Paper No. F14- Therapeutic Nutrition F14TN34- ROLE OF PUFA, MUFA AND TRANS FAT. 1. INTRODUCTION Presently the incidence of non communicable diseases is increased in most of the countries. The World Health Organization has identified that among the various contributing factors of cardiovascular diseases, diabetes mellitus, improper diet and lifestyle modifications are considered as prime factors responsible. The WHO guidelines in general is to reduce the intake of refined carbohydrate, replace the saturated fats in diet with mono and polyunsaturated fatty acids and completely restricting trans-fats. 2. OBJECTIVES To understand the concept of saturation and categorization of fats and fatty acids. To explain in detail the effects of PUFA, MUFA and TRANS FAT on health. 3. CATEGORIZATION OF FATTY ACIDS BASED ON SATURATION Fatty acids are the main building blocks of fats. They have a methyl group and a carboxyl group with a chain of carbon and hydrogen atoms. About twenty fatty acids are found in our body tissues and in the food we consume. They are categorized based on three aspects such as chain length, saturation and essential fatty acids. atoms. In this module the role of fats is dealt on the basis of saturation and the position of hydrogen Saturated fatty acid has a single bond between its carbon atoms, thus the molecule is saturated with hydrogen. Stearic acid is an example for saturated fatty acids. Unsaturated fatty acids have one or more double bonds in their molecule and are thus not saturated with hydrogen. This is further classified based on the number of double bonds as Monounsaturated fatty acids have only one double bond in the molecules. Oleic acid, found in olive oil is an example. Polyunsaturated fatty acids have two or more double bonds in the molecules. Corn oil contains PUFA. Fatty acids are also characterized by the location of their double bonds. The methyl end of the fatty acid molecule is called the omega end. If the first double bond in the fatty acid is in the third carbon atom from the methyl end, it is called omega-3 fatty acid; if the sixth carbon from the methyl end, it is called omega 6 fatty acid and when it is in the ninth carbon it is called omega-9 fatty acid. Linoleic acid (omega 6 PUFA) and Linolenic acid (omega 3 PUFA) are called essential fatty acids because 1. These are not synthesized in the human body. 2. These are required for important functions in the body and 3. These are available only through diet. Trans- fatty acids the hydrogen atoms are in the trans position. 4. ROLE OF MUFA, PUFA AND TRANS FAT IN DETAIL The epidemiological relation between the total fats, fatty acids and human health proves that different fats implicate their effect on health in a different dimension. Each fatty acid has its own biological properties and health benefits. The examples of fatty acids in food is given in table 1.
Table 1 Examples of fatty acids in foods Acetic Vinegar Butyric Butter Caproic Butter Caprylic Saturated Coconut Myristic Nutmeg and mace Palmitic Palm oil and lard Stearic Beef tallow Oleic MUFA Olive oil Linoleic Groundnut, sesame, corn oil, sunflower oil. Clupanadonic PUFA Fish oils 4.1 MONOUNSATURATED FATTY ACIDS MUFA are a better replacement for saturated fatty acids than PUFA because they are less susceptible to oxidation. Oxidised LDL is taken up by macrophages and deposited in atherosclerotic plagues. Inhibition of LDL oxidation slows the development of atherosclerosis. It was observed that high intake of PUFA resulted in some lowering of HDL cholesterol along with the levels of total and LDL cholesterol. MUFA is resistant to peroxidation and helps to lower oxidised LDL by preserving HDL levels. More recent studies reveal that high dietary PUFA ( omega 6) when SFA intake remains the same may enhance platelet aggregation while MUFA does not. Further larger proportion of MUFA in diet may be conducive to thrombolysis and may be anti inflammatory as n-3 PUFA. It is now established that substitution of SFA by MUFA lowers both total and LDL cholesterol but not HDL-C. Uncontrolled peroxidation of PUFA in cell membrane may lead to cellular damage while maintenance of a balance with MUFA is conducive to maintain cell function. Olive oil extensively used in the Mediterranean region is rich in monounsaturated (18:1) oleic acid (73 per cent). Both hyper cholesterolemia and CHD are less prevalent in USA, UK and north and central Europe. This observation lead to many studies on the benefits of high fat and high MUFA diet. The step I diet (30 per cent total fat, 10 per cent saturated fatty acid, 10 per cent mono unsaturated fatty acid) and a high MUFA diet (38 per cent total fat, 10 per cent saturated fatty acid, 18 per cent mono unsaturated fatty acid) were equally effective in lowering total cholesterol and LDL cholesterol without changing the HDL cholesterol. More recently, a Mediterranian type step I diet was shown to reduce recurrent CVD by 50 per cent. This modified step I diet emphasizes fruits, root vegetables (carrot, turnips, potatoes, onions, radishes), green leafy vegetables, breads and cereals, fish, foods high in alpha linolenic acids (flax and canola oil), vegetable oil products (salad dressing and other products made with non hydrogenated oils high in alpha linolenic acid) and nuts and seeds (walnuts and flaxseed). Although higher fat diets (low in saturated fatty acids, with mono unsaturated fatty acids as the predominant fat) can lower blood cholesterol, they should be used with caution owing to the caloric density of high fat diets and results of clinical trials, which have shown new atherosclerotic lesions in men who consume higher fat diets, similar lesions seen with diets high in SFA in animal studies. The negative association between the Mediterranean diet and coronary heart disease could be due to factors other than MUFA intake. For example, these populations consume more fruits and vegetables, bread, cereals, fish and nuts and less red meat than many populations. Olive oil is the primary source of fat and eggs are consumed zero to four times per week.
4.2 POLYUNSATURATED FATTY ACIDS The very low prevalence of CHD among Eskimos inspite of high fat diet led to the exposition of differential effects of n-3 and n-6 types of dietary PUFA. The important n3 PUFA are alpha linolenic acid, eicosapentanoic acid and docosa hexenoic acid. The n6 PUFA are linoleic acid and arachidonic acid. The EFAs have several important functions. For growth in the young and maintenance of normal healthy skin. They are the components of membranes to ensure their permeability to water and other small molecules. Precursors of eicosanoids, a group of important metabolites which regulate vascular function. The omega 3 fatty acids, DHA (Decosa hexenoic acid) and EPA (eicosa pentenoic acid) have an important role in fetal brain and eye development. These also protect against rheumatoid arthritis and cardiovascular diseases. They are used to synthesize prostaglandins which prolong bleeding time, reduce the thickness and stickiness of platelets, lowers triglycerides and very low density lipoproteins in the blood. It reduces artery blockage, inflammation and pain in certain ailments. Polyunsaturated fatty acids promote esterification of cholesterol and make into easily utilisable form. PUFA especially arachidonic acid are precursors of prostacyclins, thromboxanes and leukotrienes. Thromboxanes are vasoconstrictors while prostacyclins are vasodilators and hence help in prevention of thrombus formation. These substances also decrease the aggregation of platelets and decreasing the tendency to clot.n3 fatty acids raise endothelial derived relaxing factors. Hence PUFA reduces thrombosis. Linoleic acid prevents accumulation of cholesterol in the blood serum and walls of blood vessels and play a key role in the transport of cholesterol. PUFA decreases the synthesis of the precursor of VLDL which are associated with an increased incidence of CHD. Apart from improving the blood lipoprotein profiles, they reduce blood clotting tendency, alpha linolenic acid, reduces risk of myocardial infarction and fatal ischaemic heart disease among women. 4.2.1 Omega 6 PUFA If carbohydrate is replaced by linoleic acid, the predominant dietary omega 6 polyunsaturated fatty acids, LDL cholesterol is lowered and HDL cholesterol level is raised. When SFAs are replaced with PUFA in low fat diet, LDL and HDL cholesterol levels will be lowered. Overall, eliminating SFA is twice as effective in lowering serum cholesterol levels as is increasing PUFA. A 1 per cent increase in omega 6 PUFA would lower total cholesterol by 1.4 mg/dl; however, PUFAs have been shown to decrease very low density lipoprotein, apo B nd HDL synthesis. In the past, a polyunsaturated: saturated ratio (P:S ratio) was used to assess fatty acid composition of foods and diets; however, this ratio is not followed now. Omega 6 PUFAs are widespread in foods, but their major source is vegetable oils, salad dressings and margarine made with the oils. An increase in linoleic acid is not recommended above current intakes as larger amounts leads to increase in LDL oxidation.
4.2.2 Omega 3 PUFA The main omega 3 fatty acids- eicosapentaenoic acid (EPA) and docoda hexaenoic acid (DHA) are high in fish oils, fish oil capsules and ocean fish. Most studies have shown that omega 3 fatty acids do not affect total cholesterol; however, they do increase LDL cholesterol (5 to 10 %) and decrease triglycerides (25 to 30 %). LDL cholesterol tends to be raised in patients with hyper triglyceridemia and lowered or unchanged in normal subjects fed concentrated sources of omega 3 fatty acids. Omega 3 fatty acids lower triglyceride levels by inhibiting VLDL and apo B- 100 synthesis and by decreasing postprandial lipemia. The effects of omega 3 fatty acids on triglyceride levels are dose dependant; that is higher doses produce greater effects. Their greatest clinical utility, therefore, is with hyper lipoproteinemias in which the triglyceride level is also elevated. Omega 3 fatty acids affect many other steps in atherogenesis; most notably they are precursors of prostaglandins that interfere with blood clotting. Therefore high intakes prolong the bleeding time. It is now postulated that consumption of fish and fish oils rich in EPA and DHA will lower cholesterol, LDL, and triglycerides level with a subsequent reduction in sudden cardiac death rates. Consumption of as little as one fatty fish meal per week (5.5 g of omega 3 polyunsaturated fatty acid per month) resulted in a 50 per cent decrease in the risk of cardiac arrest after adjustment for all other risk factors. Dietary supplementation with 1 g of omega 3 PUFA daily reduced the relative risk of CVD death, non fatal MI, and non fatal stroke in patients who had recently survived an MI. Thus omega 3 PUFA has cardioprotective effects in primary and secondary prevention. 4.2.3 OMEGA 6 / OMEGA 3 RATIO It has been postulated that human evolved by consuming a diet lower in saturated fat and higher in omega 3 fatty acids than is consumed today. Humans can convert alpha linolenic acid to Eicosa pentanoic acid and the longer docosa hexenoic acid. The modern diet is rich in omega 6 fatty acids from animal protein and especially from oils extracted from grains, such as corn and safflower oils, with an estimated omega 6/ omega 3 ratio of 8:1 to 12:1. Humans can desaturate and elongate ALA into EPA and DHA but only when the omega 6/ omega 3 ratio is low. Excess omega 6 fatty acids in the diet saturates the enzymes and prevents conversion of ALA into longer EPA and DHA forms. Because the optimal ratio has been estimated to be 2:1 to 3:1, four times lower than the current intake, it is recommended that humans consume more omega 3 fatty acids from vegetable and marine sources. ALA can be obtained from flaxseed (57 per cent), canola (8 per cent ) ad soy bean (7 per cent) oils and green leaves in a few plants. Sources of the longer EPA and DHA omega 3 fatty acids are primarily marine: cod liver oil, mackerel, salmon and sardines, as well as crab, shrimp and oysters. The FAO and WHO recommend omega 6 and omega 3 fatty acid ratio to be between 4:1 and 10:1.
Those Eskimos living in Greenland and fishing community in Japan, who have a daily consumption of fish is 200 400 g, enjoy complete freedom from cardiovascular diseases. The beneficial effect of dietary fish is attributed to the fatty acid composition of the fish. Fish are good source of omega 3 fatty acids especially fatty fish such as salmon. Consumption of 100-200g of fish two to three times a week helps to prevent heart disease. Vegetable substances like mustard oil, flax seed oil, canola oil, soyabean oil and walnuts are good sources of omega 3 fatty acids. Moderate levels of linolenic acid are present in groundnut and rice bran oil. The daily consumption of 10 15 g of fish oil extract, representing 3-5 g omega 3 fatty acid is probably adequate to control moderate hyper triglyceridemia. HDL levels for regular fish eater (who donot eat meat) have been shown to be significantly higher than vegetarians, vegans and regular meat eaters. The desirable percentage of calories from different fats is given in table 2. Table 2 The desirable percentage of calories from different fats Recommended fat % of Kcal Total fat <30 Saturated 8-10 Polyunsaturated 5-8 Monounsaturated Difference Ratio omega 6 to omega 3 4-10:1 4.3 TRANS- FATTY ACIDS In natural unsaturated fatty acids, the two carbons participating in a double bond each bind a hydrogen on the same side of the bond (the cis-isomer form). Here the hydrogen gets attached in the trans position with one hydrogen on opposite sides of the double bond. Trans fatty acids raise LDL cholesterol to the same extent as myristic acid and in addition lower HDL cholesterol. Thus trans fatty acids turning out to be even more atherogenic than myristic acid. Further trans fatty acids have been found to raise lipoprotein (a) levels, thus raising the risk of CHD. Trans fatty acids in the diet come from two main sources 1. Hydrogenation of unsaturated fat can occur during anaerobic fermentation in the rumen of cows and sheep. 2. Hydrogenation of vegetable oils alter the geometric structure of the polyunsaturated fatty acids from natural cis to trans forms. Only cis forms can serve as essential fatty acids to be incorporated in cell structure. Depending on the degree of hydrogenation, trans fats in food products contain anywhere from 5 per cent to as high as 40 per cent. 50 percent of trans fatty acid intake comes from animal foods and the other 50 comes from hydrogenated vegetable oils. Elaidic acid, the trans isomer of oleic acid raises the blood cholesterol when compared to PUFA; however, it has less of a cholesterol raising effect than the saturated myristic and lauric acids. Therefore consuming trans fatty acids at level 3 per cent of kilocalories will raise the LDL cholesterol levels but to a lesser extent than SFAs such as butter. Increased trans fatty acid intakes (6 per cent of energy) also lowers HDL cholesterol. Consuming appropriately homemade low fat foods, low fat dairy products, and low fat meats will lower trans fatty acid intakes.
In the process of digestion, the enzyme lipase aids in the metabolism of fat but only in the cis form although this theory has been modified by the upcoming researches that the trans fats are metabolized but it competitively inhibits the ability to metabolize essential fatty acids including omega 3 PUFA, leading to changes in the phospholipid fatty acid proportion in the aorta of heart, thereby increasing the risk of coronary heart disease. Trans fat are metabolized by the liver with a different approach than the other fats and interferes with the delta 6 desaturase. This is an enzyme involved in the conversion of essential fatty acids to arachidonic acid and prostaglandins, which are important factors for proper cell function. 5. SUMMARY Reduced intake of refined carbohydrate. Replaced saturated fats in diet with mono and polyunsaturated fatty acids. Complete restriction of trans-fats. Textbook References 1. Sumathi R. Mudambi: M.V.Rajagopal, (2012), Fundamentals Of Foods, Nutrition And Diet Therapy, 6 Th Edition, New Age International Publishers, New Delhi. 2. Michael J Gibney, Barrie M Margetts, John M Kearneyand Lenore Arab,(2005), Public Health Nutrition, Blackwell Science, United Kingdom. 3. L.Kathleen Mahan, Sylvia Escott- Stump, (2000), Krause s Food Nutrition And Diet Therapy, Saunders Publications USA, 11 Edition. 4. B.Srilakshmi (2011) Dietetics, New Age International Publishers, New Delhi,6 Th Edition. Journal references 1. Dorola Szostatwegierek, Longina Klosiewicz- Latoszek, Wikter B Szostat, Barbara Cybulska (2013) Role of Dietary Fats for Preventing CVD- A Review.Institute of Food and Nutrition, Warsaw Poland. 64 (4) : 263-269. 2. Penny M. Kris- Etherton (1999) MUFA and risk of CVD. AHA science advisory. 100: 1253-1258.