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  1. What is cholesterol?

    Cholesterols are types of fat found in the blood. The liver produces sufficient cholesterol for the body’s requirements, but it can also be acquired from foods, particularly animal products, such as meat, egg yolks, butter, cheese and milk. Cholesterol is necessary for the body to function properly, as it is involved in the production of hormones and vitamin D, and in the digestive process.[1]  Cholesterol is not soluble in the blood and has to be transported through the bloodstream by carriers called lipoproteins (complexes of fatty acids and proteins).[1] There are two types of proteins that transport cholesterol to and from cells, high-density lipoproteins (HDL), and low-density lipoproteins (LDL). The levels of cholesterol bound to these lipoproteins in the bloodstream can be an important indicator of the risk of heart disease. A blood test commonly used by doctors to determine your ‘cholesterol level’ calculates the overall cholesterol level by adding HDL and LDL to 20% of the amount of triglyceride (another fat present in the blood). [2] LDL is commonly known as ‘bad’ cholesterol. This is because it contributes to the formation of plaques within blood vessels, which are thick hard deposits that can clog arteries and decrease their flexibility, resulting in atherosclerosis. [3] If a blood clot forms in one of these narrowed arteries, it can result in a heart attack or a stroke.[1] Excess LDL can also contribute to peripheral artery disease, which is the result of plaque narrowing an artery that supplies blood to the extremities, such as the legs.[1] HDL is known as ‘good’ cholesterol as it assists in the removal of LDL by acting as a scavenger, carrying LDL back to the liver where it is broken down and excreted.[4] 20% to 30% of cholesterol is carried by HDL.[4], [5]  However, despite its beneficial actions, studies have shown that the level of HDL in the plasma may not reliably indicate the degree of reduction of LDL and so research into this area is continuing.[6] A satisfactory level of HDL can, however, decrease the risk of heart attack and stroke and, conversely, a level that is too low increases the risk.[7]  Triglycerides are another type of fat also present in the blood. They are also produced by the liver and are additionally found in oils, meat and dairy products. Their purpose is to provide energy to the body’s cells and tissues. When excess calories are ingested they are converted to triglycerides and stored as body fat and as fatty deposits within organs and tissues.[8] Like LDL, high levels of triglycerides are also associated with atherosclerosis,[9] and many people with diabetes or heart disease have high triglyceride levels within their blood. It is also common for people with high triglyceride levels to have a high ‘overall’ cholesterol level (i.e. a high LDL level and a low HDL level). One study has shown that a healthy lipid profile (i.e. low LDL, high HDL and low triglycerides), can reduce the risk of chronic heart disease by 71%.[10] Some common causes of elevated triglyceride levels include obesity, high alcohol consumption, cigarette smoking and a diet high in saturated fats.[11] Underlying diseases, e.g. poorly controlled diabetes, an underactive thyroid (hypothyroidism), kidney disease, and alcoholism,[11] and genetic disorders such as familial hypertriglyceridemia[12] can also cause increased levels of triglycerides. The best way to maintain healthy cholesterol levels is by leading a healthy lifestyle: a varied and balanced diet, low in saturated fat and plenty of pesticide-free fruit and vegetables, in addition to sustaining a healthy weight. Exercise is another key factor in reducing or maintaining healthy cholesterol levels, although the exact mechanism for this is not yet clear.[13] Exercise is also beneficial in controlling weight. Smoking should be avoided and alcohol consumed in moderation; as well as increasing cholesterol levels, the adverse effects on health of both smoking and excess alcohol are well documented. [1] NIH (2016) What is cholesterol? Retrieved May 2016 from,  [2] Barter, P. et al. (2007) HDL Cholesterol, Very Low Levels of LDL Cholesterol, and Cardiovascular Events. The New England Journal of Medicine. 57. 1301-1310. [3] Kyle, D. (2004) Understanding lipoproteins as transporters of cholesterol and other lipids. Advances in Physiology Education. 28(3). 105-106. [4] Lee-Rueckert, M. et al. (2016) HDL functionality in reverse cholesterol transport - Challenges in translating data emerging from mouse models to human disease. Biochim Biophys Acta. 1861(7). 566-83. [5] Schwartz, CC. et al. (2004) Lipoprotein cholesteryl ester production, transfer, and output in vivo in humans. J Lipid Res. 45(9). 1594-1607. [6] Rothblat, G.H. et al. (2010) High-density lipoprotein heterogeneity and function in reverse cholesterol transport. Current Opinion in Lipidology, 21(3), 229-238. [7] University of Pennsylvania. (2016) Fat and ketoacids, cholesterol, repair. Retrieved June, 2016, from  [8] Toth, P. (2005) The “Good Cholesterol”. Circulation. 111(5). 89-91. [9] Borge, G. et al. (2007) Nonfasting Triglycerides and Risk of Myocardial Infarction, Ischemic Heart Disease, and Death in Men and Women. Journal of the American Medical Association. 298(3). 299-308. [10] Manninen, V. (1992) Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study Implications for treatment. Circulation. 85(1). 37-45. [11] University of Colorado, Denver (2016) Cholesterol and Triglycerides Retrieved August, 2016, from  [12] NIH (2016) Familial hypertriglyceridemia.  Retrieved June, 2016, from [13] Meissner, M. et al. (2010) Exercise enhances whole-body cholesterol turnover in mice. Med Sci in Sports Exercise. 42.1460-1468.
  2.   In the 20th century, the vegetable oil industry had a great impact on human nutrition. Vegetable oil is a good and accessible source of unsaturated fatty acids, having up to 80% of oleic and linoleic acids combined,[1] which are vital for health. Through the development of a chemical process called ‘hydrogenation of fatty acids’ in the early 20th century, the food industry found a way to expand the application of vegetable oils. The process allowed to obtain cheap margarine products that could be used in several different foods to provide attractive qualities, such as distinctive flavour, crispness, plasticity, creaminess etc.[2] In nature, unsaturated fatty acids are normally found in cis-fat form (see the steric arrangement of hydrogen bonds in the picture below), and only up to 2-8% of them occur naturally in trans-fat form due to bacterial fermentation in dairy products and ruminants’ meat.[3] The unsaturated fatty acids that contain double bonds in trans-fat form are called trans-fatty acids.[2] Hydrogenation is the chemical process that allows to convert unsaturated fatty acids into saturated ones by means of heating, nickel catalyst and hydrogen. Unfortunately, it is almost impossible to achieve 100% hydrogenation, and in this case, trans-fatty acids are formed as a by-product along with saturated fatty acids.[2] Although the causative link between trans fats and coronary artery disease was first published in the 1950s, it took several decades of research to understand and subsequently tackle the problem.[4] It was later found that trans fats cause an increase in LDL cholesterol (the ‘bad’ cholesterol) and a decrease in HDL cholesterol (the ‘good’ cholesterol),[5] leading to an increased risk of heart attacks.[6] The consumption of margarine, one of the most common sources of industrially produced hydrogenated fats, was found to increase the body’s natural cholesterol levels in the blood.[7] Trans fats also increase other blood lipid profiles (such as lipoprotein(a) and triglycerides), which can lead to increased cardiovascular risks.[8]  In previous researches comparing the health effects of various fatty acids – namely saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA) and trans-fatty acids (TFA) – both SFA and TFA have been found to increase cardiovascular risks, resulting in the proposal of specific policies to reduce their consumption by 1 and 7 percent of daily energy intake, respectively.[9] However, more recent studies have shown that only TFA intake is associated with all-cause mortality, while, with methodological limitations, there was mixed evidence to prove that SFA have similar negative health effects.[10]  Many studies have proved the dangers of TFA produced from hydrogenation of vegetable oils, but what about TFA intake from consuming ruminants and dairy products?[11] Researchers have shown that these naturally occurring TFA can hardly pose health risks as their levels are generally low,[3][11][12] but further research is needed.[13] For this reason, we can safely assert that the biggest health risk lies with TFA found in processed, hydrogenated-fat food, rather than the naturally occurring TFA.  The risks associated with TFA are a significant problem acknowledged by many countries. The US Food and Drug Administration has recently announced that a ban on hydrogenated fat use for processed food production will enter into force in June 2018.[14] While possible actions are still under discussion in the European Union, the European Food Safety Authority encourages consumers to opt instead for less processed food products containing less TFA. “TFA” is currently labelled on a voluntary basis only in the European Union, while it is mandatory in the USA.[15] It is anticipated that the European Food Safety Authority will soon provide the updated tolerable limits of TFA to label processed foods accordingly. Heart disease is one of the major causes of death in Europe and worldwide, and TFA are recognised as one of the factors leading to it. Other suggested negative health outcomes of excessive TFA intake include Alzheimer’s disease, diabetes, obesity and even cancer.[16][17] The general biochemical mechanism of these health effects is not yet properly understood; however, it is thought that the human body lacks lipase enzymes that are able to metabolise this artificial fatty acid, and that trans fats also impair the metabolism of essential polyunsaturated fatty acids.[18] Even though trans-fats intake declined in recent years, governments do not do their best to protect the public from TFA exposure. For this reason, food industry manufacturers are not motivated to replace harmful ingredients that provide appealing food qualities (like creaminess and crispness) at low prices with more expensive alternatives. Until TFA are banned, it is strongly recommended to avoid processed foods and consume high-fat dairy products in moderation.    [1] Orsavova, J., Misurcova, L., Ambrozova, J., Vicha, R., & Mlcek, J. (2015). Fatty Acids Composition of Vegetable Oils and Its Contribution to Dietary Energy Intake and Dependence of Cardiovascular Mortality on Dietary Intake of Fatty Acids. International Journal Of Molecular Sciences, 16(6), 12871-12890.  [2] Jang, E., Jung, M., & Min, D. (2005). Hydrogenation for Low Trans and High Conjugated Fatty Acids. Comprehensive Reviews In Food Science And Food Safety, 4(1), 22-30. [3] Lindmark Månsson, H. (2008). Fatty acids in bovine milk fat. Food & Nutrition Research, 52(1), 1821. [4] Lichtenstein, A. (2014). Dietary Trans Fatty Acids and Cardiovascular Disease Risk: Past and Present. Current Atherosclerosis Reports, 16(8). [5] Brouwer, I., Wanders, A., & Katan, M. (2010). Effect of Animal and Industrial Trans Fatty Acids on HDL and LDL Cholesterol Levels in Humans – A Quantitative Review. Plos ONE, 5(3), e9434. [6] Nestel, P. (2014). Trans Fatty Acids: Are Its Cardiovascular Risks Fully Appreciated?. Clinical Therapeutics, 36(3), 315-321. [7] Liska, D., Cook, C., Wang, D., Gaine, P., & Baer, D. (2016). Trans fatty acids and cholesterol levels: An evidence map of the available science. Food And Chemical Toxicology, 98, 269-281. [8] Ooi, E., Watts, G., Ng, T., & Barrett, P. (2015). Effect of Dietary Fatty Acids on Human Lipoprotein Metabolism: A Comprehensive Update. Nutrients, 7(6), 4416-4425. [9] Hammad, S., Pu, S., & Jones, P. (2015). Current Evidence Supporting the Link Between Dietary Fatty Acids and Cardiovascular Disease. Lipids, 51(5), 507-517. [10] de Souza, R., Mente, A., Maroleanu, A., Cozma, A., Ha, V., & Kishibe, T. et al. (2015). Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ, h3978. [11] Da Silva, M., Julien, P., Pérusse, L., Vohl, M., & Rudkowska, I. (2015). Natural Rumen-Derived trans Fatty Acids Are Associated with Metabolic Markers of Cardiac Health. Lipids, 50(9), 873-882. [12] Mozaffarian, D., Aro, A., & Willett, W. (2009). Health effects of trans-fatty acids: experimental and observational evidence. European Journal Of Clinical Nutrition, 63, S5-S21. [13] Gebauer, S., Chardigny, J., Jakobsen, M., Lamarche, B., Lock, A., Proctor, S., & Baer, D. (2011). Effects of Ruminant trans Fatty Acids on Cardiovascular Disease and Cancer: A Comprehensive Review of Epidemiological, Clinical, and Mechanistic Studies. Advances In Nutrition: An International Review Journal, 2(4), 332-354. [14] FDA Cuts Trans Fat in Processed Foods. (2017). Retrieved 23 July 2017, from [15] Trans fats (TFA) - Food Safety - European Commission. (2017). Food Safety. Retrieved 23 July 2017, from [16] Morris, M., Evans, D., Bienias, J., Tangney, C., Bennett, D., & Aggarwal, N. et al. (2003). Dietary Fats and the Risk of Incident Alzheimer Disease. Archives Of Neurology, 60(2), 194. [17] Dhaka, V., Gulia, N., Ahlawat, K., & Khatkar, B. (2011). Trans fats—sources, health risks and alternative approach - A review. Journal Of Food Science And Technology, 48(5), 534-541. [18] Calder, P. (2015). Functional Roles of Fatty Acids and Their Effects on Human Health. Journal Of Parenteral And Enteral Nutrition, 39(1_suppl), 18S-32S.
  3. Cholesterol is a fat that is both made in the body and ingested in our diets. It is transported around our bodies in the bloodstream attached to proteins which are called lipoproteins. There are two main forms of lipoprotein. Low density lipoprotein (LDL) is often referred to as the "bad cholesterol" because it plays a role in the formation of plaques. These are thick, hard deposits that are formed in arteries causing a medical condition called atherosclerosis which is a type of heart disease. In contrast, high density lipoprotein (HDL) is considered “good” because it helps to remove LDL from arteries and transports it to the liver where it is broken down and eliminated from the body.[1] Triglyceride is another type of fat and high levels of triglycerides are also associated with atherosclerosis.[2] People with high triglyceride levels often have high LDL levels and low HDL levels.[3] Eggs are a major source of cholesterol in the diet. They are also a highly nutritious, low cost food item and they provide a range of nutrients including:[3] High quality, bioavailable protein (protein which the body can digest and use) Vitamins A, B12, D, E and K Choline Folate Riboflavin Selenium The link between egg consumption and high LDL levels (and the associated risk of heart disease) is not straightforward. In order to understand the relationship between egg consumption and the risk of heart disease it is necessary to look at a lot more than just the cholesterol content in eggs. It is important to consider the effect of cholesterol content of eggs on both LDL and HDL levels and ultimately on the risk of developing heart disease. Research has provided conflicting evidence on this.[4] In fact, one study has shown that eating a lot of eggs leads to a greater increase of “good” HDL cholesterol than “bad” LDL cholesterol.[5] Recent research also suggests that dietary cholesterol in general does not play as important role in the development of heart disease as was once thought.[4] Several studies have found that people who eat eggs are no more likely to develop heart disease than those who do not eat eggs.[7] [8] [9] Studies of real populations support this. In Japan people in general eat a diet that is low in total fat and in saturated fat. During the 1980s, the incidence of heart disease fell in Japan, but at the same time, egg consumption increased and total serum cholesterol levels increased in the population. This does not support the claim that there is a link between egg consumption and heart disease. It does, however, indicate that the total diet needs to be taken into account when making recommendations relating to heart disease prevention.[10] The American Heart Association has also moved away from recommending the avoidance of particular foods and instead looks at the diet as a whole. It recommends that the total daily cholesterol intake should not exceed 300 mgs per day and as one egg contains between 150 and 300 mgs of cholesterol, it would be no more than one egg a day.[11] In addition to diet, the individual’s physiology is also important. One study has identified a sub-group of the population who have been termed ‘hyper responders’ because of the way in which their bodies reacted to cholesterol in their diet. The study found that in 70% of the study subjects, egg consumption did not alter blood levels of LDL but in 30% (the hyper responders) it did go up slightly due to genetic condition (familial hypercholesterolaemia).[12] Furthermore, diabetics who consume more eggs are more likely to develop heart disease than those who do not.[13] Research is underway to identify ways in which the fatty acid composition of yolk lipids could be changed. The aim of this is to alter the way in which egg consumption affects blood cholesterol levels. It is possible to change the nutritional content of eggs by feeding supplements to the chickens that lay them. For example, they can be enriched with Omega-3 by feeding flaxseed, fish oil or microalgae to chickens.[14] It has been shown that consumption of Omega-3 enriched eggs was associated with a significant (16-18%) decrease in blood serum triglycerides, but with no significant difference in serum LDL-cholesterol and HDL-cholesterol.[15]   To conclude, when making recommendations on egg consumption (which are a useful source of nutrition) it is important to recognise both diversity of diet and individual physiology which both affect the way in which an individual’s body will react to dietary cholesterol intake. The consumption of one or two eggs per day, when part of a low fat diet, does not adversely affect cholesterol levels. However, there are some specific conditions, such as diabetes, for which lower limits of egg consumption should be recommended and there are also certain individuals for whom a lower limit would be advisable because of their individual physiology. For these reasons the most appropriate advice is that eggs can be part of a healthy diet for healthy individuals and providing you have no physiological condition ‘familial hypercholesterolaemia’. Until you know your physiology for sure, when consuming eggs you are better to regularly monitor your LDL cholesterol level.      [1] Sharrett, A., Ballantyne, C., Coady, S., Heiss, G., Sorlie, P., Catellier, D., & Patsch, W. (2001). Coronary Heart Disease Prediction From Lipoprotein Cholesterol Levels, Triglycerides, Lipoprotein(a), Apolipoproteins A-I and B, and HDL Density Subfractions: The Atherosclerosis Risk in Communities (ARIC) Study. Circulation, 104(10), 1108-1113. [2] Njike, V., Faridi, Z., Dutta, S., Gonzalez-Simon, A., & Katz, D. (2010). Daily egg consumption in hyperlipidemic adults - Effects on endothelial function and cardiovascular risk. Nutrition Journal, 9(1). [3] Fuller, N., Sainsbury, A., Caterson, I., & Markovic, T. (2015). Egg Consumption and Human Cardio-Metabolic Health in People with and without Diabetes. Nutrients, 7(9), 7399-7420. [4] Katz, D., Evans, M., Nawaz, H., Njike, V., Chan, W., Comerford, B., & Hoxley, M. (2005). Egg consumption and endothelial function: a randomized controlled crossover trial. International Journal Of Cardiology, 99(1), 65-70. [5] Rong, Y., Chen, L., Zhu, T., Song, Y., Yu, M., & Shan, Z. et al. (2013). Egg consumption and risk of coronary heart disease and stroke: dose-response meta-analysis of prospective cohort studies. BMJ, 346(jan07 2), e8539-e8539. [6] Lee, A., & Griffin, B. (2006). Dietary cholesterol, eggs and coronary heart disease risk in perspective. Nutrition Bulletin, 31(1), 21-27. [7] McNamara, D. (2000). Dietary cholesterol and atherosclerosis. Biochimica Et Biophysica Acta (BBA) - Molecular And Cell Biology Of Lipids, 1529(1-3), 310-320. [8] OKAYAMA, A., UESHIMA, H., MARMOT, M., NAKAMURA, M., KITA, Y., & YAMAKAWA, M. (1993). Changes in Total Serum Cholesterol and Other Risk Factors for Cardiovascular Disease in Japan, 1980–1989. International Journal Of Epidemiology, 22(6), 1038-1047. [9] Kritchevsky, S. (2004). A Review of Scientific Research and Recommendations Regarding Eggs. Journal Of The American College Of Nutrition, 23(sup6), 596S-600S.  [10] Fernandez, M. (2006). Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations. Current Opinion In Clinical Nutrition And Metabolic Care, 9(1), 8-12.  [11] Hu, F. (1999). A Prospective Study of Egg Consumption and Risk of Cardiovascular Disease in Men and Women. JAMA, 281(15), 1387. [12] Fraeye, I., Bruneel, C., Lemahieu, C., Buyse, J., Muylaert, K., & Foubert, I. (2012). Dietary enrichment of eggs with omega-3 fatty acids: A review. Food Research International, 48(2), 961-969. [13] Bovet, P., Faeh, D., Madeleine, G., Viswanathan, B., & Paccaud, F. (2007). Decrease in blood triglycerides associated with the consumption of eggs of hens fed with food supplemented with fish oil. Nutrition, Metabolism And Cardiovascular Diseases, 17(4), 280-287.