigue.


Disclaimer: The entire contents of this article is based upon the opinions of the author, unless otherwise stated. The information in this article is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of the author and his community. The author encourages you to make your own health care decisions based upon your own research and in partnership with a qualified health care professional. If you are pregnant, nursing, taking medication, or have a medical condition, consult your health care professional before using products based on this content.  This content may be copied in full, with copyright, contact, creation and information intact, without specific permission, unless if used for commercial purposes.






[1]  Expert Rev Clin Pharmacol. 2015 Mar;8(2):201-10

[2] Science Daily February 15, 2015

[3] Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99.

[4] Wellness Resources February 16, 2015

[5] Although it was proposed to add a black box warning to statins stating this, the US Food and Drug Administration (FDA) decided against it in 2014.

[6] Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99.

[7] Professor of neurology and vice chair for research at Penn State College of Medicine

[8] Movement Disorders January 14, 2015

[9] Medical News Today February 20, 2015

[10] European Journal of Pharmacology April 24, 2013

[11] Canadian Journal of Physiology and Pharmacology 02/2013; 91(2):165-70

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