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Dietary fats & blood lipids

An in-depth review

This HEART UK Nutrition Academy webpage has been funded by Novartis Pharmaceuticals UK Ltd who have had no input into the content or development of this material.

Welcome to the first of our four-part blog series, where we will explore essential dietary interventions for achieving optimal blood lipids.

Dietary advice is pivotal in lipid management for optimal cardiovascular health. The leading cardiology organisations, such as the American Heart Association1, European Society of Cardiology2, and NICE3, have aligned their primary and secondary prevention guidance with similar dietary recommendations.

A critical dietary aspect of lipid management hinges on the quality of fats consumed and is the focus of our first blog.

The balance of dietary fats consumed by an individual can significantly influence the quality of plasma lipids: low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol and triglycerides (TGs)2,4–6.

Plasma lipids and cardiovascular risk

It is well established that elevated plasma LDL cholesterol is atherogenic and both raised LDL cholesterol and TGs are directly associated with increased cardiovascular disease (CVD) risk2,6–9.

With regard to HDL cholesterol, studies have found an inverse association with atherosclerotic CVD as a consequence of HDL's role to remove cholesterol from peripheral tissue and the circulation and return it to the liver for removal. However, recent evidence indicates a U-shaped correlation, with very high levels potentially increasing risk2,10. Furthermore, intervention studies trialling medication to increase HDL cholesterol have failed to demonstrate a benefit in cardiovascular outcomes11,12. Protective effects of HDL cholesterol seam to peak at levels around 1.3-1.4 mmol/L with little additional benefits seen at levels beyond 1.4mmol/L13.

Table 1. Target blood lipid levels in primary care14.  This table is a general guide for ideal cholesterol and triglyceride levels for healthy adults in the UK. Blood lipid targets for secondary prevention should be tailored to each patient i.e., for those with high cholesterol or at higher risk e.g., existing heart disease or diabetes, target levels may be lower.

Blood lipids mmol/L
Total cholesterol <5
Non-HDL cholesterol <4
LDL cholesterol <3
HDL cholesterol

>1 for men; >1.2 for women

Ideally, around 1.4.

Very high levels may not give extra protection.

Fasting triglycerides <1.7
Non-fasting triglycerides <2.3

Non-HDL cholesterol includes all the atherogenic lipoprotein particles: LDL, very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL).

The primary role of dietary and pharmaceutical interventions is to lower plasma LDL cholesterol and elevated TGs. In particular, elevated LDL cholesterol levels and the duration of exposure are now undisputed (through Mendelian, observational and randomised controlled trials) direct causal risk factors for the development of atherosclerotic CVD2,6,7.

1 mmol/L reduction in LDL cholesterol has been associated with6:

  • A 23% reduced risk of atherosclerotic CVD over a period of 5 years
  • Over a 12 year period, the reduced risk can be as much as 30%
  • Over 50 years, the risk reduction is as much as 50%

UK prevalence & impact of high cholesterol

Dietary fats: quality over quantity

It is the balance of the different types of dietary fats rather than the quantity of fat in the diet that will determine the impact on plasma lipids1,2,5,6,15.

Saturated fat

Saturated fats, especially those rich in lauric (C12:0), myristic (C14:0) or palmitic (C16:0) fatty acids significantly increase LDL cholesterol6,15,16.

The mechanism: high saturated fatty acids reduce liver LDL receptor numbers and expression, thus reducing the liver's capacity to take up cholesterol from the circulation for removal via bile acids.

What replaces saturated fat will determine the impact on lipids

The nutrient replacing saturated fat in the diet is crucial in determining whether plasma lipids improve, remain unchanged, or deteriorate6,15–17. Thus, when considering outcomes of clinical studies investigating the impact of dietary fats, it is important to critique the methodology and ensure the saturated fat replacement is identified.

Table 2. The impact on blood lipids of replacing 5% dietary energy from saturated fats with other fats and carbohydrates15

Nutrient replacing 5% energy from saturated fat Change in blood lipids - mmol/L






Polyunsaturated fatty acids
(PUFA - in the main n-6)
-0.28 -0.05 -0.02
Monounsaturated fatty acids (MUFA) -0.21 -0.02 -0.01
Carbohydrates* -0.17 +0.55 -0.05

*carbohydrate's impact on lipids will vary depending on whether refined or whole grain carbohydrates replace saturated fats.

MUFA and PUFA for optimal LDL cholesterol reductions

Replacing saturated fats with either monounsaturated fatty acids (MUFA) or polyunsaturated fatty acids (PUFA) significantly reduces LDL cholesterol with little impact on HDL cholesterol or TGs6,15. Additionally, PUFA lowers LDL cholesterol to a greater magnitude than MUFA.

Mechanism: unlike saturated fats, unsaturated fats increase hepatic LDL receptors and expression, enhancing cholesterol uptake and clearance from the bloodstream.

Plant vs animal sources of MUFA

Meat and animal fats as well as plant fats can be significant sources of MUFA. However, the World Health Organization (WHO) has undertaken an extensive review of the evidence and demonstrated that plant food sources of MUFA are superior to animal-sourced MUFA with regard to both coronary heart disease (CHD) incidence and mortality5. Large cohort studies have concurred that plant sources of MUFA are cardioprotective, while consuming animal sources of MUFA can be detrimental to overall health18.

This should not be surprising as animal foods providing MUFA will also be a source of saturated fat, while plant food sources of MUFA will predominantly provide other unsaturated fatty acids.

What about omega-3?

Omega-3 unsaturated fatty acids have long been associated with reduced CVD and CHD risk. However, the evidence is not clear about the direct association19,20.
What is known is that replacing saturated fats with unsaturated fats (which includes omega-3), will lower LDL cholesterol which is a well-established causal factor for atherogenic CVD. Additionally, diets rich in oily fish, which is a major source of long-chain omega-3, such as the Mediterranean diet, have also been associated with lower CVD risk21.

Marine long-chain omega-3 fats, eicosapentaenoic acid (EPA; C20:5) and docosahexaenoic acid (DHA; C22:6) at pharmacological doses (2-4g daily), may be used therapeutically to lower elevated TGs by 20-30%8,20,22–24. In the updated Cochrane systematic review and meta-analysis, increasing intakes of EPA and DHA were associated with small improvement in CHD events and reduction in mortality20.

Short-chain plant omega-3 fats (alpha-linolenic acid; ALA C18:3). An extensive review of the studies investigating ALA supplements on cardiovascular health outcomes, suggests that ALA may reduce risk of CVD events and arrythmias, but more evidence is needed20.


The type of carbohydrate that replaces saturated fats in the diet will also play a critical role on plasma lipids25. Refined carbohydrates have been shown to increase TGs significantly and have little impact on LDL cholesterol, whereas whole grains (particularly those rich in viscous fibre) have been demonstrated to reduce both LDL cholesterol and triglycerides.

Dietary cholesterol

The focus of dietary intervention for lipid management seldom focuses on dietary cholesterol due to a number of reasons including:

  • Typical intakes are low and below recommended maximum daily intakes of 300mg
  • Saturated fats, due to the higher quantity they are consumed in, are far more potent at elevating serum LDL cholesterol levels
  • Foods high in saturated fats are also often key sources of dietary cholesterol. Thus, reducing intakes of foods high in saturated fat, will automatically lower cholesterol intakes.

Individuals with familial hypercholesterolemia (FH) are the exception to this rule26. Due to their genetic predisposition, FH patients have exceptionally high levels of serum cholesterol. Dietary advice for FH thus focuses on dietary cholesterol with stricter maximum allowance (no more than 200mg per day). However, saturated fat reductions are still prioritised.

Trans fatty acids

Although naturally occurring trans fatty acids (TFA) can be found in red meat and dairy products, the concern lies with industrially produced TFAs. Industrially produced TFAs have been shown to increase LDL cholesterol and reduce HDL cholesterol, significantly raising CVD risk far more than saturated fats6,15,27,28. These TFAs are a result of the partial hydrogenation process used with vegetable oils to make them more solid and improve their technical qualities. This process was common in the 1970s, but as the harmful effects of TFAs became known, food regulations and manufacturing practices changed28,29. Consequently, TFAs are no longer a concern in most developed countries. In the UK, average intakes remain well below the 5g daily limit set30.

The impact of dietary fats on CHD outcomes

Studies have consistently demonstrated a similar pattern when comparing the impact of dietary saturated fat substitution with other macronutrients on CHD risk. Replacing saturated fat with TFAs increases CHD risk whilst replacement with MUFA, PUFA and (to a lower degree) whole grains reduces risk CHD27.

UK intakes vs recommendations

Current recommendations

  • UK public health recommendation31: no more than 10% of energy from saturated fat.
    • For adults aged 19-64 years, this equates to no more than 22g for women and 28g for men
  • UK NICE guidelines for individuals with elevated cholesterol levels and/or high risk of CVD3: no more than 7% of energy from saturated fat
    • For adults aged 19-64 years, this equates to no more than 16g for women and 19g for men

Current intakes

Intakes have persistently exceeded recommended daily limits over the last decade30.  Current intakes: 12.3% of energy from saturated fat (adults 19-64 years)

Key food sources

62% of the saturated fat in the UK diet comes from three main sources30:

  • Meat and meat products
  • Cereal products (mainly ready meals, buns, cakes, pastries, and biscuits)
  • Milk and dairy.

Good food sources of unsaturated fats

Food source Type of unsaturated fat
Olive oil and avocados Mono-unsaturated fat
Nuts and seeds and their oils, most vegetable oils and their spreads except coconut and palm Polyunsaturated fat - Omega-6
Rapeseed oil (standard vegetable oil), walnuts and walnut oil, hemp and flaxseeds and their oils Polyunsaturated fat - Alpha linolenic acid (ALA) - omega-3
Oil rich fish and algae supplements Polyunsaturated fats - eicosapentaenoic acid (EPA) and docosahexaenoic (DHA) - omega-3



  1. Maintain fat intake at 30-35% of total energy.
  2. Reduce sources of saturated fat in the diet.
  3. Encourage a mix of MUFA and PUFA (omega-6 and omega-3) to replace saturated fats.
  4. Substitute refined carbohydrates with whole grains



  • Reduce red and processed meat consumption; fully or partially replacing it with beans, tofu, or mycoprotein.
  • For cooking, use rapeseed or other vegetable oils (except for palm or coconut oil).
  • Opt for olive, walnut or other seed or nut oil in salads.
  • Add seeds and nuts to breakfast cereals, porridge, stir-fries, salads, stews.
  • Replace savoury and sweet snacks with seeds, nuts, or fruit.
  • Choose oat-based breakfast cereals and switch to wholemeal breads, chapattis, wraps, pasta, and brown rice.
  • When shopping, check front-of-pack traffic light nutrition labelling. Aim for green labels primarily, amber occasionally, and avoid red altogether



  1. Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;140(11):e596-e646. doi:10.1161/CIR.0000000000000678

  2. Visseren FLJ, Mach F, Smulders YM, et al. 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice: Developed by the Task Force for cardiovascular disease prevention in clinical practice with representatives of the European Society of Cardiology and 12 medical societies With the special contribution of the European Association of Preventive Cardiology (EAPC). European Heart Journal. 2021;42(34):3227-3337. doi:10.1093/eurheartj/ehab484

  3. NICE. Cardiovascular disease: risk assessment and reduction, including lipid modification. Clinical guideline CG181. Published May 2023. Accessed September 29, 2023.

  4. Feingold KR. The Effect of Diet on Cardiovascular Disease and Lipid and Lipoprotein Levels. In: Feingold KR, Anawalt B, Blackman MR, et al., eds. Endotext., Inc.; 2000. Accessed January 3, 2024.

  5. Reynolds AN, Hodson L, de Souza R, Pham HTD, Vlietstra L, Mann J. Saturated Fat and Trans-Fat Intakes and Their Replacement with Other Macronutrients: A Systematic Review and Meta-Analysis of Prospective Observational Studies. WHO; 2022:164.

  6. Christensen JJ, Arnesen EK, Rundblad A, et al. Dietary fat quality, plasma atherogenic lipoproteins, and atherosclerotic cardiovascular disease: An overview of the rationale for dietary recommendations for fat intake. Atherosclerosis. 2024;389:117433. doi:10.1016/j.atherosclerosis.2023.117433

  7. Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. European Heart Journal. 2017;38(32):2459-2472. doi:10.1093/eurheartj/ehx144

  8. Virani SS, Morris PB, Agarwala A, et al. 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia. Journal of the American College of Cardiology. 2021;78(9):960-993. doi:10.1016/j.jacc.2021.06.011

  9. Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and Cardiovascular Disease. Circulation. 2011;123(20):2292-2333. doi:10.1161/CIR.0b013e3182160726

  10. Razavi AC, Jain V, Grandhi GR, et al. Does Elevated High-Density Lipoprotein Cholesterol Protect Against Cardiovascular Disease? J Clin Endocrinol Metab. 2024;109(2):321-332. doi:10.1210/clinem/dgad406

  11. Kosmas CE, DeJesus E, Rosario D, Vittorio TJ. CETP Inhibition: Past Failures and Future Hopes. Clin Med Insights Cardiol. 2016;10:37-42. doi:10.4137/CMC.S32667

  12. The AIM-HIGH Investigators. Niacin in Patients with Low HDL Cholesterol Levels Receiving Intensive Statin Therapy. New England Journal of Medicine. 2011;365(24):2255-2267. doi:10.1056/NEJMoa1107579

  13. HEART UK. The latest thinking on HDL cholesterol: our HEART UK update for health professionals. HEART UK - The cholesterol charity. Published October 7, 2020. Accessed June 24, 2024.

  14. HEART UK. Understanding your cholesterol test results. HEART UK. Published May 2024. Accessed May 28, 2024.

  15. Mensink RP, World Health Organization. Effects of Saturated Fatty Acids on Serum Lipids and Lipoproteins: A Systematic Review and Regression Analysis. World Health Organization; 2016. Accessed October 16, 2023.

  16. Fernandez ML, West KL. Mechanisms by which Dietary Fatty Acids Modulate Plasma Lipids1. The Journal of Nutrition. 2005;135(9):2075-2078. doi:10.1093/jn/135.9.2075

  17. Briggs MA, Petersen KS, Kris-Etherton PM. Saturated Fatty Acids and Cardiovascular Disease: Replacements for Saturated Fat to Reduce Cardiovascular Risk. Healthcare (Basel). 2017;5(2):29. doi:10.3390/healthcare5020029

  18. Guasch-Ferré M, Zong G, Willett WC, et al. Associations of Monounsaturated Fatty Acids from Plant and Animal Sources with Total and Cause-Specific Mortality in Two U.S. Prospective Cohort Studies. Circ Res. 2019;124(8):1266-1275. doi:10.1161/CIRCRESAHA.118.313996

  19. Hamilton-Craig C, Kostner K, Colquhoun D, Nicholls SJ. Omega-3 fatty acids and cardiovascular prevention: is the jury still out? Internal Medicine Journal. 2023;53(12):2330-2335. doi:10.1111/imj.16283

  20. Abdelhamid AS, Brown TJ, Brainard JS, et al. Omega‐3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews. 2020;(3). doi:10.1002/14651858.CD003177.pub5

  21. Laffond A, Rivera-Picón C, Rodríguez-Muñoz PM, et al. Mediterranean Diet for Primary and Secondary Prevention of Cardiovascular Disease and Mortality: An Updated Systematic Review. Nutrients. 2023;15(15):3356. doi:10.3390/nu15153356

  22. DiNicolantonio JJ, O’Keefe JH. Effects of dietary fats on blood lipids: a review of direct comparison trials. Open Heart. 2018;5(2):e000871. doi:10.1136/openhrt-2018-000871

  23. Elagizi A, Lavie CJ, O’Keefe E, Marshall K, O’Keefe JH, Milani RV. An Update on Omega-3 Polyunsaturated Fatty Acids and Cardiovascular Health. Nutrients. 2021;13(1):204. doi:10.3390/nu13010204

  24. Oscarsson J, Hurt-Camejo E. Omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and their mechanisms of action on apolipoprotein B-containing lipoproteins in humans: a review. Lipids Health Dis. 2017;16:149. doi:10.1186/s12944-017-0541-3

  25. Hollænder PLB, Ross AB, Kristensen M. Whole-grain and blood lipid changes in apparently healthy adults: a systematic review and meta-analysis of randomized controlled studies. Am J Clin Nutr. 2015;102(3):556-572. doi:10.3945/ajcn.115.109165

  26. Diamond DM, Alabdulgader AA, de Lorgeril M, et al. Dietary Recommendations for Familial Hypercholesterolaemia: an Evidence-Free Zone. BMJ Evid Based Med. 2021;26(6):295-301. doi:10.1136/bmjebm-2020-111412

  27. Sacks FM, Lichtenstein AH, Wu JHY, et al. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. Circulation. 2017;136(3):e1-e23. doi:10.1161/CIR.0000000000000510

  28. WHO. Trans fat. World Health Organisation. Published January 2024. Accessed May 28, 2024.

  29. EFSA. Trans fat in food - European Commission. European Commission - Food Safety. Published April 24, 2019. Accessed May 28, 2024.

  30. PHE. NDNS: results from years 9 to 11 (2016 to 2017 and 2018 to 2019). GOV.UK. Published December 11, 2020. Accessed January 3, 2024.

  31. PHE. Government Dietary Recommendations: Government Recommendations for Energy and Nutrients for Males and Females Aged 1 – 18 Years and 19+ Years. PHE; 2016:12.


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