by Dr Jess Braid

reading between the lines

Dr Jess says: If you’ve recently had a cholesterol test, you may be a little confused with what the results actually mean. That’s because it isn’t a simple yes/no thing – if you’ve read my article on what is cholesterol, you’ll already understand that not all cholesterol is bad, but that some types are more problematic than others. If you’ve taken a more advanced test, things only get more confusing! Of course, you should always discuss any test results with your healthcare provider and if you do wish to work on reducing your cholesterol levels, working with a functional medicine expert is a great place to start, as they can help advise on lifestyle factors to consider and show you how to try to use diet and lifestyle changes to transform your cholesterol levels, rather than relying on medications such as statins.

test results – what should my cholesterol be?

It’s really easy to get tested for your cholesterol levels these days. Most GPs, pharmacies and private lab testing companies offer this service as a standard blood test, although a fast finger-prick blood test is also available (though these are potentially less accurate). 

normal values for cholesterol (blood taken after fasting is always more reliable):

Total cholesterol: 3.5-5 mmol/L (<190 mg/dL)

LDL – cholesterol<3 mmol-L (115 mg/dL)

non-HDL cholesterol: <4 mmol/L (130mg/dL)

HDL cholesterol: ≥1 mmol/L  (40mg/dL) in men and ≥1.2mmol/L (45mg/dL) in  women

Triglycerides: ≤1.7mmol/L (150mg/dL)

cholesterol ratios (you can calculate these yourself!):

Total: HDL ratio – ≤4 this ratio is determined by dividing the total cholesterol by the HDL. Studies have shown that a raised total/HDL cholesterol ratio is associated with early atherosclerosis.1

LDL: HDL ratio – Below 4 is ideal. Above 11 is considered to be high risk. This figure is calculated by dividing the LDL by the HDL number. This ratio is of uncertain importance when it comes to the prediction of atherosclerotic plaques,2 or risk of death3, but studies have shown a high LDL/HDL ratio is associated with sudden cardiac death4.

HDL: Triglyceride ratio – you get this figure by dividing your HDL number by your triglycerides. Less than 2 is ideal. If it is above 4 it is high and indicates an increased risk of heart disease. It has been shown that the HDL/triglyceride ratio is one of the best predictors of whether you will have a heart attack5 (if it’s high, it can be up to a 16x higher risk5) so it’s important to work on lowering your triglycerides and increasing your healthy HDL.

what if my cholesterol tests are normal?

If your standard cholesterol panel is normal you can always work on increasing your functional HDL and keeping a good balance of omega 3 fats in your diet. Your diet shouldn’t include harmful seed oils like rapeseed and sunflower oil. You may still wish to check your Lp(a) levels on a blood test, as this can be raised even with normal cholesterol results. 

You may also want to look at other risk factors like blood tests for hsCRP (an inflammatory marker that is predictive of heart disease risk) and HbA1c (a blood sugar measure that should be lower than 36) and consider genetic testing for your ApoE type (see below). 

Cholesterol should be checked every 2-4 years, depending on your age and general health. 

what can I do if my standard cholesterol test is abnormal?

If your total cholesterol is raised – this may not be an issue if your LDL (or non-HDL from some labs) and triglycerides are normal and your HDL is high (but read our section on HDL, to understand the importance of healthy HDL). 

If your total cholesterol is 7.5 or over, it is important to consider familial hypercholesterolemia, especially if you are under 30 years (or if your cholesterol is ≥9 if you are over 30). 

A raised LDL may not indicate a high risk of cardiovascular disease if further testing of LDL particles, subfractions and oxidised LDL is assessed to be low risk (see the section on LDL). 

An LDL of 5 or over is highly suggestive of familial hypercholesterolemia, which is shown to carry significant risks. It is important you are assessed by your medical provider if this is the case. Further advanced cholesterol testing is particularly useful to properly assess the risk, if you have high LDL.

Raised triglycerides – If your triglycerides are high, then it may be worth doing further testing but as these are such a strong risk factor for heart disease and metabolic syndrome, it is important to concentrate on reducing the sugar, carbohydrate and inflammatory oils in your diet. In Dr Jess’s experience, 99.9% of cases will resolve with diet and lifestyle changes.  

A low HDL cholesterol is an independent risk factor for heart disease, stroke and overall risk of death. The best way to increase your HDL is through lifestyle changes such as diet, stopping smoking and exercising regularly. You should also consider your blood sugar control and tackle any inflammation. 

A high HDL, especially if >1.5, may mean it is useful to look at whether your HDL is healthy (functional), which can be assessed by a more in-depth look at the size of the HDL particle. Smaller, denser particles can be a high risk, as they are for LDL. 

You can take this advanced blood testing with a test by Genova CV Health, plus genomics. You can also look at myeloperoxidase levels. Raised myeloperoxidase makes it very likely that your HDL is unhealthy. Although this test is more difficult to find in the UK, it can be done with Cleveland HeartLab in America. 

If your cholesterol test is abnormal, make sure to ask your doctor to test your:

HbA1c (glycated haemoglobin) – Recent evidence makes it likely that higher HbA1c is a cause of raised total cholesterol, LDL cholesterol and raised triglycerides6. HbA1c is a measure of your blood sugar levels over time (the last 4-6 weeks) and shows the importance of controlling blood sugar for cholesterol. It is a simple blood test and the normal range is 31-41mmol-L (5-6%). 

However, with 40mmol/L being pre-diabetic, if you are creeping into the high thirties you need to make changes. Dr Jess has found that by encouraging patients onto a low sugar and low carbohydrate diet she can bring down HbA1c levels to 35 mmol/L (5.4%) and under. In many patients, she has observed an improvement in cholesterol with this approach too. 

HbA1c is an extremely important marker, even in non-diabetics.7 It’s also important for your long-term health to have good blood sugar control. A rise in HbA1c is a late stage of blood sugar problems (blood insulin levels rise several years before blood sugar problems). 

Thyroid function – Low or subclinical hypothyroidism (low thyroid function) likely contributes to a higher risk of atherosclerotic plaques developing in your coronary arteries (the blocking of the arteries). Low thyroid function (or raised TSH can contribute to raised cholesterol, triglycerides and LDL – it also makes oxidised LDL more likely and more dangerous. It is a particularly bad combination if you also have raised blood sugar.8 

It’s important to check your thyroid function blood test is in the normal range if you have abnormal cholesterol and if it isn’t, to take appropriate action. 

other privately available testing:

*Lipoprotein a/ Lp(a) is an independent risk factor that’s associated with a higher risk of heart disease, stroke and blood clots. It has a strong genetic component and should be tested for if your cholesterol test is abnormal. You can have this test done via the NHS by a lipid clinic if you have a strong family history of heart problems. Otherwise, labs like Medichecks, Genova or Doctors Data offer these privately.  

LDL particle number/ LDL-P – this test is more useful than a standard LDL cholesterol test for assessing LDL levels and is a much better predictor of risk. This can be combined with the tests below to give you a better picture of your LDL.

*LDL subfractions – Smaller, denser particles of LDL are the ones that are likely to be damaging to health, whereas the larger size particles are likely protective.

*Oxidised LDL/ OxLDL – LDL is much more dangerous when it is oxidised (damaged) and more likely to cause inflammation and atherosclerosis (plaques in the arteries).  Measuring the level of your LDL that is oxidised is a good measure of your overall risk. Even if you have a normal LDL, it’s important to work on reducing this level if it is high.  

HDL particle number/ HDL-P – Like LDL, this test is more useful than a standard HDL cholesterol test for assessing HDL levels and is a much better predictor of risk. 

VLDL – This correlates with your level of triglycerides, as it is involved in carrying them. High triglycerides are a strong indicator of your risk of heart disease, as is high VLDL.  

Apolipoprotein A1/ Apo A1This is another way to look at the amount of ‘good’ cholesterol (HDL) in your blood, as it is the protein that makes up HDL. Apo A1 is anti-inflammatory and protects against autoimmune diseases9 and dementia.10 Levels of Apo A1 should be greater than 120mg/L in men and 140mg/L in women. The amount found decreases with a diet high in carbohydrate and polyunsaturated fats, and increases with fish-based omega 3s and a low carb and plant-rich diet.11 The ratio of Apo B:ApoA1 can be used to assess risk (in a similar way to the LDL:HDL  ratio, but this method is possibly more accurate).

Apolipoprotein B/ Apo BThis protein makes up most of the proteins in LDL and can be more accurately measured in the blood to assess LDL. High levels of Apo B and a poor ratio of Apo B:Apo A1 (a ratio of >0.8 is a higher risk) are associated with an increased risk of atherosclerosis. 

*Lp-PLA2/ PLACThis enzyme breaks down oxidised LDL in the blood vessel wall. Higher levels indicate that you have oxidised LDL in your blood vessel walls and a high risk of atherosclerosis, heart attack and stroke. Even if the rest of your tests are normal and you have no symptoms, if this test is raised you have an increased risk of heart disease. There is some evidence that early treatment with statin medications lowers this risk.12

*HomocysteineShould be <16µmol/L. Homocysteine is a chemical that can be measured in your blood that when raised can show a deficiency of folic acid, B12 or B6 or a genetic issue (see MTHFR in the genetic section below) but high levels have also been shown to increase your risk of strokes, heart attacks and DVT. 

If your homocysteine is high, there is evidence that supplementing with B vitamins and folate can decrease the levels of homocysteine and lower the risk of stroke.13 High homocysteine has been associated with dementia. B vitamins and folate can significantly improve signs of early dementia.14

*Fibrinogen – fibrinogen is a protein in the blood that helps the blood to clot. It is also involved in injury repair, blood vessel growth and inflammation. Fibrinogen levels can be tested in the blood and several studies have shown when fibrinogen is raised, it is a significant marker for the risk of heart disease and atherosclerosis.15 It may be raised due to genetic tendencies from SNPs –  single nucleotide polymorphisms, which act as genetic markers. If your levels are high, consider taking supportive herbs like ginkgo biloba, which has been shown to improve blood clot resolution.16

Myeloperoxidase – Currently this test is difficult to get in the UK (myeloperoxidase levels are not the same as the more common myeloperoxidase antibodies test), but this test can be done by the American lab Cleveland Heartlab, which accepts samples couriered from the UK. A raised myeloperoxidase indicates inflammation in the blood vessels and damaged lipoproteins, both creating a much higher risk of atherosclerosis and many forms of heart disease and stroke.17

Trimethylamine-N-oxide/ TMAO – Increasing interest and debate over TMAO levels in recent years has led to available testing. Raised TMAO has been shown in multiple studies to increase cardiovascular risk18 as it makes the blood more likely to clot and increases plaques. High levels of TMAO show an increased risk of atherosclerosis, heart attack and stroke.19 As with myeloperoxidase, this test is difficult to get in the UK but is available from Cleveland Heartlab in America. TMAO is produced from the breakdown of choline, betaine and L-carnitine (in our diet) by our gut bacteria. This area of research is showing a new link between our gut health and heart disease.20

*High sensitivity CRP/ hsCRPthis is a relatively inexpensive private blood test for inflammation, costing around £40 and is available from companies like Medichecks on a fingerprick home test. It is an excellent marker for heart disease and stroke risk and if you have raised LDL cholesterol this is a good test to help you assess your risk.21 If raised, it is important to work on inflammation.

Many of these tests are not currently available on the NHS. If you are concerned about your cholesterol, then you can be referred to a lipid clinic who can perform Lp(a) testing, especially if you have a strong family history of heart problems (it is primarily genetic). Homocysteine tests can also be done by the NHS (your GP is usually able to do this test). 

Some of the best overall private checks of the blood markers discussed above are available from Genova Diagnostics and Regenerus labs in the UK. The Genova CV Health test is around £260 for many of the most important risk markers, or £500 if you also test for genetic markers (SNPs), although you would only need to test once for the genetic markers as they don’t change. 

Regenerus labs through Doctors Data offer the Cardiometabolic serum test for around £260 that is comprehensive and also looks at markers of insulin resistance (blood sugar control) We would suggest you consider working with a functional medicine practitioner to interpret the results of these tests and decide on the best diet and lifestyle strategies to deal with any abnormal results. 

In all cases, whether or not you are able to do some of the private tests, abnormal cholesterol should be assessed alongside any symptoms, your family history, blood sugar control and improving chronic (long term) inflammation.

apolipoprotein E/ APOE 

Apart from familial hypercholesteremia, there are a range of important gene variations that you should consider if you have abnormal cholesterol. These are called SNPS – single nucleotide polymorphisms, they are tested for with a simple mouth swab by private companies like Genova diagnostics. The most important one to know for cholesterol is APOE.

Apolipoprotein E is a type of lipoprotein involved in cholesterol clearance and metabolism and is the main cholesterol carrier in the brain. There are three gene types E2 (best), E3 or E4 (worst) and you get one from each parent, so we each have a combination of the two: e.g. E 3/4.  

Your APOE gene type affects your risk of heart disease. If you have any E4 present,  you have an increased risk of high cholesterol and LDL, low HDL, diabetes, heart disease and Alzheimer’s. This risk is worsened if you smoke or drink alcohol, so try to avoid both.22 You can do a simple mouth swab DNA test to find out which genotype you are.

If you have an E4 gene type, it is important to work on diet and lifestyle. Consider seeing a functional medicine practitioner and taking supplements like red rice yeast extract. Some people with E4 variations may need to limit fat in their diet. With regular testing, it should be possible to predict how much impact fat has on your cholesterol markers. 

(Dr Jess has E3/4, as do one in five of the population so try not to worry. It just means you have to think more carefully about preventing long-term health problems through your diet.) 

is there anything else that can cause abnormal cholesterol?

  • chronic kidney disease – significantly increases cholesterol, VLDL, oxidised LDL and triglycerides, decreases HDL23
  • hypothyroidism – increases cholesterol and triglycerides24
  • pregnancy (can increase cholesterol) – statins in pregnancy can cause damage to the developing baby and may cause brain development issues.25
  • multiple myeloma, a bone cancer, can show low levels of LDL cholesterol26
  • steroids can increase cholesterol, LDL and triglycerides, and lower HDL27
  • excess alcohol intake (can increase triglycerides and VLDL)28
  • oral contraceptive pill (can increase cholesterol, LDL, HDL and triglycerides)29
  • beta-blocker medications (can increase triglycerides and lower HDL)30
  • smoking (can increase cholesterol and lower HDL, increases oxidised LDL)31
  • low fat or vegetarian diets (lower HDL)32

other articles in this series:


  1. Acevedo M, Krämer V, Tagle R, Corbalán R, Arnaíz P, Berríos X, Navarrete C. Relación colesterol total a HDL y colesterol no HDL: los mejores indicadores lipídicos de aumento de grosor de la íntima media carotidea [Total/HDL cholesterol ratio and non HDL cholesterol as predictors for increased intima media thickness]. Rev Med Chil. 2012 Aug;140(8):969-76. Spanish. doi: 10.4067/S0034-98872012000800001. PMID: 23282768.
  2. Nimkuntod P, Tongdee P. Plasma Low-Density Lipoprotein Cholesterol/High-Density Lipoprotein Cholesterol Concentration Ratio and Early Marker of Carotid Artery Atherosclerosis. J Med Assoc Thai. 2015 May;98 Suppl 4:S58-63. PMID: 26201135.
  3. Fulks M, Stout RL, Dolan VF. Association of cholesterol, LDL, HDL, cholesterol/ HDL and triglyceride with all-cause mortality in life insurance applicants. J Insur Med. 2009;41(4):244-53. Erratum in: J Insur Med. 2011;42(2-4):108. PMID: 20666103.
  4. Kunutsor SK, Zaccardi F, Karppi J, Kurl S, Laukkanen JA. Is High Serum LDL/HDL Cholesterol Ratio an Emerging Risk Factor for Sudden Cardiac Death? Findings from the KIHD Study. J Atheroscler Thromb. 2017 Jun 1;24(6):600-608. doi: 10.5551/jat.37184. Epub 2016 Oct 26. PMID: 27784848; PMCID: PMC5453685.
  5.  Gaziano JM, Hennekens CH, O’Donnell CJ, Breslow JL, Buring JE. Fasting triglycerides, high-density lipoprotein, and risk of myocardial infarction. Circulation. 1997 Oct 21;96(8):2520-5.
  6. Jia X, Hou Y, Xu M, Zhao Z, Xuan L, Wang T, Li M, Xu Y, Lu J, Bi Y, Wang W, Chen Y. Mendelian Randomization Analysis Support Causal Associations of HbA1c with Circulating Triglyceride, Total and Low-density Lipoprotein Cholesterol in a Chinese Population. Sci Rep. 2019 Apr 2;9(1):5525. doi: 10.1038/s41598-019-41076-6. PMID: 30940890; PMCID: PMC6445078.
  7. Cavero-Redondo I, Peleteiro B, Álvarez-Bueno C, Rodriguez-Artalejo F, Martínez-Vizcaíno V. Glycated haemoglobin A1c as a risk factor of cardiovascular outcomes and all-cause mortality in diabetic and non-diabetic populations: a systematic review and meta-analysis. BMJ Open. 2017 Jul 31;7(7):e015949. doi: 10.1136/bmjopen-2017-015949. PMID: 28760792; PMCID: PMC5642750.
  8. van Tienhoven-Wind LJ, Dullaart RP. Low-normal thyroid function and novel cardiometabolic biomarkers. Nutrients. 2015 Feb 16;7(2):1352-77. doi: 10.3390/nu7021352. PMID: 25690422; PMCID: PMC4344592.
  9. Kravitz MS, Pitashny M, Shoenfeld Y. Protective molecules–C-reactive protein (CRP), serum amyloid P (SAP), pentraxin3 (PTX3), mannose-binding lectin (MBL), and apolipoprotein A1 (Apo A1), and their autoantibodies: prevalence and clinical significance in autoimmunity. J Clin Immunol. 2005 Nov;25(6):582-91. doi: 10.1007/s10875-005-7828-2. PMID: 16380821.
  10. Slot RE, Van Harten AC, Kester MI, Jongbloed W, Bouwman FH, Teunissen CE, Scheltens P, Veerhuis R, van der Flier WM. Apolipoprotein A1 in Cerebrospinal Fluid and Plasma and Progression to Alzheimer’s Disease in Non-Demented Elderly. J Alzheimers Dis. 2017;56(2):687-697. doi: 10.3233/JAD-151068. PMID: 28035918.
  11. Jones JL, Fernandez ML, McIntosh MS, Najm W, Calle MC, Kalynych C, Vukich C, Barona J, Ackermann D, Kim JE, Kumar V, Lott M, Volek JS, Lerman RH. A Mediterranean-style low-glycemic-load diet improves variables of metabolic syndrome in women, and addition of a phytochemical-rich medical food enhances benefits on lipoprotein metabolism. J Clin Lipidol. 2011 May-Jun;5(3):188-196. doi: 10.1016/j.jacl.2011.03.002. Epub 2011 Mar 11. PMID: 21600524.
  12. White HD, Simes J, Stewart RA, Blankenberg S, Barnes EH, Marschner IC, Thompson P, West M, Zeller T, Colquhoun DM, Nestel P, Keech AC, Sullivan DR, Hunt D, Tonkin A; LIPID Study Investigators. Changes in lipoprotein-Associated phospholipase A2 activity predict coronary events and partly account for the treatment effect of pravastatin: results from the Long-Term Intervention with Pravastatin in Ischemic Disease study. J Am Heart Assoc. 2013 Oct 23;2(5):e000360. doi: 10.1161/JAHA.113.000360. PMID: 24152981; PMCID: PMC3835245.
  13. Spence JD. Homocysteine lowering for stroke prevention: Unravelling the complexity of the evidence. Int J Stroke. 2016 Oct;11(7):744-7. doi: 10.1177/1747493016662038. Epub 2016 Jul 26. PMID: 27462097.
  14. Smith AD, Smith SM, de Jager CA, Whitbread P, Johnston C, Agacinski G, Oulhaj A, Bradley KM, Jacoby R, Refsum H. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial. PLoS One. 2010 Sep 8;5(9):e12244. doi: 10.1371/journal.pone.0012244. PMID: 20838622; PMCID: PMC2935890.
  15. Canseco-Avila LM, Jerjes-Sánchez C, Ortiz-López R, Rojas-Martínez A, Guzmán-Ramírez D. Fibrinógeno. Factor o indicador de riesgo cardiovascular? [Fibrinogen. Cardiovascular risk factor or marker?]. Arch Cardiol Mex. 2006 Oct-Dec;76 Suppl 4:S158-72. Spanish. PMID: 17469344.
  16. Naderi GA, Asgary S, Jafarian A, Askari N, Behagh A, Aghdam RH. Fibrinolytic effects of Ginkgo biloba extract. Exp Clin Cardiol. 2005 Summer;10(2):85-7. PMID: 19641664; PMCID: PMC2716226.
  17. Ndrepepa G. Myeloperoxidase – A bridge linking inflammation and oxidative stress with cardiovascular disease. Clin Chim Acta. 2019 Jun;493:36-51. doi: 10.1016/j.cca.2019.02.022. Epub 2019 Feb 21. PMID: 30797769.
  18. Yang S, Li X, Yang F, Zhao R, Pan X, Liang J, Tian L, Li X, Liu L, Xing Y, Wu M. Gut Microbiota-Dependent Marker TMAO in Promoting Cardiovascular Disease: Inflammation Mechanism, Clinical Prognostic, and Potential as a Therapeutic Target. Front Pharmacol. 2019 Nov 19;10:1360. doi: 10.3389/fphar.2019.01360. PMID: 31803054; PMCID: PMC6877687.
  19. 54. Zhang Y, Wang Y, Ke B, Du J. TMAO: how gut microbiota contributes to heart failure. Transl Res. 2021 Feb;228:109-125. doi: 10.1016/j.trsl.2020.08.007. Epub 2020 Aug 22. PMID: 32841736.
  20. Denegri A, Boriani G. High Sensitivity C-reactive Protein (hsCRP) and its Implications in Cardiovascular Outcomes. Curr Pharm Des. 2021;27(2):263-275. doi: 10.2174/1381612826666200717090334. PMID: 32679014.
  21. Bouhairie VE, Goldberg AC. Familial hypercholesterolemia. Cardiol Clin. 2015 May;33(2):169-79. doi: 10.1016/j.ccl.2015.01.001. PMID: 25939291; PMCID: PMC4472364.
  22. Marais AD. Apolipoprotein E in lipoprotein metabolism, health and cardiovascular disease. Pathology. 2019 Feb;51(2):165-176. doi: 10.1016/j.pathol.2018.11.002. Epub 2018 Dec 28. PMID: 30598326.
  23. Dincer N, Dagel T, Afsar B, Covic A, Ortiz A, Kanbay M. The effect of chronic kidney disease on lipid metabolism. Int Urol Nephrol. 2019 Feb;51(2):265-277. doi: 10.1007/s11255-018-2047-y. Epub 2018 Dec 5. PMID: 30519980.
  24. Kotwal A, Cortes T, Genere N, Hamidi O, Jasim S, Newman CB, Prokop LJ, Murad MH, Alahdab F. Treatment of Thyroid Dysfunction and Serum Lipids: A Systematic Review and Meta-analysis. J Clin Endocrinol Metab. 2020 Dec 1;105(12):dgaa672. doi: 10.1210/clinem/dgaa672. PMID: 32954428.
  25. Carson RA, Rudine AC, Tally SJ, Franks AL, Frahm KA, Waldman JK, Silswal N, Burale S, Phan JV, Chandran UR, Monaghan AP, DeFranco DB. Statins impact primary embryonic mouse neural stem cell survival, cell death, and fate through distinct mechanisms. PLoS One. 2018 May 8;13(5):e0196387. doi: 10.1371/journal.pone.0196387. PMID: 29738536; PMCID: PMC5940229.
  26. Tirado-Vélez JM, Benítez-Rondán A, Cózar-Castellano I, Medina F, Perdomo G. Low-density lipoprotein cholesterol suppresses apoptosis in human multiple myeloma cells. Ann Hematol. 2012 Jan;91(1):83-8. doi: 10.1007/s00277-011-1246-8. Epub 2011 May 3. PMID: 21538060.
  27. McCullough D, Webb R, Enright KJ, Lane KE, McVeigh J, Stewart CE, Davies IG. How the love of muscle can break a heart: Impact of anabolic androgenic steroids on skeletal muscle hypertrophy, metabolic and cardiovascular health. Rev Endocr Metab Disord. 2021 Jun;22(2):389-405. doi: 10.1007/s11154-020-09616-y. Epub 2020 Dec 2. PMID: 33269425; PMCID: PMC8087567.
  28. Klop B, do Rego AT, Cabezas MC. Alcohol and plasma triglycerides. Curr Opin Lipidol. 2013 Aug;24(4):321-6. doi: 10.1097/MOL.0b013e3283606845. PMID: 23511381.
  29. Naz F, Jyoti S, Akhtar N, Afzal M, Siddique YH. Lipid profile of women using oral contraceptive pills. Pak J Biol Sci. 2012 Oct 1;15(19):947-50. doi: 10.3923/pjbs.2012.947.950. PMID: 24159692.
  30. Ritter MM, Richter WO, Schwandt P. Die Auswirkungen von Betablockern auf den Lipoproteinstoffwechsel [Effects of beta blockers on lipoprotein metabolism]. Fortschr Med. 1992 Oct 10;110(28):507-10. German. PMID: 1356899.
  31. Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004 May 19;43(10):1731-7. doi: 10.1016/j.jacc.2003.12.047. PMID: 15145091.
  32. Yokoyama Y, Levin SM, Barnard ND. Association between plant-based diets and plasma lipids: a systematic review and meta-analysis. Nutr Rev. 2017 Sep 1;75(9):683-698. doi: 10.1093/nutrit/nux030. PMID: 28938794; PMCID: PMC5914369.