Saturated Fat

Saturated Fat─Biggest Contributor to Blood Cholesterol

  • Differences in coronary artery disease (CAD) mortality worldwide is explained by differences in saturated fatty acid (SAFA) intake and resulting serum TC levels in 40 countries, except for France, Finland, and India.1-3 Dietary saturated fatty acids (SAFA) are dietary factor with the strongest impact on LDL-C.4 In sharp contrast, unsaturated fat consumption reduces risk of CVD. Replacing 10% of energy from saturated fats with unsaturated fats reduces CAD risk by about 20-30%.5, 6
  • It is worth highlighting that atherosclerosis in experimental animals is produced by adding saturated fat in the form of coconut in the chow (see reduce coconut consumption).7
  • In the Seven Countries Study the saturated fat intake ranged from 3% in Japan to 24% in Finland and 22% in the USA and paralleled  the cholesterol levels and the CAD rates.8-10The SAFA intakes in the US and UK average at around 13% ─nearly double the maximum recommended intakes of 7% of food energy. There are strong, consistent and graded relationships between saturated fat intake, blood cholesterol levels and mass occurrence of CVD.11
  • A substitution of 10% energy from these SAFAs with carbohydrates results in 12 mg/dl decrease in LDL-C, 16 mg/dl and monounsaturated fat and 20 with polyunsaturated fat.5, 6 In typical Western diets replacing 60% of SAFA by other fats and avoiding 60% of dietary cholesterol would decrease LDL-C by 25 mg/dl. This  degree of reduction in LDL-C  would result in 100,000 to 150,000 lives saved in the USA per year.5
  • Although saturated fats as a whole increase the LDL, the LDL raising property is limited to lauric, myristic, and palmitic acids. The cholesterol raising ability of myristic acid is 50% higher and lauric acid is 33% less than palmitic acid.  Stearic acid (high in  cocoa and meat) in contrast to other SAFA (lauric, myristic, and palmitic) fatty does not increase LDL levels.12, 13
  • The greatest reduction in CVD risk is achieved by LDL-lowering by reducing saturated fat intake, which  is best accomplished by reducing the intake of high-fat dairy, and replacing it with low fat dairy and fiber-rich foods. 
  • The preferred substitution for saturated fat is monounsaturated fat (abundant in olive oil and canola oil)  or polyunsaturated fat (abundant in soybean and sunflower oil)  and both results in decrease in LDL and triglycerides.14  A  substitution of 40% of the energy intake from  corn oil to coconut oil can increase blood cholesterol levels by 130to 160 mg/dl.15
  • Substitution of healthy fat for unhealthy fat is more effective in preventing CAD than reducing overall fat intake.16, 17 Substituting saturated fat with carbohydrates decreases LDL but makes LDL small dense and more dangerous (by increasing triglycerides).16 
  • Substituting carbohydrates with monounsaturated fat decreases LDL, triglycerides, and increases HDL. Both poly and monounsaturated fats increase insulin sensitivity and decrease the risk of type 2 diabetes.18
  • Current guidelines recommend a diet that provides  25-35% calories from dietary fat  <7% saturated fat, <10% polyunsaturated fat and up to 20% monounsaturated fat.18  Reduction of saturated fat intake to less than 7% of the daily energy can translate to 10 g for women on a 1200 Kcal diet and 12 g for men on a 1500 Kcal diet.
  • This can be achieved by limiting the consumption of the following foods: beef, lamb, pork, bacon, sausage, ribs, poultry with skin, butter, ghee, vanaspathi  desserts, bakery products (cakes, biscuits, cookies, donut), cheese, ice cream, full-fat milk, and tropical oils (coconut, palm kernel and palm oils). (Table 015).
  • Most fast food items are high in SAFA and trans fat. For example, McDonalds 32  oz triple thick milk shake contains 1110 calories, 26 g of fat and 16g saturated fat. 
  • Dietary cholesterol seems to have a relatively small impact on serum lipids compared with dietary saturated fat and trans fat. Reducing the dietary cholesterol by 100 mg  a day reduces the cholesterol by 1%. However, there is marked individual variation in the way serum cholesterol responds to dietary cholesterol.19


1. What is a fat tax?

A. Denmark introduced the world’s first food fat tax. Foods are now subject to the tax if they contain more than 2.3% saturated fat. The tax applies to meats, including chicken and pork, cheese, butter, edible vegetable oil, margarine and other foods such as potato-based snacks. The tax, imposed on domestic and imported food, is levied on the weight of saturated fat contained in these foods, and charged at the rate of DKK13.50  (USD 2.4 or Rs 125 approx) per kg of saturated fat. This will cause the prices of high fat foods to go up and thus discourage people from buying them. A similar fat tax in India would more than double the price of palm oil and coconut oil both of which are very high in saturated fat.


1. Artaud-Wild SM, Connor SL, Sexton G, Connor WE. Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland: A paradox. Circulation. 1993;88(6):2771-2779.

2. Aravanis C, Corcondilas A, Dontas AS, Lekos D, Keys A. Coronary heart disease in seven countries. IX. The Greek islands of Crete and Corfu. Circulation. Apr 1970;41(4 Suppl):I88-100.

3. Kimura N, Keys A. Coronary heart disease in seven countries. X. Rural southern Japan. Circulation. Apr 1970;41(4 Suppl):I101-112.

4.  Saturated fatty acids in vegetable oils. Council on Scientific Affairs. Jama. Feb 2 1990;263(5):693-695.

5. Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. Jan 11 1997;314(7074):112-117.

6. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr. May 2003;77(5):1146-1155.

7. Waqar AB, Koike T, Yu Y, et al. High-fat diet without excess calories induces metabolic disorders and enhances atherosclerosis in rabbits. Atherosclerosis. Nov 2010;213(1):148-155.

8. Keys A. Diet and blood cholesterol in population surveys–lessons from analysis of the data from a major survey in Israel. Am J Clin Nutr. 1988;48(5):1161-1165.

9. Keys A. Diet and the epidemiology of coronary heart disease. J Am Med Assoc. Aug 24 1957;164(17):1912-1919.

10. Keys A, Menotti A, Karvonen MJ, et al. The diet and 15-year death rate in the seven countries study. Am J Epidemiol. 1986;124(6):903-915.

11. Graham I, Atar D, Borch-Johnsen K, Boysen G, Durrington PN. European guidelines on cardiovascular disease prevention in clinical practice: executive summary: Fourth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (Constituted by representatives of nine societies and by invited experts). Eur Heart J. Oct 2007;28(19):2375-2414.

12. Catapano AL, Reiner Z, De Backer G, et al. ESC/EAS Guidelines for the management of dyslipidaemias The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). Atherosclerosis. Jul 2011;217 Suppl 1:1-44.

13. Enas EA. Indian diet and cardiovascular disease: An update. In: Chatterjee SS, ed. Update in Cardiology Hyderabad: Cardiology Society of India.; 2007.

14. WHO. Prevention of cardiovacular disease. World Health Organization, Genewa Switzerland2007.

15. Ahrens E. H. J, Insull W, Jr., Blomstrand R, Hirsch J, Tsaltas TT, Peterson ML. The influence of dietary fats on serum-lipid levels in man. Lancet. May 11 1957;272(6976):943-953.

16. Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease. Jama. Nov 27 2002;288(20):2569-2578.

17. Hu FB, Stampfer M, Manson J, et al. Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med. 1997;337(21):1491-1499.

18. Enas EA, Senthilkumar A, Chennikkara H, Bjurlin MA. Prudent diet and preventive nutrition from pediatrics to geriatrics: current knowledge and practical recommendations. Indian heart journal. Jul-Aug 2003;55(4):310-338.

19. Katan MB, Beynen AC, de Vries JH, Nobels A. Existence of consistent hypo- and hyperresponders to dietary cholesterol in man. Am J Epidemiol. Feb 1986;123(2):221-234.

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