by Dr Jess Braid

Jess says: Reducing cholesterol is something that many of us don’t even consider until we are of an age where we are offered a cholesterol test at the pharmacy or doctors, only to discover that ours is high. 

Or you may have seen adverts on TV for cholesterol-lowering foods and know there is a connection between heart attack risk and cholesterol, but you’re not sure what that connection is and if it is something you should be concerned with. 

Here, we’ll look at how you can reduce your cholesterol if yours is high, and don’t forget to also read our article on natural ways to reduce your cholesterol, which discusses the foods and supplements that you can take if your cholesterol is high. We also have more in-depth articles for what to do if your cholesterol test results are high

what is cholesterol?

Cholesterol – as is evident from its name, is a sterol, a fatty type of substance that is present in the blood and in most cell membranes. Our bodies need cholesterol to function correctly as it helps to regulate our hormones, bile salts and keeps our cell membranes lubricated and fluid. As a fat, cholesterol won’t dissolve in water and so it is attached to a protein carrier and called a lipoprotein. 

There are two main cholesterol-carrying lipoproteins in our body, LDL (low-density lipoprotein) and HDL(high-density lipoprotein). HDL and LDL are measured as part of a standard blood test to measure cholesterol. Learn more about interpreting your test results here.

how will I know if I have high cholesterol and am I at risk of heart disease or stroke?

Six out of 10 adults have raised cholesterol in the UK. The idea that by lowering our cholesterol, we also reduce our risk of heart disease and stroke is one of the biggest health myths out there.1

For years, people have been taught that high cholesterol = bad and low cholesterol = good, but it isn’t that simple. To prove that point, as a nation, the Swiss have one of the highest rates of cholesterol, yet one of the lowest rates of heart disease. 

Standard cholesterol testing has a long way to go before it can accurately assess your risk of contracting heart disease or suffering a stroke. Private testing, however, can now differentiate between the different types of cholesterol and give a much clearer picture of an individual’s risk, including whether there are cholesterol-based particles in your blood that could increase your risk of cardiovascular (heart and blood vessel) disease.2 

Our bodies need cholesterol to function effectively. It is used for the vitamin D, hormones, cell membranes and essential brain and nerve cell function. There are several studies demonstrating that low cholesterol and low LDL (one of the types of cholesterol) increases the risk of death from other causes3,4. A recent British Medical Journal review also showed that elderly people with high LDL (the so-called ‘bad’ cholesterol) may live longer than those with low LDL,5 challenging the cholesterol theory entirely. 

This all makes it more likely that we need to look at cholesterol levels alongside other health markers, not on its own. More sophisticated cholesterol testing can evaluate a range of associated markers simultaneously. This can help with prescribing more useful treatments for patients. 

Cholesterol results should be taken in the context of other tests as part of a comprehensive health assessment. By assessing your other risk factors such as your age, family history, other medical conditions, raised blood sugar or evidence of inflammation, you can make more informed choices. Working with a functional medicine practitioner alongside your medical specialist can be a great idea to help find the best ways to optimise your health and personal risk factors. If you are diagnosed with familial hypercholesterolaemia, medication is nearly always needed. 

ways to reduce your cholesterol 

It is a MYTH that the answer is to reduce saturated fat. Large-scale randomised trials have shown that replacing saturated fats with inflammatory oils (those containing linoleic acid and seed oils like rapeseed, sunflower, canola, safflower, corn, canola etc.) actually increases the risk of heart disease and dying from heart disease.6 Healthy fats include butter, meat fats, coconut oil, ghee and good quality olive oil. 

Inflammatory oils are much more dangerous than saturated fat. Inflammatory oils increase oxidised LDL and are unstable with heat, easily creating damaging particles called free radicals that are inflammatory.7 By contrast, saturated fats like meat fats and coconut oil are stable at higher temperatures and are safe to cook with. Much of our processed food is made using inflammatory oils (check your packets) and unfortunately when we eat out, much of the food that we eat is cooked in these oils. 

Sugar is also a major culprit for increased risk of heart disease. An Italian study showed that two-thirds of those who had heart attacks have diabetes or prediabetes,8 but only 50% of people who die from heart attacks have abnormal cholesterol!9. Sugar also drives inflammation and raises triglycerides.

Reduce your inflammation. Atherosclerosis and heart disease are inflammatory processes, so reducing your inflammation is extremely important – likely more important than your cholesterol balance.6 

Your waist-to-hip ratio is calculated by measuring around the smallest part of your waist (just above your belly button whilst standing straight and breathing out) and dividing it by the measurement around the widest part of your hips. The ratio should be 0.8 or below for women and 0.95 or below for men. It is an important indicator of how much visceral fat (fat around your internal organs there is) and also how likely you are to have a heart attack. This is particularly true in women, where a waist/hip ratio that is greater than 0.8 more than doubles their risk.10 By reducing excess weight, you can substantially reduce your risk of heart problems. 

Eat more vegetables. Vegetables are one of the best sources of dietary fibre. As well as being packed with antioxidants, they are beneficial for your gut health and are anti-inflammatory. Eating more vegetables and whole foods is an important way to reduce total cholesterol and reduce LDL cholesterol and triglycerides. Vegetables are a natural source of cholesterol-lowering plant sterols.11

Exercise improves your HDL cholesterol (the good type that is protective). Exercise has been shown to increase your HDL and the amount of functional (good) HDL you have. Exercise reduces atherosclerosis, inflammation and oxidative stress, so is extremely important for cardiovascular health. Just 30-40 minutes of aerobic exercise three times a week (such as cycling or brisk walking) can increase HDL between 2-8mg/DL. The amount of exercise seems to be more important than how hard you work in that exercise.12,13,14

Eat more omega 3 fats (high in DHA), or take a supplement. Omega 3s, especially DHA and EPA omega 3 fats from fish and possibly algae are shown to be protective against atherosclerosis and reduce the risk of sudden death from a heart attack. They have been shown to improve the balance of cholesterol. Even when not lowering it overall, they lower triglycerides and improve the TG:HDL ratio and inflammation.15 A diet which is high in DHA has been shown to reverse the risk of the APOE4 genetic variation (high risk for heart disease and Alzheimer’s).16 Omega 3 is especially important if you are on statin medications, as a large trial found the risk of heart attack and stroke was 25% lower in those with risk factors taking an EPA-based omega 3 supplement.17

Optimise your vitamin D levels – cholesterol is needed for us to synthesise vitamin D and cholesterol deposits. According to recent research, atherosclerosis (the plaque which hardens the arteries) may be less likely to form when taking a vitamin D supplement. 18 

Dr Jess says: After three months of making the above changes and using the supplements to lower cholesterol (which can be extremely effective) it is appropriate to have a repeat cholesterol blood test. If your results have improved, discuss continuing your dietary changes and supplement management as a viable alternative to medication. Regular blood tests can help establish suitable baseline levels that reflect your personal risk factors. If you do choose to continue to use medication, be sure that you fully understand the benefits and risks. 

medications to lower cholesterol

Even if you are not a fan of taking over-the-counter medication, there are some instances (like familial hypercholesterolemia) where it may be necessary to help lower your cholesterol. This is why working with a functional medical practitioner, alongside your GP can be the best solution to allow you to reduce your cholesterol as naturally as possible. 


Statin medications (atorvastatin, simvastatin, pravastatin, rosuvastatin) can lower the production of LDL cholesterol (by blocking an enzyme involved in its production by the liver). 

They take up to four weeks to reach maximum effect and should be taken at night. Statin medications have the following possible side effects:

  • Nearly 1 in 10 patients experience digestive symptoms including: pain, flatulence and constipation
  • Muscle pain (myalgia) is experienced by up to 1 in 7 people; this risk increases the higher the dosage of statin19
  • Cough experienced by 1 in 20 people, rarely permanent lung disease can develop from statin use (interstitial lung disease)20
  • Changes in liver enzymes and creatinine kinase (a muscle marker) on blood tests; very rarely liver damage
  • Small increased risk of diabetes21
  • Headaches and joint pain, possible but less common
  • Rarely muscle breakdown and kidney failure (rhabdomyolysis)

They should not be taken in pregnancy or by those with liver disease.

If you are unsure about taking a statin, consider making changes to your lifestyle such as those in our article about foods and supplements to help lower cholesterol. Regular testing can check for improvements. In many cases there are many measures to try, before a statin is medically necessary.

Other medications: Those who can’t tolerate statins or find they don’t fully control their cholesterol may be offered:

  • Fibrates (ciprofibrate, bezafibrate, gemfibrozil), which can reduce triglycerides, increase HDL and lower the levels of small, dense LDL by affecting cholesterol metabolism in the liver. They may cause kidney problems and gallstones and may cause digestive disturbance, liver and muscle enzyme changes on blood tests and headaches. 
  • Ezetimibe prevents you from absorbing cholesterol in your gut. It can lower LDL cholesterol, raise HDL cholesterol and lower triglycerides, but it is unknown whether it changes your risk of dying from heart disease or stroke. Common side effects are headache, abdominal pain and diarrhoea, rarely it may cause allergic reactions including skin rashes and mouth and throat swelling.

If you are advised to take statins, working on diet and lifestyle changes to reduce inflammation can also be a huge help to counteract any negative effects of taking the statins. 

Also consider taking a coenzyme Q10 supplement, as statins block coenzyme Q10 production,22 which has a wide range of important antioxidant and anti-ageing roles in the body.23 Coenzyme Q10 supplements can also reduce any muscle pain from taking statins (Dr Jess recommends 100mg daily of the ubiquinol form).24

For those who have familial hypercholesterolemia, there is a very strong argument for using medication for cholesterol reduction (if you cannot reduce it with other measures), due to the high risk of heart attack or stroke. Although it may be possible to use red rice yeast extract with monitoring, there are also other supplements that you may wish to consider. Our article on supplements to help lower cholesterol can be a great starting point. 

other articles in this series:


  1. Ravnskov U. The fallacies of the lipid hypothesis. Scand Cardiovasc J. 2008 Aug;42(4):236-9. doi: 10.1080/14017430801983082. PMID: 18615352.
  2. German CA, Shapiro MD. Assessing Atherosclerotic Cardiovascular Disease Risk with Advanced Lipid Testing: State of the Science. Eur Cardiol. 2020 Jul 15;15:e56. doi: 10.15420/ecr.2019.18. PMID: 32742310; PMCID: PMC7387892.
  3. Zhou L, Wu Y, Yu S, Shen Y, Ke C. Low-density lipoprotein cholesterol and all-cause mortality: findings from the China health and retirement longitudinal study. BMJ Open. 2020 Aug 16;10(8):e036976. doi: 10.1136/bmjopen-2020-036976. PMID: 32801200; PMCID: PMC7430481.
  4. Simes RJ. Low cholesterol and risk of non-coronary mortality. Aust N Z J Med. 1994 Feb;24(1):113-9. doi: 10.1111/j.1445-5994.1994.tb04446.x. PMID: 8002849.
  5. Ravnskov U, Diamond DM, Hama R, Hamazaki T, Hammarskjöld B, Hynes N, Kendrick M, Langsjoen PH, Malhotra A, Mascitelli L, McCully KS, Ogushi Y, Okuyama H, Rosch PJ, Schersten T, Sultan S, Sundberg R. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open. 2016 Jun 12;6(6):e010401. doi: 10.1136/bmjopen-2015-010401. PMID: 27292972; PMCID: PMC4908872.
  6. Malhotra A, Redberg RF, Meier P. Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions. Br J Sports Med. 2017 Aug;51(15):1111-1112. doi: 10.1136/bjsports-2016-097285. Epub 2017 Apr 25. PMID: 28442474.
  7. Ramsden CE, Zamora D, Majchrzak-Hong S, Faurot KR, Broste SK, Frantz RP, Davis JM, Ringel A, Suchindran CM, Hibbeln JR. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ. 2016 Apr 12;353:i1246. doi: 10.1136/bmj.i1246. PMID: 27071971; PMCID: PMC4836695.
  8. Mozaffarian D, Marfisi R, Levantesi G, Silletta MG, Tavazzi L, Tognoni G, Valagussa F, Marchioli R. Incidence of new-onset diabetes and impaired fasting glucose in patients with recent myocardial infarction and the effect of clinical and lifestyle risk factors. Lancet. 2007 Aug 25;370(9588):667-75. doi: 10.1016/S0140-6736(07)61343-9. PMID: 17720018.
  9. Sachdeva A, Cannon CP, Deedwania PC, Labresh KA, Smith SC Jr, Dai D, Hernandez A, Fonarow GC. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. Am Heart J. 2009 Jan;157(1):111-117.e2. doi: 10.1016/j.ahj.2008.08.010. Epub 2008 Oct 22. PMID: 19081406.
  10. Cao Q, Yu S, Xiong W, Li Y, Li H, Li J, Li F. Waist-hip ratio as a predictor of myocardial infarction risk: A systematic review and meta-analysis. Medicine (Baltimore). 2018 Jul;97(30):e11639. doi: 10.1097/MD.0000000000011639. PMID: 30045310; PMCID: PMC6078643.
  11. Maćkowiak K, Torlińska-Walkowiak N, Torlińska B. Dietary fibre as an important constituent of the diet. Postepy Hig Med Dosw (Online). 2016 Feb 25;70:104-9. doi: 10.5604/17322693.1195842. PMID: 26943307.
  12. Ruiz-Ramie JJ, Barber JL, Sarzynski MA. Effects of exercise on HDL functionality. Curr Opin Lipidol. 2019 Feb;30(1):16-23. doi: 10.1097/MOL.0000000000000568. PMID: 30480581; PMCID: PMC6492243.
  13. Woudberg NJ, Mendham AE, Katz AA, Goedecke JH, Lecour S. Exercise intervention alters HDL subclass distribution and function in obese women. Lipids Health Dis. 2018 Oct 10;17(1):232. doi: 10.1186/s12944-018-0879-1. PMID: 30301473; PMCID: PMC6178267.
  14. Palazón-Bru A, Hernández-Lozano D, Gil-Guillén VF. Which Physical Exercise Interventions Increase HDL-Cholesterol Levels? A Systematic Review of Meta-analyses of Randomized Controlled Trials. Sports Med. 2021 Feb;51(2):243-253. doi: 10.1007/s40279-020-01364-y. PMID: 33064295.
  15. Holub BJ. Docosahexaenoic acid (DHA) and cardiovascular disease risk factors. Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):199-204. doi: 10.1016/j.plefa.2009.05.016. Epub 2009 Jul 9. PMID: 19545988.
  16. Kariv-Inbal Z, Yacobson S, Berkecz R, Peter M, Janaky T, Lütjohann D, Broersen LM, Hartmann T, Michaelson DM. The isoform-specific pathological effects of apoE4 in vivo are prevented by a fish oil (DHA) diet and are modified by cholesterol. J Alzheimers Dis. 2012;28(3):667-83. doi: 10.3233/JAD-2011-111265. PMID: 22057027.
  17. Preston Mason R. New Insights into Mechanisms of Action for Omega-3 Fatty Acids in Atherothrombotic Cardiovascular Disease. Curr Atheroscler Rep. 2019 Jan 12;21(1):2. doi: 10.1007/s11883-019-0762-1. PMID: 30637567; PMCID: PMC6330561.
  18. Riek AE, Oh J, Bernal-Mizrachi C. 1,25(OH)2 vitamin D suppresses macrophage migration and reverses atherogenic cholesterol metabolism in type 2 diabetic patients. J Steroid Biochem Mol Biol. 2013 Jul;136:309-12. doi: 10.1016/j.jsbmb.2012.12.019. Epub 2013 Jan 17. PMID: 23333932; PMCID: PMC3687029.
  19. Abd TT, Jacobson TA. Statin-induced myopathy: a review and update. Expert Opin Drug Saf. 2011 May;10(3):373-87. doi: 10.1517/14740338.2011.540568. Epub 2011 Feb 23. PMID: 21342078.
  20. Fernández AB, Karas RH, Alsheikh-Ali AA, Thompson PD. Statins and interstitial lung disease: a systematic review of the literature and of food and drug administration adverse event reports. Chest. 2008 Oct;134(4):824-830. doi: 10.1378/chest.08-0943. Epub 2008 Aug 8. PMID: 18689579.
  21. Thompson PD, Panza G, Zaleski A, Taylor B. Statin-Associated Side Effects. J Am Coll Cardiol. 2016 May 24;67(20):2395-2410. doi: 10.1016/j.jacc.2016.02.071. PMID: 27199064.
  22. Lieberman A, Lyons K, Levine J, Myerburg R. Statins, cholesterol, Co-enzyme Q10, and Parkinson’s disease. Parkinsonism Relat Disord. 2005 Mar;11(2):81-4. doi: 10.1016/j.parkreldis.2004.07.012. PMID: 15734664.
  23. Garrido-Maraver J, Cordero MD, Oropesa-Avila M, Vega AF, de la Mata M, Pavon AD, Alcocer-Gomez E, Calero CP, Paz MV, Alanis M, de Lavera I, Cotan D, Sanchez-Alcazar JA. Clinical applications of coenzyme Q10. Front Biosci (Landmark Ed). 2014 Jan 1;19:619-33. doi: 10.2741/4231. PMID: 24389208.
  24. Qu H, Guo M, Chai H, Wang WT, Gao ZY, Shi DZ. Effects of Coenzyme Q10 on Statin-Induced Myopathy: An Updated Meta-Analysis of Randomized Controlled Trials. J Am Heart Assoc. 2018 Oct 2;7(19):e009835. doi: 10.1161/JAHA.118.009835. PMID: 30371340; PMCID: PMC6404871.