Although statins are often beneficial, they can cause certain side effects which can be minimised by taking co-enzyme Q10.

Maintaining a low cholesterol level is undoubtedly beneficial for health, as having a raised ‘bad’ LDL-cholesterol is closely linked with your future risk of heart attack and stroke which together account for 245,000 deaths each year in the UK.

Although cholesterol levels are often reduced by dietary and lifestyle changes, many people inherit genes that stop them lowering their total cholesterol through diet and exercise alone. Drug treatment is then needed to reduce the risk of premature death, especially in people with other risk factors for heart disease such as smoking, high blood pressure, overweight or diabetes.This is where the group of drugs known as statins come in.

HOW STATINS WORK

Statins (atorvastin, fluvastatin, pravastatin, rosuvastatin and simvastatin) reduce cholesterol production in your liver by inhibiting an enzyme which is involved in the production of both cholesterol and co-enzyme Q10.

Several large trials show that taking statins for at least five years can reduce the risk of coronary heart disease (CHD) by around one third and can reduce overall mortality by approximately a quarter for those who have already had a heart attack^1-5M. Taking a statin also reduces the risk of non-haemorrhagic stroke by up to 29% in those with CHD^6-7.

Initially, statins were prescribed for people at high risk of coronary heart disease and stroke who had a raised cholesterol level. Then, in 2002, the Heart Protection Study which involved over 20,000 people showed that statins appeared to reduce the risk of major cardiovascular events in everyone, even those with an ideal total cholesterol level of <5.0mmol/l. There did not seem to be a lower cut-off for cholesterol levels beneath which the benefits ended⁸.

Statins are now recommended for anyone whose likelihood of developing CHD over the next 10 years is 20% or greater. This risk is calculated from charts, based on your gender, age, smoking status, blood pressure, cholesterol levels and whether or not you have diabetes. The general aim of treatment is to lower your LDL cholesterol to <3.0mmol/l and your total cholesterol to <5.0mmol/l, or by 30%, whichever is greater, but the decision to prescribe a statin is no longer based on your cholesterol level alone. This all sounds like good news, so where’s the problem?

SIDE EFFECTS

Like all drugs, statins have the potential to cause side effects such as headache, nausea and bowel disturbances. In particular, 1-5% of people taking a statin develop muscle problems such as pain, inflammation and weakness. Out of every 100,000 people taking a statin for a year, one person will also develop a rare condition called rhabdomyolysis, in which muscle fibres break down. If this affects the heart, it is obviously serious, but muscle pigments (myoglobin) entering the circulation can also damage the kidneys.

As well as switching off cholesterol production in the liver, statins also switch off production of co-enzyme Q10 (CoQ10) and this is believed to cause the muscle problems associated with statin drugs⁹. In fact, the original patent filed for the first statin drug suggested that it should be given together with Co-Q10 supplements to prevent muscle side effects.

CO-ENZYME Q10

Co-Q10 is needed for energy production by all body cells and is especially important in muscle, including the heart. When Co- Q10 levels are low, cells cannot produce adequate energy, function less well and are more likely to become diseased. Biopsies from people with various forms of heart disease have shown, for example, that between half and three-quarters are deficient in Co-Q10.

While statins can reduce cholesterol levels by 40-50%, they also reduce Co-Q10 by the same amount - and often more quickly. In fact, taking a statin can halve your circulating blood levels of Co-Q10 within just two weeks¹⁰. Although lowering Co-Q10 levels may not cause difficulties for healthy volunteers¹¹, it can worsen heart problems in some people¹². As a result, all statins sold in Canada are now required to carry a warning that they may seriously deplete Co-Q10 levels in the body, which can lead to impaired cardiac functioning in people with congestive heart failure.

Importantly, taking Co-Q10 supplements has been shown to maintain blood levels of Co-Q10 without affecting the cholesterol-lowering effect of the statin drug¹³. And a recent study showed that combining simvastatin with 60mg Co-Q10 produced improved heart health benefits compared with taking simvastatin alone¹⁴. Co-Q10 supplements appear to be especially important for those on statins who have familial hypercholesterolemia (inherited raised cholesterol levels) or heart failure or who are over 65 years of age¹⁵.

VITAMIN E

Although less well-known, statins also lower blood levels of fat-soluble vitamin E by 17%¹⁶. As a result of reduced Co-Q10 and reduced vitamin E levels, LDL-cholesterol is less able to withstand oxidative stress in people taking a statin¹⁷. If you are taking a statin, it’s worth ensuring your supplement regime also includes vitamin E - ideally along with other antioxidants that support its action, such as vitamin C, selenium, carotenoids, alpha-lipoic acid and l-carnitine.

^*References available on www.healthspan.co.uk

CHOLESTEROL FACTS

• Cholesterol is an important building block for making cell membranes and hormones.
• There are two main sources of blood cholesterol- you make around 800mg per day in your liver and obtain around 300mg per day preformed in your diet.
• There are two main types of cholesterol in your circulation:
  1. Low-density lipoprotein (LDL) cholesterol - often referred to as ‘bad cholesterol’ as it is linked with hardening and furring-up of arteries.
  2. High-density lipoprotein (HDL) cholesterol - usually referred to as ‘good cholesterol’ as it protects against heart disease by transporting LDL - cholesterol away from the arteries and back to the liver for processing.
• Ideally, your total cholesterol level should be less than 5mmol/l.
• It is estimated that as many as 72% of men and 69% of women in the UK aged 35 to 64 have total cholesterol levels above 5mmol/l.
• The average total cholesterol level in adults aged 35 to 64 is currently 6.1mmol/l.

^1. Downs JR et al. 1998. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. JAMA. 279: 1615-22
^2. Shepherd J et al. 1995. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med. 333: 1301-7
^3: Scandinavian Simvastatin Survival Study Group. 1994. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 344: 1383-9< br /> ^4: Sacks FM et al. 1996. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med. 335: 1001-9
^5: Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. 1998. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 339: 1349-57
^6: Byington RP et al. 2001. Reduction of stroke events with pravastatin. The Prospective Pravastatin Pooling Project. Circulation.103:387-92
^7: Hebert PR et al. 1997. Cholesterol lowering with statin drugs, risk of stroke, and total mortality. An overview of randomized trials. JAMA. 278:313-21.
^8: Heart Protection Study Group. 2002. Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002;360:7-22.
^9: Lamperti C et al. 2005 Muscle coenzyme Q10 level in statin-related myopathy. Arch Neurol. 62;11:1709-12.
^10: Rundek T et al. 2004. Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke. Arch Neurol. 61;6:889-92.
^11. Bleske BE et al. 2001 The effect of pravastatin and atorvastatin on coenzyme Q10. Am Heart J. 142;2.
^12: Krum H, McMurray JJ. 2002 Statins and chronic heart failure: do we need a large-scale outcome trial? J Am Coll Cardiol. 39;10:1567-73.
^13. Bargossi et al. 1994. Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMG-CoA reductase inhibitors. Mol Aspects Med. 15 Suppl:s187-93
^14:Chapidze G et al. 2005. Prevention of coronary atherosclerosis by the use of combination therapy with antioxidant coenzyme Q10 and statins. Georgian Med News. 1:20-5.
^15: Levy HB, Kohlhaas HK.2006. Considerations for supplementing with coenzyme Q10 during statin therapy. Ann Pharmacother. 40;2:290-4
^16: Colquhoun DM et al. 2005. Effects of simvastatin on blood lipids, vitamin E, coenzyme Q10 levels and left ventricular function in humans. Eur J Clin Invest. 35;4:251-8.
^17: Palomaki A et al. 1997. Enhanced oxidizability of ubiquinol and alpha-tocopherol during lovastatin treatment. FEBS Lett. 410(2-3):254-8.

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